Can asymptomatic people spread covid-19?

Covid-19 spreading asymptomatically in a crowd

One of the most contentious issues when it comes to covid-19 is whether or not people who are asymptomatic can spread the disease. The reason is that there are major ramifications depending on the answer. If only those with symptoms spread the disease, then telling people who are completely symptom free to stay at home and avoid social contacts makes zero sense. But if even those without symptoms can spread the disease, then there is at least some theoretical basis for quarantining asymptomatic people, a.k.a. lockdowns.

My personal intuition has been that covid probably does spread asymptomatically. This intuition is based on the fact that the virus has spread so rapidly and successfully around the world, and also on the complete and utter uselessness of lockdowns (I’ll explain my thinking on this further along in the text). This is very diferent from MERS and SARS, which were both rapidly and easily contained, probably because there was no asymptomatic spread, thus making it easy to identify and quarantine those who were infectious.

Back in November I wrote an article about a study conducted on US marine corps recruits. These recruits were forced to quarantine at home for two weeks before beginning their training, and were only allowed to begin the training if they had been symptom free during that entire two week period. In spite of this, the virus was able to sneak in to the training camp and spread among the recruits. Of the recruits that were determined to have brought the virus in to the camp, most remained symptom free throughout. To me, this in itself is pretty powerful evidence that asymptomatic spread does happen. But of course, 18 year olds are not known for being reliable – maybe they were so keen to start their military careers that they went to the training camp in spite of a sore throat and head ache, and just pretended to be asymptomatic.

Since then, however, more data has been published, which can perhaps help to answer the question more definitively. And to be fair, we don’t just want to know if asymptomatic spread can happen, we also want to know to what extent it happens in reality, and what the difference in infectiousness is between people who are symptomatic or pre-symptomatic and those who stay asymptomatic. If people with symptoms are 100 times more infectious than people without symptoms, then that is for all practical intents and purposes the same as if people without symptoms are not infectious, because it means that it should be enough to contain only those with symptoms in order to effectively stop the spread of the disease. If on the other hand they’re only slightly more infectious, then efforts to contain the disease by quarantining only those with symptoms are unlikely to be successful.

An article was published in The Lancet in January that sought to establish the relative infectiousness of people with symptomatic as opposed to asymptomatic disease. It used data from Singapore’s screening and track and trace programs. Singapore screens large segments of the population for covid-19 on a regular basis. When someone tests positive for covid through the screening program, all recent contacts that have spent more than half an hour within two meters of that person are also tested. Both the “index case” and the contacts are then placed in quarantine until they test negative.

This has allowed the Singaporean government to catch a lot of people with asymptomatic infection, and to see the extent to which they are able to pass the infection on to others. This data can then be compared with the data from people who have symptomatic infection and their close contacts. So, what the authors of the study did was to take the data on everyone who spent time in quarantine as a result of being a close contact of someone with covid between August 1st and October 11th 2020, and compare the relative rates of secondary infection among those exposed to someone with symptomatic covid and those exposed to someone with asymptomatic covid, as diagnosed by PCR.

A total of 628 index cases and 3,790 close contacts were identifed (roughly six close contacts per index case). 5.2% of the contacts of symptomatic index cases developed covid-19 (i.e. switched from having a negative to a positive PCR test) during their quarantine period, as compared with 1.6% of asymptomatic index cases. On the face of it, this would suggest that people with symptomatic disease are roughly three times more infectious than those with asymptomatic disease.

Of course, there is a factor that makes this result more difficult to interpret, and that is the false positive rate of the PCR test. Data from real world testing suggests that the false positive rate of the PCR test is well below 1%. In Australia, as few as 0.2% of tests have been positive for much of the pandemic. If we assume that this number is in the ballpark, and subtract 0.2% from the two numbers provided above from the Singaporean data, that would give us 5.0% infected among contacts of symptomatic people, and 1.4% infected among contacts of asymptomatic people, which would still suggest that people with symptomatic infection are roughly three to four times more infectious than people with asymptomatic infection.

One major issue with this study, however, is the fact that all of this is observational data. The contacts haven’t only been in close contact with the known index cases. They’ve interacted with lots of other people too. How do we know that the supposed index case is the person that actually infected them? We don’t. So technically, it could actually be the case that every single one of the people that became infected after spending time with an asymptomatic person was actually infected by someone else who was symptomatic. If that’s the case, then people who are symptomatic are infinitely more infectious than people who are asymptomatic. It’s impossible to know for certain.

In order to be able to figure that part out, you would need a randomized trial, where you keep your study objects in a cage and cut them off from all contact with other people for a month or so, then introduce them to someone with either symptomatic or asymptomatic covid-19 and see if they become infected. Well… I guess it doesn’t have to be a cage…

Since that trial design would be difficult to get approved by an ethical review board, we have to look around for an observational study that accomplishes something similar. Luckily, a Japanese study, recently published in the International Journal of Infectious Diseases, does just that. Like Singapore, Japan has had an extensive track and trace system in place since the beginning of the pandemic. The study describes the first cluster of cases identified in Japan, back in January 2020. At that time there was virtually zero societal spread in Japan, so for anyone who was a close contact of a known index case, and who subsequently developed covid-19, we can be reasonably certain that it was the known index case that infected them.

It began with a tourist from Wuhan. The tourist infected a person who subsequently went to a party in Tokyo on January 18th, at which ten people were infected, four with symptomatic covid, and six with asymptomatic disease (it must have been quite a party!). Of the six asympomatic people, one went on to infect two people. One of these developed symptomatic disease while the other remained asymptomatic. The asymptomatic person then went on to infect two more people, both of whom developed symptomatic disease, one of whom died.

What does this prove? Well, it’s observational data, so it’s hard to say that it proves anything. But considering how little societal spread there was at the time, it seems highly likely that the people identified as having spread the infection to others further down the chain actually were the spreaders. This study therefore provides pretty strong support to the notion that people with asymptomatic disease, who remain asymptomatic (i.e. who aren’t just pre-symptomatic), can spread the disease on to others, who then go on to develop symptoms.

Overall, 36 people were identified in the cluster of infections arising from the tourist from Wuhan. 23 of these were symptomatic, while 12 remained asymptomatic (one had unknown symptom status). Overall, people with symptomatic infection were estimated to be 3.7 times more infectious than people with asymptomatic infection. However, the confidence interval was wide due to the small number of cases, with the lower bound estimate being that people with symptomatic disease are over thirty times more infectious than those with asymptomatic disease, while the upper bound estimate is that people with asymptomatic disease are almost as infectious as those with symptomatic disease.

When taken together, I think these two studies show that people with asymptomatic covid-19 can and do spread the disease, and the best estimate from both studies is that those with symptomatic disease are about three to four times more infectious than those with asymptomatic disease. That is not a huge difference. Even though people with symptoms are a couple of times more infectious than people without symptoms, those without symptoms could still be causing more infections overall.

The reason is that people with symptomatic disease will for the most part stay at home and avoid contact with other people, at least from the moment they start to have symptoms (by which time they could, of course, already have infected plenty of other people). People who are asymptomatic, on the other hand, will continue to lead their lives as normal, for example going to work at a care home or hospital, where they will come in to close physical contact with frail elderly people for extended periods. Considering that the evidence from randomized trials shows that face masks provide little to no benefit, they will then likely spread the infection on regardless of how rigorously they follow mandates to wear face masks at work. And that’s probably why lockdowns haven’t had any noticeable effect on the number of people dying of covid. Telling 30 year old office workers to work from home won’t stop the virus circulating in hospitals and care homes. Those at risk of serious disease will therefore still be exposed and infected.

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212 thoughts on “Can asymptomatic people spread covid-19?”

  1. Early on in the “pandemic” we were told that the virus can exist for periods of time on surfaces, for different lengths of time depending on the sort of surface it is. Hence the “sanitising stations” all over the place, and the preference for using card instead of cash payments.

    However, one can only do so much to avoid touching surfaces or things that may have “The Virus” lurking on them. So even if people are put in a cage/lockdown, they still have to eat etc and so various objects will still be passing in and out of their domain. Obviously in a proper experiment these objects can be cleaned before being passed to the participants, other than food of course…but in real life situations, even those who are isolating are likely to be exposed to things that may transmit the virus.

    So my thoughts are that maybe scientists should think about other ways people can get infected rather than just from the supposed “asymptomatic spreader”?

    1. I’m not sure about this article. It seems certain that the start of the pandemic was in October at the latest, there was no mass mortality until governments and medics worldwide intervened. There is no mention above of Dr Hope-Simpson who in the 1990’s following a lifetime of keeping records of influenza outbreaks put forward an explanation that explains asymptomatic infection and the rapid appearance of the disease in populations. This happened before mass air travel so was obviously mainly person to person

      1. I don’t wish to not-pick but the issue Hope-Simpson was addressing was the replacement of one strain by another over wide geographic areas in a single season. There are certainly ‘variants’ becoming successively dominant but we have yet to see any example of Hope-Simpson’s antigenic ‘shift’ though his ‘drift’ is obviously happening. Hope-Simpson’s book also discusses ‘persistent viral infection’ and the role of DIPs (defective interfering particles) in maintaining this infectious state without causing symptomatic disease. He notes that when the production of DIPs is diminished, disease results.
        We are aware of virus ‘interference’ which is similar to DIPs in its effect of suppressing disease by slowing replication, so we may have here yet another ‘confounder’, transmission may be easy and highly effective, but only causes disease in those who are virus ‘naive’ and without ‘interference’.
        It would be good to find out if this virus produces DIPs as the less pathogenic influenza viruses do, because if it does then things will get much worse when it stops.

    2. I’m not sure of this. dr Michael Yeadon stated that asymptomatic must have symptoms to spread. When the virus is in your body your immune system starts to fight it and you get symptoms. He’s adamant that asymptomatic do not spread the disease.

      1. I too aggree with Dr Yeadon about asymptomatic. I also think that controversy and its consequent uncertainty prolong fear and stress, neither of which are good for good health. BUT some of the controversy is due to linguistics: –
        1 ‘Herd immunity’ was recently redefined.
        Some use it to mean both naturally acquired immunity and vaccine-induced immunity, others mean only vaccine-induced immunity. Hence different opinions.
        2 The words ‘infection’, ‘infectious’, ‘contagion’, and ‘contagious’ seem used differently by different cultures.
        In English (UK) ‘infection’ and ‘infectious’ refer to air-borne and ‘contagion’ and ‘contagious’ to by touch. AND an ‘infection’ is not necessarily ‘infectious’ nor a ‘contagion’ necessarily ‘contagious’.
        BUT some cultures use ‘infection’ and others use ‘contagion’ for all 4 meanings.
        3 Varied use of the word ‘infection’ aids controversy about ‘asymptomatic’ and ‘pre-symptomatic’. As do coming up with the results the ‘funder’ wants and the non-rigorous nature of epidemiology compared to that of research. Epidemiologists often re-discover the already discovered wheel.

  2. Thanks for the review. Once an environmentally robust respiratory transmitted virus is established in a population that can be transmitted by aerolization, it cannot be eliminated. As the virus can stay airborne for a period of time in the aerosol, the methodological limitations of contact tracing preclude meaningful assessment as it would need to include anyone who was in the area 15 minutes before the now symptomatic person entered the area. And by definition, such a person would be unknown. I think the idiom, “closing the barndoor after the horses has left” is apt.

  3. How to explain the relative uselessness of masks and lockdown? I think that when the conclusions of a study are counterintuitive, authors should try to explain it from a physiological point of view when possible. Otherwise, can’t we hypothesize that the results are simply invalid (flawed study) ?? Agreed that, for example, most of the spreading may have taken place before the patient or the contact is put in lockdown. But what about masks???

  4. I may be missing something here, but I still don’t see anywhere in the article where the evidence is that asymptomatic people spread the disease. I was under the impression that the most of the PCR tests were generating false positives as a result of high cycle rates. Further, if asymptomatics are capable of spreading COVID, then I would think asymptomatics would also be spreading the common cold and the flu. We never responded to those infections the way we’ve responded to C19. So is this the new norm…when the regular flu season comes around, are we going to lock down, be compelled to social distance and mask up? If so, count me out.

    1. If we assume the false positive rate is 0,2%, based on the real world data from places with very low spread, then the odds that a positive test in someone, where we have a strong suspicion of infection, actually is a false positive, is low. Only one in 500 tested people will produce a false positive result. So if you test say 50 people and get five positive results, then that is so unlikely just by chance that most or all of those positives are almost certainly true positives.

      The false positive rate is a problem if you’re doing mass screening, i.e. testing people in which there is no suspicion of disease, in a population where the disease has a very low prevalence. For example if the actual prevalence in the tested population is 0,2% and the false positive rate is 0,2%, then 50% of positive tests will be false positives.

      1. Sebastian, I’m not medically trained so happy to be shown to be incorrect here, but..
        You’re claim that Australia shows the false positive rate is 0.2% seems wrong. There ARE positive cases most days in Australia, but they are in hotel quarantine having arrived from overseas (currently still restricted to under 10,000 people per week). If the false positive rate was as high as 0.2%, then when they are testing 40,000+ people a day in the community (as they are in NSW and Victoria at this very moment), they would be turning up WAY more positives which would then be found to be false results. But they aren’t. There were two positives found the other day. Otherwise false positives are barely ever mentioned.
        Have I missed something here?

      2. I didn’t say the false positive rate is 0,2% – I said it seems to be at worst 0,2%, to set a worst case scenario as a basis for discussing the risk of false positives interfering with the results. It could well be (and probably is) much better.

      3. Is there standardization of the number of PCR cycles done? It seems that with enough cycles you can generate a false positive quite easily.

        This Lancet paper put the false positive rate at between 0.8% and 4%, quite lot higher than your number.

      4. I may be wrong, since I’m no expert on lab technique (maybe someone who is can chip in?), but I think this is due to the fact that in the reviewed studies, only one primer was being used, but in reality multiple primers are often used, which improves specificity enormously if you only consider a test positive if it’s positive with all different primers. Last summer, many countries had very low rates of positive tests, often well below 1%. The false positive rate cannot be higher than the total positive rate.

      5. But you suggested 0.2% is “in the ballpark” for the false positivty rate, when Australia tests tens of thousands a day and generally has no false positives. If that’s not what you meant by that statement in the article, it certainly comes across this way.
        At least in Australia, the false positive rate must surely be much much lower than 1 in 500.

      6. Ok, maybe I expressed myself poorly. My point was that even if the false positive rate is as high as 0,2%, then that still isn’t enough to meaningfully impact the results of the study.

      7. What was or is the CT used in Australia? Under 25 or over 35?

      8. Dr. Rushworth
        Is the PCR test supposed to detect the actual virus, or just the antibodies to the virus?

      9. Taking Australia’s rate of positivity as proof of the false positive rate does not work. The total number of positive cases here are so low that all positive samples are retested and sequenced. They include weak positives in their data but are able to exclude false positives.

      10. To add my thoughts into the mix and potentially answer a few questions in this reply thread. In Australia, every state except Victoria has had a 0.1% positivity rate. The VICs have done more tests and obviously have had more virus so they lead to a national average of 0.2%.

        I spoke with a lab where I live (I am in Australia) and they said the CT threshold used for positive varies between manufacturers, but quoted one as being 41 cycles.

        In terms of the ‘false positives’ I think over time we have been talking about two different things. The first is whether the test itself produced an incorrect positive (ie a true false positive). The second is whether the person who tested positive actually had viable virus (not simply dead RNA fragments). In Australia the labs don’t attempt to culture swabs to see if the positive PCR was live virus. There have been studies that seem to show that beyond about 25 cycles, there is little chance of someone being infectious, so it is likely we’ve isolated a lot of people due to a positive PCR when they weren’t infectious. If you count those with high CT positive results as potentially ‘false positives’ then there’s probably been a lot of these, but without knowing the cycle threshold that generated the positive result (which they don’t publish) it’s hard to be sure. Recently in Victoria, the Government reclassified two cases that were originally ‘positive’ to ‘negative’. These may have been false positives. And the big deal is that the Victorian CMO called the variant ‘a beast’ on the back of the two incorrect positives….and of course the media latched on and everyone hid under their doonas

        Back to your article Dr Rushworth, I’m wondering why in the Japan study they didn’t conduct genomic testing to link index cases with secondary infections. That would answer the question as to whether the secondary case caught the virus from the index case or not.


      11. What about the ‘cycles’ run with the PCR – anything over 25-28 cycles is known to be replicating fragmented DNA virus particles but with absolutely little context. Like the toxicologist says “the poison is in the dose”. If you need to run the PCR into the 30-40 cycles to get a viral DNA fragment particle – in the context of the patient – what does that even mean? They are completely asymptomatic yet deemed positive – positive for what (having had and successfully immunologically beat it)?

      12. As ‘they’ say, a lie will travel half way around the world before the truth gets their pants on…

        Introduce the theory of asymptomatic spread, gin it up with dubious epi stats from Wuhan public health type people, WHO eats it up with nil due diligence as they are ‘managing messaging’ from the CCP and the rest of the ‘studies’ or ‘meta studies’ just muddy our rational thinking of transmission of virus.
        “Some might conclude that that study lacks the credibility one might expect for a paper published in Nature; it is claimed, for example, that they PCR-tested 92% of Wuhan’s population (~10m individuals) over a 19-day period at the end of May, and found just 300 positive PCR tests, implying a FPR of no greater than 0.003%. Further, it is claimed that while 100% of the 300 PCR positive cases were asymptomatic, there were zero symptomatic PCR positive cases out of ~10m tested during a period only a few weeks after the epidemic had peaked in Wuhan.

        If this seems incredulous, then surely that has serious implications for the way in which earlier studies from China – data from which formed a significant part of the worldwide evidence base for asymptomatic transmission – should be regarded.

        (bite of an aside -but pertinent)
        One last thing – first published in JAMA 1919, Dr Milton Roseneau did a rather stringent experiment of transmission of Spanish Flu – an utterly fascinating account of trying to INFECT subjects with the flu with little effect (worth the read). The link I post is the synopsis of the JAMA 1919 letter he submitted.

      13. How do you know that a disease has low prevalence? PCR? What is the mean false negative rate of PCR tests? What is the specificity at 27 cycles? What is the specificity at 37 cycles?

        What is the sensitivity of influenza tests?

      14. I was under the impression that the false positive rate in Australia was so low because the incidence of actual infection was low there too, and that in places where infection rates are higher, then the false positive rate will be higher too – due to several possible reasons including contamination, viral fragments in people without infection etc. So is it correct to use this low figure when considering this?

  5. In order for an asymptomatique person to spread the disease, they have to have a substantial amount of it in their respiratory tract in order to expel amounts that would lead to an infection. Is this possible without the virus replicating there and can it replicate without causing symptoms?

  6. If we run with asymtomatic spread does exist and that the vast majority of people catch covid, either have no symptoms or just slightly get sick then eventually natural herd immunity should take place shouldn’t it.

    The next question is how to handle the sickly person. Some of these can improve their health so that they’re nolonger at major risk (obesity rates have skyrocketed in most countries) According to a study by the National Institute Of Health plus other sources obesity, type-2-diabetes plus other lifestyle disorders are the leading cause of hospitalization as it pertains to covid.

    I would like to see a big push by governments and the major mass media promoting improved personal health but at least in Canada not a word in fact they close all forms fitness facilities – No money made off healthy people

    1. There are many truths in your post. The lab origin, PCR tests, asymptomatic spread (children are vectors!), denial of ivermectin (and other safe, effective therapeutics) and immunity post-true virus symptoms/experience are very serious discussions that are taking place very late in this pandemic and are causing distraction from the true goal: experimental shots.
      The shots cause serious short term harm (especially when compared to the risk of getting the virus in certain age/health strata) and we are learning of the serious long term harm in ovaries, spleen, and prostrate (to name a few). Pharma is making a boat load of money and creating patients for the academics (lots of new studies) and more pharmaceuticals to “fix” the problem.
      Sadly, science has been extensively corrupted. The distrust held by many informed, intelligent people is warranted. I watch this with great sadness as harm is being done to innocent lives. I look forward to the legal system catching up. We must demand the dissolution of those bodies of science (including scientific journals and government funding of academia) and accountability who’s intent was to do harm to benefit pharma shareholders. Criminal charges must filed. Those of us in the “progressive” west look on to a group of determined lawyers in India demanding the WHO stop the campaign against Ivermectin.

      1. Its definately going to be harder in the future if we accept this technocratic power grab Sebastian – what do you mean bu this? Any reistance to the shit show that is happenign now is good IMHO.

  7. PCR number of cycles are a problem. About the false positives, it must be remembered that there is no such thing as a perfect test : high sensibility means low specificity and vice-versa. Moreover, if the rate of infection in the population is low, even a test with a low percentage of false positives will look bad.

    1. No this is wrong. It is perfectly possible to have both sensitivity and specificity high Sensitivity is the number of people with the disease AND a positive test divided by the number of people with the disease. Specificity is the reverse, the number of people without the disease AND a negative test divided by the number of people without the disease. They are completely independent properties of the test.

      1. That is correct allright, but a point to consider is the very low PPV (positive predictive value) of the test at the low virulence level we’re (and probably will stay) in now. The (vast) majority of the positive tests will be false positives (by necessity), if we continue to test masses of asymptomatic people.
        So, the question of the asymptomatic spread really is of utter importance; as long as we stick to it, we will have reason to test at this level, and (by necessity) will quarantaine lots of people for no good reason.

      2. Oups! I should have said that to have a very high sensitivity (the test catches every infection) you have to sacrifice a bit of specificity (it also catches non existent infection). This is an accepted concept in epidemiology I think.

  8. Could you please review the actual dangers of wearing masks? I am under the impression they are few to insignificant. This might be likened to wearing condoms? The risk of wearing one is zero. The benefits (beyond planned parenthood) of protection in the relatively small chance a non-promiscuous person is likely to contract or spread an std, are clear.

    So, could you shead light on the current disputes over “harm” in wearing a mask? I may be mistaken. But when the benefits of a prophylactic against spread of disease out weigh the risks of practicing (by an order of 1m to 1,) considerate prophylactic humanism, to argue against using the prophylactic seem counter logical, counter science, if the risk of using the prophylactic are zero to none. Thoughts?

    1. Psychological harms are one that practically no one seems interested in talking about. I am done with the charade of outdoor mask wearing despite it being mandated here.

    2. I suggest you direct that question to e.g. 3M who make the FP3 masks that could be slightly effective, to ask what is the medical basis for their recommendation that a FP3 mask should not be worn for more than 1 hour. They clearly don’t fall apart in 1 hour so the reason must be medical.

      1. Here is what UK dental association says (not 3m). Interesting practical facts.. But not so useful epidemiologally.

        FFP3 masks – HSE says not for more than one-hour use

        The dental industry widely deploys disposable FFP3 masks. Yet HSE guidance doesn’t recommend continuous wear of more than one hour.

        Disposable FFP3 masks are commonly the first line of defence against COVID-19 for high risk COVID environments. In particular AGPs (aerosol generating procedures).

        Yet HSE guidance HSG53 (respiratory protective equipment at work, fourth edition, page 16) states that clinicians should only use disposable half mask-particle filters (which include FFP3 masks) for a continuous wear time of less than one hour.

        The two forms of RPE (respiratory protective equipment) it recommends for use for more than one hour are powered masks and powered hoods.

        The issues associated with the continuous wearing of disposable masks for more than one hour include a less reliable seal, and discomfort including pressure sores or skin damage on the face.

        Powered hoods or powered air purifying respirators (PAPRs) use a fan to draw air through a HEPA filter. This creates a positive pressure of clean air within the hood. Thus removing the need to seal the hood to the face.

        PAPRs are reusable and are more comfortable for long-term use, as they do not form a direct seal to the face.

      2. This paper is/was interesting, but I understand that it has been removed from Oralhealth for obvious reasons – ‘Why Face Masks Don’t Work: A Revealing Review of Their Inadequacies. Yesterday’s Scientific Dogma is Today’s Discarded Fable.’ By John Hardie, BDS, MSc, PhD, FRCDC in oralhealth October 2016.
        The gist is that in use there is no evidence of mask efficacy in dentists’ surgeries but, and this is important in the context of the current discussion of transmission of disease, dentists as a profession of mask users have greater immunity to more aerosol virii than other medical professions, almost certainly due to daily exposure to asymptomatic harbourers of transmissible diseases. The constant exposure to low levels of pathogens seems to be a good way to maintain a strong immune system!

      1. Thanks. It seems logical that “claustrophobic” anxiety “could” increase, yes, as the good article points out. I wouldn’t reject that that happens. Any epidemiological estimates would help. This comment is NOT directed toward you.

        But it is curious to me that of the core covid-19 skeptics who believe that their chance of severe injury or death, or their chance of infecting another, from it is so low, they would rather take the risk of getting it and spreading it that use a prophylactic against it. Sounds reasonable. Yet their risk of adverse reaction to a vaccine, if my maths are correct, are even less than getting severely or spreading the virus.

        Its like saying: here is a revolver with 1oo,ooo chambers and one bullet in one of them. Here is another revolver with 200 000 chambers and one bullet in one of them. You are to choose one revolver, and point it at your elderly mother or neighbor who is someoneelse’s mother, spin the chamber and pull the trigger once a day, every day (spinning the chamber before every shot). And the person chooses the 100 000 chamber revolver because being told to choose the 200 000 chamber revolver infringes on his right to choose. I never will get that.

      2. Re: pointing revolvers. Fifteen months ago, someone a mile from my house died of COVID. Since COVID is so contagious, I’ve likely been exposed to the disease. No matter what I do, everyone will be exposed to it. The novel vaccine, on the other hand? I haven’t been exposed to it, don’t know what the long-term effects are, and the risks aren’t zero. Many drugs that were FDA approved (not just EUA) eventually got a black-box warning or were taken off the market due to their side effects.

      3. IF vaccines work somewhat to reduce mortality and morbidity from covid, THEN they might be worth the risk of ADE’s down the road. However, the vaccine trials don’t boost my confidence in them.

        Meantime, it seems that trying to stay healthy and have a decent diet with a backup of elderberry concentrate (anglo-saxon folk medicine) looks like the way to go.

    3. For what they’re worth, if anything, my personal thoughts on masks: –
      1 Our faces are our personal identity. Bank-robbers wear masks because no ID is no responsibility, thence no inhibitions about robbing.
      2 Pathogens tend to thrive in warm and damp environments. e.g. warm, damp, airless bathrooms rapidly culture black moulds.
      Masks become warm and damp. Air we exhale is not sterile, nor are masks worn for hours, or repeatedly, or after being dropped on the floor.
      Incubated pathogens inhaled from masks give our immune system more to combat than from unenclosed air.
      Operating theatres are sterilised and masks used there clinically disposed of.
      BUT masks used in public are not treated as clinical waste.
      3 The tiniest particles from the mask fabric or from detergents used for washing masks are inhaled into the deepest part of our lungs.
      AND stay there, damaging our lungs and reducing ability to breathe from then on.
      Particularly in atopic persons, life-long respiratory illness caused by micro-particles can be seriously debilitating.
      Masks are made from and/or coated with chemicals and are recently popular.
      BUT so was asbestos.

    4. Quite apart from protective aspect (or not), we are likely breathing tiny polypropylene fibers from the masks into our lungs. Could this have long term effects on lung disease, particularly in children? Also, many brands of masks have been found to contain heavy metals and dangerous chemicals like formaldehyde. What will be their effect on health for people who have to wear them all day (e.g., school kids).

      Then there’s the environment impact of disposing of something like *100 billion* masks worldwide a month.

      1. Thank. Interesting speculations. Some people do wear them as part of work, daily for years. Do we have any data on health injuries to surgical nurse?

        Disposal is an issue. Like with pop cans, I can imagine a solution could be found?

      2. Sweet,



        Wearing masks in a climate-controlled operating suite while uninfected with an ILI is very different from wearing masks in high humidity environments like New Orleans or while wearing masks while infected with an ILI in a dry climate. Masking in high humidity environments risks bacterial infections. Masking while infected in a dry environment risks re-breathing one’s own exhaled virus, which includes virus from large droplets.

        Going unmasked prevents inhaling virus from large droplets because they simply fall to the floor.

        Masking in a dry environment _might_ reduce viral output to 70% of unmasked output, if large droplets are ignored.

        Masking in a humid environment is really too dangerous to advocate for public health.

  9. There are contact tracing studies, which you seem to have missed, that demonstrate that very few asymptomatic PCR-positive patients spread the disease, even to close family members living in the same household.

    Annals of Internal Medicine, contact tracing study shows that asymptomatic patients don’t spread the virus; the virus is predominantly spread via prolonged contact with household members. The virus was least likely tp spread in public transportation and most likely in the household. Severity of symptoms is directly correlated with risk of infecting others.

    Another contact tracing study shows asymptomatic patients don’t spread the virus.

    JAMA meta-analysis confirms that asymptomatic patients don’t spread the virus.

    1. Actually, the Annals study showed that asymptomatic people do spread the virus, but at a lower rate than people who are symptomatic, which is what the studies discussed here found.

      The second study is a case study of contacts of a single person. There’s plenty of evidence to suggest that most people with covid are not infectious, while a minority are highly infectious. So finding that one person didn’t spread their infection to anyone else doesn’t prove anything.

      The third study is a meta-analysis, and the conclusions concerning spread of infection within households from symptomatic vs asymptomatic people come from different studies using different methodologies, not studies that have directly compared symptomatic vs asymptomatic spread. In other words, the comparison is highly suspect.

      1. If the asymtomatic are infectious, then it is hard to explain the fact that a very small number of comunity dwelling ‘vulnerables’ have gotten the disease. Even with lockdowns, the elderly in the community have some contacts, and one can assume that all of these are asymptomatic. The risk of catching Covid in Canada turns out to be high for those in instutional settings – care homes, prisons and hospitals. All the latter have air circulation between rooms, usually with some sort of Hepa filtration.

        I am afraid that govenments were paniced into a strategy that it is hard to back out of. Add to that a bunch of backroom health personnel being suddenly given star billing in the news, income support for millions of layabouts, and people on fixed incomes too stupid to realize they will pay for it all with inflation. In case you think that ‘layabout’ is too severe, business people I know are now being told “I can only work 2 days/week or I’ll lose my benefits” when they try to hire – all those I know are having this problem.

  10. This is ridiculous. You don’t diagnose someone with a disease with a PCR test. If you don’t have symptoms, you aren’t sick and you certainly aren’t contagious. In order to be contagious (shedding virus), you have to reach a certain viral threshold. By then, you will have symptoms. There is no asymptomatic spreader. That was the deliberate lie to justify all of the BS lockdowns and mask mandates. They’ve been searching for the mythical asymptomatic spreader the whole time and haven’t found one yet. A positive PCR test means nothing. At the cycle rate they’re using, the false positives are around 85%. You would need to follow up with an antigen test to verify an actual infection. The number of actual infections and actual covid caused deaths is much, much lower than what they’re claiming. There’s an agenda here.

    1. ” If you don’t have symptoms, you aren’t sick and you certainly aren’t contagious. In order to be contagious (shedding virus), you have to reach a certain viral threshold. By then, you will have symptoms”

      Dr Rushworth’s review of the evidence suggests this statement is completely false. Please review the evidence yourself and comment on why his interpretation is not correct.

      1. Dr. Rushworth’s analysis is inadequate. One thing we can be certain about is the incredible amount of uncertainty about PCR with respect to unculturable positives and Dr. Rushworth’s analysis relies upon the uncertainty of PCR positives without any confirmation using viral culturing.

        Indoor spread is a bigger problem than asymptomatic spread and perhaps hospitals and private parties (perhaps just a party of two) are the locations where spread looks to have been done. People don’t stop having sex just because an epidemic is on. Also, private parties don’t care about lockdowns.

        And consider people who cannot afford to take time off just because they may have symptoms. In the US, illegal immigrants cannot afford to take time off and frequently live packed in apartments.

      1. Dr. Rushworth made a statement of faith when he claimed that science and faith are mutually exclusive. I haven’t seen any RCTs backing his claim.

    2. One of the problems is that the symptoms may be pretty subtle – a bit of a headache or stuffy feeling, not full of normal energy. But since you had that fight with boss/girlfriend, drank a couple of glasses of wine, got woken by a thunderstorm…….. the night before, you attribute the symptoms to the normal stresses of life. It is probable that common garden colds and flu are spread by people who are not really sick enough to feel sick, but at a lower rate than the person who goes to work streaming and coughing.

      Is this a reason to shut down all normal activity? There is risk in living, but living is preferable to this crazy state of panic induced by government and media fear porn.

  11. Didn’t think I’d need to point out that PCR is not an indicator of infectiousness. The low false positive mentioned pertains to whether the test incorrectly detected the presence of a molecule. But in mainstream discourse, positive PCR has been conflated with infectiousness, even at cycle counts like 40 in common use.

    1. Absolutely, the PCR test in itself says nothing about whether you are currently infectious. A PCR test can mean you had the infection a month ago and are now only producing viral remnants, or that you were infected four days ago and are now shedding live virus. This could actually make those who are asymptomatic seem less infectious than they are, because those with symptomatic infection will be discovered at a time point when they are shedding virus, while those with asymptomatic infection found through screening can be found at any point during the time period where they have some virus in their respiratory tract, which could be long after they stopped shedding virus.

      1. Sebastian , so the Swedish Fotball player that had Covid 19 in January and still have antibodies and now have a positive PCR test again, is probably not having Covid 19 ? It is then a “false poistive” test. I have a friend that had the same, but in his case it was more than a year between the first infection (yes he still had antibodies after more than a year) and the 2nd positive PCR test. So a positive PCR test if you have had Covid does not say you have it again ?

      2. It could be a false positive. Or it could be reinfection. Immunity doesn’t mean you can’t be reinfected, just that the immune system reacts much more quickly and effectively the second time around.

      3. Thanks for your thoughtful and balanced review of asymptomatic transmission. The only comment I have is that covid symptoms are so general, variable and often so mild that ‘asymptomatic’ may not be a very useful term for what is actually a low grade infection with, e.g. a headache and an occasional cough. Semantics are definitely part of the reason this debate is so contentious.

        PCR, of course, is the main reason we have so little good data, that and the seemingly deliberate obscurantism of governmental health bodies. If only tests that demonstrated actual infection, such as viral protein tests are supposed to do, were used, then we would have a much better idea of what is going on.

        Thanks also for mentioning the very low rate of false positives in Australia. That does seem to undermine the claims of high levels of false positives – at least in countries with well run testing programs.

        My impression here is that the Australian testing has been well designed, but it is just an impression from reading guidelines that fairly thoroughly cover the things that could go wrong – not from any knowledge of how things have been done in practice.

  12. Virus mania is a book that is well worth reading.
    The authors explain that orthodox virology is completely wrong and show that the claims of the ‘expert’ virologists are based on the most shoddy science imaginable.
    It is well worth a read, if you are like me (a lay person), you will probably be shocked at how poor/fraudulent orthodox virological science actually is.
    Those that claim that sarscov2 has not been properly isolated, identified and proven to cause the disease covid19 are correct, the mind blowing thing is that no virus has ever been isolated, identified and proven to cause the disease attributed to it.
    If the authors are correct then not only is the sarscov2 virus a colossal fraud then so is pretty much all of virology, and given the fiasco of the lockdowns and the vaccines who would doubt the possibility?

    1. So far it’s been an interesting read. I’m curious about the opinions of others who have read it.

      1. I reread your article on the recruits study.
        “Overall, 1,9% of participants became PCR positive during the two week period, in spite of all the measures taken to prevent spread, although only four people developed symptomatic covid.”
        These measures taken (wear face masks at all times, always be at least six feet apart, wash their hands regularly, were not allowed access to electronics or other items that might contribute to surface transmission of the virus, all movement was unidirectional, and every building had separate entry and exit points, to keep people from getting too close to each other ) clearly betray a huge bias for spread primarily by large respiratory droplets.
        “In some ways I find this the most interesting result of the whole study. The fact that you can go from a single infected person to nine infected people in one platoon over the course of a two week period, in spite of the use of extraordinarily stringent methods to prevent spread, shows how unbelievably infectious SARS-CoV-2 can be. ….. This study clearly shows how effectively the virus spreads even when extremely repressive methods are being used to contain it. In spite of strict physical distancing, rigorous hand and surface hygiene, face masks, PCR based screening, daily symptom checks, and two weeks of quarantine before even arriving at campus, the virus still snuck in and was still able to spread effectively among the recruits. The stringency of the measures that were put in place among the recruits was far more extreme than anything that could be accomplished in a civilian setting. And yet, in two of the platoons, the virus still spread like wildfire.”

        My point is: these extraordinarily stringent methods to prevent spread probably are of very little use, if the virus is airborne. If the virus is airborne, as I conclude from the relevant research, these results are by no means a proof for the unbelievable infectionousness of sars cov-2 (as you rightly state at the end, “there is no control group, so it’s impossible to say what would have happened had there been no lockdown-like restrictions”; there should have been). They seem to validate though your hypothesis that some are/can be very infectious, others hardly.
        You have not convinced me, so far.

    1. On an individual level it’s impossible. So we have to look at the relative statistical probability that someone is a true positive or a false positive. That’s why the Japanese study is useful.

      1. And the relative statistical probability is still based on PCR tests. You are going down the wrong road.

        Assuming that flu is tested with PCR and cycled at 27 and covid is cycled at 37, what are the odds of a flu misdiagnosis versus a covid misdiagnosis?

        Even using an increasing positive rate for evaluating where a population is on the Gompertz curve is full of potential pitfalls (confounders). What if people are tested multiple times? What if testing increases? What if major employers begin testing? What if people start traveling because of vacation season or ski season? There is no alternative to doing viral culturing when evaluating population spread of covid or viral transmission for research purposes. If you are relying on viral transmission PCR data without viral culturing, you are simply fooling yourself.

      1. This approach to pin down spread on asymptomatic people is rooted in germ theory. It puts the cart before the horse.

        If you look at this from the perspective of terrain theory, you’ll see that the wrong questions are being posed here.

        We need to look at the overall health of an individual first before assigning blame to an asymptomatic vector. This applies to Typhoid Mary, who carried a microorganism, but her body’s healthy immune response was able to keep it in-check.

      2. Typhoid fever is a bacterial disease (Salmonella enterica), as you know. It is not surprising that a bacterium can replicate, inside a host, without producing symptoms. The bacterium merely requires to obtain nutrients from the host.

        A virus, by contrast, can replicate only by commandeering the host’s cells. The phenomenon of cells becoming virus factories possibly qualifies as a symptom, in its own right, but, regardless, seems highly likely to become macroscopically observable (i.e. to cause symptoms perceptible to patient or doctor), once it’s occurred to a material extent.

        Thus, I suggest the history of Mary Mallon adds little credence to the theory of asymptomatic CoViD-19 transmission.

      3. Well, there are plenty of viral diseases that are known to be able to replicate asymptomatically in the human body and spread from an asymptomatic host to another person – HIV, EBV, hepatitis B, hepatitis C, HPV, herpes simplex, to name a few.

      4. There is limited evidence that Typhoid Mary carried salmonella in her body–basically stool samples. And there is evidence that she did not which were samples she provided. None of the theories of asymptomatic spread rely on RCT evidence. The Typhoid Mary case is anecdotal at best from a time when germ theory was poorly understood. Quite possibly Mary Mallon simply was a vector whenever she cooked and salmonella was carried in some cooking ingredient used by Mallon.

      5. I see Typhoid Mary brought up all the time, and I have read as much as I can find about her, but the claim she had no symptoms is not based on evidence. Sure, she didn’t exhibit severe typhoid symptoms but you are asking me to believe she never had diarrhoea (or constipation), a slight fever, or never felt a bit unwell?

        It seems more likely to me that Mary Fallon had a tolerated but chronic infection – my understanding is that there are others with similar infections that are better studied. It may be that the covid induces similar infections in some people, but there is no data supporting widespread asymptomatic spread of the disease.

  13. Once again, thank you for clearly analyzing and explaining the data re. these issues. I appreciate it!

  14. I’d think there would be two types of asymptomatic, those infected according to their PCR test who later developed symptoms (i.e. pre-symptomatic) and those who never really knew they had anything except an iffy PCR test told them so. Would be interested in what the minimum infective dose is.

    Rat studies have found just one Virion can infect, but that’s in the lab. Other estimates are 500 – 1000 Virions in the real world. I have no idea how accurate these estimates are.

    I’d speculate that the lower the minimum infective dose, then the more likely it’s an escaped bioweapon.

    The insistent mainstream narrative of zoonotic origin (which one top doc puts at Far Less than 1% in his 193 pp Bayesian analysis) might be motivated by a desire to stop bioweapon speculation, and that we’re now in the era of biowarfare (and the Devil take the hindmost).

    1. I have seen figures of 300 virions to cause an infection and 1 minute of talking by a symptomatic carrier produces 750,000 .

  15. What about the Wuhan study of 1 million individuals Sebastian – the rate of asymptomatic spread was very low as far as I remember?

    1. Well, firstly it’s a Chinese study and I don’t trust anything coming out of China that relates to covid, because it’s been vetted by the Chinese government, who have probably told the researchers what results to produce.

      Secondly, they found 300 positive tests, not one of which had any symptoms, out of 10 million tested people. That result in itself defies belief. Most studies have found that 50-70% of those infected with covid develop symptomatic infection, but here they’re saying that 100% were asymptomatic. Considering only 300 positive tests out of 10 million, and all asymptomatic, the only reasonable conclusion, if you decide to actually believe the numbers, is that all 300 are false positives. Even if all are false positives, that still gives by far the lowest false positive rate estimate I’ve seen anywhere. Additionally, all 300 had negative cultures when cultured, which confirms that these 300 were all false positives.

      So the Wuhan study isn’t useful. The only thing it shows is that the Chinese authorities claim to have completely eliminated covid in Wuhan by May 2020. That’s a claim that I am very skeptical of.

      1. ‘Secondly, they found 300 positive tests, not one of which had any symptoms, out of 10 million tested people. That result in itself defies belief. ‘

        If you set your PCR test for a sufficiently low number of cycles you could get zero positive results if that what you want, set it high enough and you will get hundreds of thousands.
        Isn’t this the beauty of the PCR when organising an international pandemic fraud such as cv19?

      2. Thanks Sebastian – But by the same token I don’t trust any research unless is clearly independent. Let’s face it – it is probable that both the Chinese and the Americans know where the virus came from and who released if. I don’t believe for one moment that the the origin of the virus would not have been traced by now. Conspiracy theory is now transitioning to conspiracy fact and Even the narrative in the MSM is finally starting to shift to one that accepts that it was almost certainly lab based. Heck, even Twitter have deemed it Tweetable. This is an information war and a biological war (now) – its hard to parse out truth but your honest and open analysis certainly helps. Much appreciated.

      3. “I don’t trust anything coming out of China that relates to covid”

        And you DO trust stuff coming out of the West? Christ.

        The Chinese probably lie about some things some of the time. The West lies about everything, all of the time. Wake up.

  16. I’m so sick with so many diseases, luckily I’m symtom free, maybe I need a test to put my mind at rest, better still just lock me up so i can’t spread it around, vaccinate me and feed me BS.

    1. I called my employer and told them I need to go on paid sick leave because I have asymptomatic typhus.
      Zero symptoms is how you know you have it, typhus is just as sneeky as covid.

  17. The subject of whether asymptomatic individuals can spread this, and possibly by extension other respiratory viruses, is I feel the most important aspect we need to understand about this whole pandemic and is the thing that in my view has caused the use of lockdowns, and mask wearing, etc to become the standard response across most of the western world.

    Traditional pandemic response plans never looked at quarantining healthy people, only those who are sick. The Swedish response of informing the population of the risks of the disease and, for the most part, only recommending the minimal modification of individual behaviour by encouraging modest social distancing, personal hygiene, isolating if ill etc effectively followed those pre-COVID pandemic plans.

    However, because it was believed that with SARSCOV2, correctly according to this article,
    asymptomatic people can spread the virus it was rationalized that anyone, anywhere at anytime could be unknowingly infected and therefore placing others at risk unless their behaviour was controlled by the state with lockdowns, mandatory mask wearing etc. . This results in the fear campaigns such as the ‘Act As If You Have It’ in the UK and leads the population to become fearful of their fellow citizens since any one of them might be a vector of a deadly disease which will make them ill or cause their death or that of their loved ones.

    My biggest concern is that this fear is now so ingrained in the population it will not leave us for a very long time and an unfortunately large segment of the population will be calling for these types of restrictions every year when the respiratory season arrives as it always does.

    I’m concerned that as we come out of this pandemic if the public isn’t properly informed that because the virus spreads by, as we now know, aerosols, and mainly indoors, things like lockdowns and masks have minimal if any effect on viral spread but major effects on other health and economic impacts. If this isn’t widely promoted to society the population will continue to believe that lockdowns and masking worked and this will be the default response going forward.

    Governments and the media have been complicit in giving the public the sense that everyone is not only at risk of catching this virus, which is true, but also of dying from it which we know is not the case but try convincing a frightened population of this.

    Here is a great blog post from Canada that looks at the official government of Canada data on deaths from COVID and in whom and where they occurred which I think is relatively consistent with what happened in other countries. Deaths are mainly in the old and health compromised population and occurred primarily within institutionalized settings such as care homes, hospitals, prisons etc.

    In British Columbia where I live we have a population of 5-5.5 million and have had around 1700 deaths over the course of the pandemic yet I still see on average 50 to 90% of people wearing masks outdoors when it is known that outdoor spread poses minimal risk.

    I fear for our future

    1. The Swedish experience (and that of anti lockdown US states) proves that lockdowns, distancing, masks, forced business closures, school closures, abolition of group events and protesting (unless protesting for politically correct causes) were all a colossal waste of time.
      We have been relentlessly lied to and propagandised so as to get people to accept the rushed gene therapy injections and as a way of imposing the vaccine passport system.

      1. The Chinese experience — BRIEF, VERY EARLY lockdowns, with that precious time used to develop effective treatment protocols, institute contact tracing, etc. — were spectacularly successful. In the West, it was different. TOO LATE, TOO LATE, TOO LONG, and with the time squandered (no good contact tracing, and especially NO EFFECTIVE TREATMENT ALLOWED)… result was disaster.

  18. How can you say that somebody is “diseased” when he has no symptoms at all??? That is just nonsense isn’t it. That would mean that if I got tested for rhinovirus and the test came back positive, I had an asymptomatic cold? Sounds crazy

    1. It sounds crazy because it is. You already have had lots of previous aliments, but recovered, because you had a healthy immune response. What is being done here with asymptomatic testing is trying to prove that your healthy immune response is not good enough for society.

  19. Not Dr. Rushworth’s fault of course but once again the depressing conclusion is that we don’t really know. Basically we have made zero progress since spring 2020 apart from the vaccines of course (if they turn out to really work) There is no cure and all we did is inflict terrible harm with basically useless NPIs, when we should have just carried on with our lives and let natural immunity build up, the outcome would have been largely the same I suspect.

  20. You’ve left me confused? My understanding is that SARS-Cov-2 is the virus of which the disease Covid-19 is a relatively unusual consequence that affects mainly the old and already unwell. So, with that understanding, younger healthy people could spread SARS-Cov-2 but not COVID-19?

  21. This study suggests that asymptomatic spread is related to specific covid variants. It might explain some of the differences in study outcomes: some showing asymptomatic spread, some showing none or minimal.

    Decoding Asymptomatic COVID-19 Infection and Transmission
    “One of the major challenges in controlling the coronavirus disease 2019 (COVID-19) outbreak is its asymptomatic transmission. The pathogenicity and virulence of asymptomatic COVID-19 remain mysterious. On the basis of the genotyping of 75775 SARS-CoV-2 genome isolates, we reveal that asymptomatic infection is linked to SARS-CoV-2 11083G>T mutation (i.e., L37F at nonstructure protein 6 (NSP6)). By analyzing the distribution of 11083G>T in various countries, we unveil that 11083G>T may correlate with the hypotoxicity of SARS-CoV-2. Moreover, we show a global decaying tendency of the 11083G>T mutation ratio indicating that 11083G>T hinders the SARS-CoV-2 transmission capacity. Artificial intelligence, sequence alignment, and network analysis are applied to show that NSP6 mutation L37F may have compromised the virus’s ability to undermine the innate cellular defense against viral infection via autophagy regulation. This assessment is in good agreement with our genotyping of the SARS-CoV-2 evolution and transmission across various countries and regions over the past few months.”

  22. your “intuition“ tells you! are you a marabout or a doctor? asymptomatic transmisson has NEVER been the major driver of the spread of a respiratory virus! one who presents NO symptoms has either beaten off the virus with a strong immune system and/or has been subjected to a low viral load. in either case if they where to shed any virus it could only be beneficial to others, like a natural vaccine!

  23. My wife says: Never trust a man’s intuition. My 40 y. experience living with her tells me to trust hers. My personal male intuition has been that covid very probably does not spread asymptomatically.
    You state: “….. while a minority are highly infectious.” Wouldn’t it be logical to suspect that this minority at least should be symptomatic? How could an asymptomatic person be highly infectuous? Johnny Ray seems to be right when he states: “In order to be contagious (shedding virus), you have to reach a certain viral threshold. By then, you will have symptoms. There is no asymptomatic spreader.”
    To me the idea of someone being ill while being and staying asymptomatic is, well, is ridiculous: either you show symptoms and therefore are, more or less, ill, or you show no symptoms and are, well, healthy. The idea that someone who is healthy (a presymptomatic ill person is not healthy) can make another healthy person sick is somehow very unlikely and seems to be, if at all, the exception and not the rule.
    You consider ‘Typhoid Mary’ (some 100 y. ago) to be a counterexample to my intuition. Typhoid – a bacterial disease – is not a respiratory disease, it spreads along other paths than coronavirusses. Even when it is a well enough documented case: it still is exceptional, isn’t it?
    I consider the aerosol theory – viral spread through little droplets – to be very plausible. One of the consequences is that spread takes place (almost completely) inside and not outdoors (allthough it is not impossible), implying that distance to a spreader is (far) less relevant than the viral load that is actually in the air and the spreader could long be gone and still continue infecting others.
    There are more questions to be asked . Does, e.g., showing symptoms (that are in no way symptomatic for covid19 only), in combination with a positive pcr test prove someone actually has covid19? It could be a false positive, or a true positive after say 35 cycles in combination with a soar throat or whatever symptom from another virus or whatever cause.

    1. There appears to be a widespread misunderstanding that symptoms are caused by the pathogen. Symptoms are rather the visible expression of the immune system’s defence against the pathogen. It was well established long before covid that people with respiratory viral infections are shedding the most virus immediately before the onset of symptoms. The moment the immune system starts to react, for example by raising body temperature, viral shedding drops precipitously. So there is nothing remotely implausible about the idea that people with asymptomatic infection can be infectious. But I don’t personally care either way. All I care about is what the evidence shows, and the evidence that exists at this point strongly suggests that people with asymptomatic covid do spread the infection.

      1. I would call this pre-symptomatic spread (“immediately before the onset of symptoms”). That is not just a difference in semantics . What would be a semantic discussion is what one would call a ’cause’. “Symptoms are rather the visible expression of the immune system’s defence against the pathogen.” Well, if the immune system’s defence is caused by the pathogen, why wouldn’t it be permissable to call the pathogen the cause of the symptoms through causing the immunesystem tot react?
        In this and the november article you seem to suggest that asymptomatic spread without any onset of symptoms is evidenced. I have commented on the recruits article above, considering that from the perspective of airborne spread this study is by no means a valid support for this hypothesis.

      2. What is the impact on infected cells when SARS-COV-2 exits? If SARS-COV-2 isn’t prevented from multiplying, won’t it eventually destroy so many cells that some sort of symptoms will occur at some point? What mechanism is there to limit the multiplication of virus once infected other than the immune system?

        Are there asymptomatic spreaders who never clear SARS-COV-2? Any studies showing this? And if asymptomatic people eventually clear the virus, how does this happen? And how can it happen without symptoms?

        Can SARS-COV-2 go dormant? Any studies?

        I would have more confidence if someone bothered to culture SARS-COV-2, which _must_ be done in research into viral transmission.

      3. I find it very hard to believe that perfectly healthy people without any disease symptoms can spread viral disease, and it seems like immunologist professor emeritus Beda Stadler agrees. He says that the idea of asymptomatic transmission is ‘a ridiculous assumption’…

        ‘If people without symptoms could spread viral diseases, every school boy could claim that he had to stay home from school for two weeks because he had influenza without symptoms.’

      4. Dr Rushworth – “So there is nothing remotely implausible about the idea that people with asymptomatic infection can be infectious. ”

        Is someone claiming it is implausible? I think most people arguing with you are claiming that the data to support widespread asymptomatic spread is just not there. You have convinced me that is possible, just not that it is probable.

        I can imagine that someone with a poor immune system could be breathing out viruses without showing symptoms, but not that person being very healthy for very long. I find it very difficult to imagine someone with a healthy immune system shedding many virions for any length of time.

        So, you claim that you think that asymptomatic spread is real, but you are not giving any mechanism for how this could be occurring.

  24. …and all this is the basis on which governments will cherry pick the data to support further lockdowns,and mandatory vaccinations and vaccination passports,and MORE CONTROL…has scientific research always been so lacking in determining a consensus ,on so many of these covid 19 issues?
    Or is it the first time that many non scientists can see that peer reviewed science in the reality of interpretation, has such scope for inaccuracy?

  25. A related question is, how random is the spreading of Sars-cov-2?
    What I hear from people who were infected is that they know with some certainity when and how and from whom they got the virus.

    Of course, it is impossible to kno
    w with for sure. But, it seems to always be a family member, friend, class mate or co-worker… And, its typically someone that should’ve
    stayed at home because they had mild symptoms. Am I wrong?
    What they call “cluster-transmission”…

    Furthermore, wasn’t there a study related to symptomatic vs asymptomatic illness done by FoHM in the last couple of months? I can’t seem to find it now but I remember they concluded that very very few are truly asymptomatic throughout the course of the disease.

  26. I can’t get ouf of my mind the video of Kary Mullins, the inventor of the PCR test, saying that his test cannot tell anyone if they have a disease or not. They can though, if you turn the cycle rate high enough , find some genetic material of almost every molecule and virus on earth, but of course it does not tell you if the virus or other particle is live, dead, contagious, a partial segment or actually infectious. That means it cannot tell if anyone has a covid infection. I am using the word infection in the old fashioned way, meaning one has clear recognizable symptoms and needs to go to the hospital.

    Thus it is crystal clear what should have been done And that is what was done in all other similar pandemics, including a typical flu, in our modern history, which is to identify the vulnerable which was the old, the frail and those with one or more chronic diseases and put them in a save place, and let everyone else go a abut out their business, inhale what ever else is in the air including covid-19 particles, and get some immunity which would have caused the spread to be over a long time ago The frail would then do what they always do when flu bug comes around , which is avoid exposure by the vulnerable until it passes and or wait for a vaccine

    Instead, because of the evil and/or ignorance of our political class in Washington D.C. of both parties who put political power seeking and personal financial gain ahead of everything, there is a good chance we may have forever bankrupted and destroyed the USA as we once knew it.

    I truly think this is our fall of Rome.

    1. If you culture virus along with a PCR test, you can determine if someone has a viral disease. PCR by itself will only tell you if you have been exposed.

  27. A few questions on the case of the Japanese party:

    1. What was the total number of attendees at that party? I presume not all were infected.
    2. Was the original tourist from Wuhan symptomatic or not.
    3. Was the friend of the infected Wuhan tourist symptomatic or not?

    Am I correct in seeing the same numbers and percentages repeated from our original “laboratory” case of the Diamond Princess?

  28. Yes its a very contentious and debated issue. The problem I have with the whole COVID issue is all the resources allocated to quash the spread and deprivation of “living a life” has failed to stop the spread, so why even bother with that?? Yes old or sick or weak people will die, but are they not the ones that make up the obituaries every day. We are rolling out experimental injections for everyone, and the majority of people (old and /or sick people) that are dying from receiving injections are the very people that we are trying to protect from COVID. I think the calculation is approx 98% of the population that are infected isolate for 14 days at home watching Netflix, a tiny percentage require hospitalisation and some old sick people will die. Wouldn’t it make more sense to quarantine the old and the sick, and let the rest of us just catch COVID, develop our own immunity and put this behind us.
    I for one will not be injected, I will take the risk of catching SARSCOV2, the small risk of it developing from an infection to COVID19 disease and allow my body to develop its own immunity. Sure there is a risk that it may kill me and I may die, but life is a risk full stop. If this happens to me I will not blame anyone for not doing enough, I have no fear of this risk. Also I will not feel guilty if I infect someone else and they do not do so well, it would not be an intentional act on behalf to do so but its much the same with any infectious disease. If I caught influenza and passed it on to someone else and they died because they are old or sick would I be guilty of a heinous act? This has been happening since the dawn of time. Its called natural selection, survival of the fittest. The human race wont be wiped out by COVID19 because humans exposed to a pathogen like coronavirus will develop an immunity to it in 98% of cases. Injections for coronavirus will only make the virus mutate more quickly and delay natural herd immunity.

  29. Hi Dr. Rushworth…this is a very interesting post to say the least. I am no expert on any of this stuff and don’t in the least claim to be, however, you’ve criticized “observational data” in the past so I am actually surprised you are saying that there is evidence of asymptomatic spread based on one person from one party in Japan would indicate, indeed, this virus could be spread asymptomatically. Unfortunately, whether we think it’s credible or not, the only study with enough data that makes it more realistic is the one out of Wuhan, China. All studies are at risk of producing a desired result would they not be? Would not the vaccine safety and efficacy studies also be guilty of this since their data is limited in scope and long term trials don’t wrap up until 2023 or 2024?

    Before this virus, I had never heard of asymptomatic spread before. Did this happen with the first Sars? The swine flu, etc.? Are other diseases like this? I think someone else commented that the reason for all these lockdowns was the fact that you could have the virus, not even know it (aka asymptomatic) and be spreading it around, therefore, the whole “don’t kill gran” meme. It would also explain why they are so eager to get a shot into everyone’s arms even though the studies on safety on efficacy may not be conclusive as of yet (as I mentioned above).

    So, would you not conclude by this very simple observational Japanese data, that asymptomatic spread is inconclusive at best?

    1. Like I wrote earlier in the thread, the Wuhan study does not say anything about asymptomatic infection. I really don’t understand why so many people think it does.

      Observational studies have limitations, but in the absence of randomized trials, they’re what we have to go on. The advantage with the Japanese study is that there was basically zero spread of covid in Japan at the time, so it is very likely that the people identified as the spreaders actually were. The Japanese study is in line with the earlier US marine corps study and the Singapore study. All the studies that have actually seriously looked in to asymptomatic spread are pointing in the same direction.

  30. I think most people here understand the PCR test is garbage and was never meant to diagnose an infectious virus. After reading these articles below, and the accompanying videos, I really think this is a Plan-demic after all. These lawsuits are apparently focusing on the German Drosten PCR test, which specifies 45 cycles(!) and wasn’t even based on the SARS-COV-2 “virus”:

  31. My best guess at this point is that asymptomatic infection is very common (>50%) as with influenza, but asymptomatic trasmission is negligible. So one symptomatic person transmits to 10 people; of these secondary infections only 1 is symptomatic, and they transmit on to 10 others (or 100) – your so-called super-spreaders. Occasionally an asymptomatic person will transmit the virus, but only under certain circumstances (ie: within a household), and most times they will turn out to be presymptomatic anyway. This is the only model that satisfactorily explains why the pandemic has both so hard to track and so prolonged. Gomes and others demonstrated very early on in the pandemic that transmission was highly heterogeneous.

  32. Aren’t there are two components of disease: symptoms which are reported by the patient but cannot objectively be observed, such as headache, fatigue, fir example; signs which can be observed, cough, sneezing, bleeding for example.

    We hear that one of the primary features of SARS CoV 2 is the mildness of the symptoms it produces and how short lived, so mild that many people have said they weren’t aware they had it, or confused it with something else. Main symptoms are headache, cough, fatigue, fever – those are shared with many things from allergy, heavy night down the pub, stress, a Cold, overwork.

    And of course anyone who has dealt with the public either in medical care or criminal investigation will know people are the most unreliable witnesses and very suggestible; they also do not tell the truth, the whole truth and nothing but the truth.

    Any research that relies mostly or exclusively on what a person says is unreliable. And of course research carried out to support the hypothesis of asymptomatic spread, certainly will.

    So when there is talk of asymptomatic cases, could it be they were in fact symptomatic but victims did not report any, them being so mild, or confused with something else, so have been classed as asymptomatic? Asymptomatic ‘cases’ have been declared based on neither signs nor symptoms, but a lab test… PCR… which is not a diagnostic test for disease. A PCR positive test, whether true or false, cannot be a sign of disease, it is an indication that a viral fragment was present at some past time, but is no indicator of disease past or present.

    Is it not likely then that the quick spread is because infected people appear asymptomatic but in fact are not. And would this not explain the success of the virus, how quickly it spreads by not immobilising those whom it infects and being so stealthy they may not even be aware of their symptoms?

    But wait. For such a fast spreading virus, each new variant being even more so than the last (horror!), how can it be that after more than a year, not enough of the population has been in contact with it and immunised, and so we need mass vaccination: she we all have been infected by now?

    Either it is a fast spreading virus or it isn’t. And if it’s effect clearly is so mild or unnoticeable why try and stop the spread? We don’t do this with many other fast spreading viruses, some of an equally lethal nature for some.

  33. As I understand it, vaccines don’t prevent infection. Rather, they stimulate the immune system to fight off the infection. Are vaccinated people then potential asymptomatic spreaders between the time they are infected and the time they eliminate the virus from the body?

    1. In a word: yes

      That is correct. Someone who is vaccinated will have a positive PCR test result.

      1. To be clear: Once infected, the body never truly eliminates a pathogen completely, but rather the immune system keeps it in-check with the antibodies it produces. So basically a signature of the pathogen is registered by the body’s immune system for life.

        If you come down with something in the future, like say the common cold or flu, it is because the body’s immune response has been weakened due to lack of sleep, poor nutrition, and stress, and the immune response cannot generate enough antibodies fast enough to deal with the most current variant of the season. Hence the body goes into overdrive and starts producing symptoms, until the variant’s differences are accounted for by the new antibodies the body was already producing in the background.

        Getting injected with a vaccine is akin to bypassing all of our natural immune system defences and getting the pathogen in a high concentration, or in the case of mRNA injections — artificially have our own cells create the “garbage/waste” aka. “spike protein”that the pathogen produces, whether we want it or not. So we intentionally and acutely stress the body’s immune system from the inside out, instead of the outside in. It’s important to note that the timeframe for this immune response is also dramatically shortened, unnaturally.

    2. One last point: in all of history, vaccines have always followed the peak infection and spread rate of a disease.

      This is because by definition, the vaccine is produced after the disease has spread throughout society. So to say that a vaccine has “helped” eliminate a disease is a far stretch.

      A pathogen spreads like wildfire. Much faster than anything we can humanly produce in months and months of research to then “replicate” through an injection to re-produce an immune response in the body so that it is “protected” in the future—just in case the pathogen spreads again.

      So this world exercise of “immunization” for a variation of the common cold (which is also a corona pathogen/aka. “virus”) is a moot point.

  34. Good article, but something is boggling my mind since I read the marine story on your book:

    The study assumed infection were only possible through direct contact between virus bearers and healthy people. At the time, aerosols were not an option for an infection vector, only ballistic particles and surfaces.

    But the marines were sharing the same space. On the study, if one marine (that was never in contact with a symptomatic person, only asymptomatic) later tested positive, they assumed asymptomatic persons were infectious.

    But we now know SARS-CoV-2 is airborne, so this marine could be infected by particles remaining in the room from a symptomatic person that was earlier in the room, right?

    What do you think?

    1. The thing is that all the positive cases were gene sequenced and genomes were compared, which minimizes the risk that the person was infected by someone other than the known index case. No infections happened across platoons, with one exception, where people from two platoons were sharing a bed room. All the others happened within platoons, and most between people sharing a bed room, i.e. all infections happened between people who were in close direct contact, which suggests that the virus doesn’t hang around very long in the air with the ability to spread infection.

      1. I think that you’d have to look at the physical circumstances of the Marine bedrooms to use this study to discount aerosol transmission. Were windows kept open? What was the time to 100% turnover of the air in the room? Does packing people in transport play a role? What about parties lasting five hours or more?

        Any self-reporting by Marines should be viewed with extreme skepticism as Marine culture places a premium on the ability to deceive–including doctors and bureaucrats, who are often viewed as the enemy. Doctors can exclude Marines from duty, which is at odds with the Marines’ mission.

        The MIT mask study is pretty convincing that aerosols are the major vector. It looked at several other studies of indoor transmission. (But those didn’t do viral culturing either, so maybe they are fatally flawed. Certainly, they are no worse than the Japanese or Singapore studies.)

        “A guideline to limit indoor airborne transmission of COVID-19”

      2. You would have to know the probabilities of genetic mutations in the community, including the presence of viral mutants among the non-participants before using a viral mutation map would make sense.

  35. This virus is somehow unpredictable, no clue how it chooses its victims.
    My cousin, got quite sure infected by a non symptomatic friend. The only person he decided to meet after weeks of distancing himself.
    Soon after they had lunch together that friends mother got mild symptoms, 3 days later then the friend and like 1-2 days later my cousin.
    On the other side my brother in law had some “mild cold” after which he felt often weak and tired. He decided to test himself and got a positive result. His wife and daughters never showed symptoms or a positive result so far…
    I … (un)fortunately still healthy 😀

  36. “My personal intuition has been that covid probably does spread asymptomatically. This intuition is based on the fact that the virus has spread so rapidly and successfully around the world, and also on the complete and utter uselessness of lockdowns…”

    Sebastian, the virus has spread rapidly and successfully around the world because there have not been any real lockdowns. The only real lockdown was implemented in Wuhan in early 2020 and it was a huge success. The “lockdowns” implemented around the world have mostly been a joke. Your conclusion about uselessness of lockdowns is based on false premises.

    1. New Zealand and Australia have been successful with their lockdowns as well. A successful lockdown is the one which lasts until there isn’t any community transmission anymore. Also, it requires strict border control.

      The vast majority of countries around the world have had half-hearted, partial lockdowns and borders wide open. Of course, such false lockdowns have been a failure, and it’s wrong to call them lockdowns.

      1. The countries that managed well are those that could and did close their borders quickly. Rather than whether or not they locked down…Internally, Australia and New Zealand haven’t been so strictly locked down.

        But the population of those countries are still naive to the virus and can be very badly hit at any point in time. So they need some sort of prophylaxis or vaccine before they can get going again…

        Look at eastern europe last autumn, very small first wave spring 2020 compared western europe but then the eastern countries were hit badly in autumn / winter.

  37. The Japanese Study. Those who caught covid from asymptomatic carriers, was this discovered via a PCR Test? I suppose you know where I’m going with this…

  38. Wuhan study finding no asymptomatic spread.
    300 asymptomatic in population of 10m.
    Understand your scepticism of the results. Unfortunately, our science everywhere is now being corrupted by funding, career, and agenda.
    (e.g. Lancet publishes paper rubbishing HCQ, and then has to withdraw a week later. How did this happen? Why are governments suppressing effective treatments?)

    1. Because it’s about bringing in vaccination as a way of identifying individuals – coupling this to your digital ID for the impending technocratic imprisonment of the 4th industrial revolution that they are neglecting to tell people about. It. Ever was about Covid unfortunately.

  39. I am a little bit surprised at your conclusions, bearing in mind you are talking about PCR tests being used to confirm the ‘infection’. Are you serious?

    1. PCR is actually not bad when there is strong suspicion of infection. The test has a very good specificity. The situation where PCR is problematic is when there is very low suspicion, for example when screening a population where the overall prevalence is low, because in that scenario there is a significant probability that a positive result will be a false positive, as I tried to explain higher up in this thread.

      1. What a bout a positive PCR when you have antibodies from a previous infection ? Is this a false positive or can you get Covid multiple times ? I have a friend that tested positive on 2 different occasions (PCR test for travel) and still having antibodies after more than a year. Same as the Swedish Football player today, who tested positive again and still having antibodies.

      2. You probably believe the 2020 flu statistics, too.

        Prevalence estimates rely on PCR and false negatives early on were very high. I assume most everyone has a one or two day turnaround for PCR, but that might be a false assumption. False negatives would be heavily impacted by delays between sampling and running the PCR.

  40. It is sad to read so much good intended thinking that seems to over look the catastrophic spread and death in India. I mean no ill-will. But how can we sit here, privileged as we are and simply not recognize that the deadly virus is deadly and the world does not look like the bubbles from which we ruminate over the decisions of our governments. Questioning if there really are the numbers of dead here, by throwing all sorts of data and test speculations laden with assumptions of ignorance, greed and/or both when we watch it roll across and kill 100s of k, as predicted, in places far less fortunate, less rich, less privileged and less prepared as most of us living, writing here? Reading this thread would lead one to tell places like India, get used to it, it’s not as bad as you are experiencing. Lock away your older folk, your weak, and good luck?🤧🥵

    1. The deadly virus is actually only deadly to those whose immune systems are compromised (age, co-morbidities, obesity and perhaps some due to inadequate vitamin D for correct immunomodulation).

      The Indians to their credit have deployed Ivermectin and other prophylactics to good effect. They don’t need good luck – they are behaving scientifically and rationally unlike some other countries wanting to foist vaccines on young people where they are not required and which countries are discounting the effects of drugs like invermectin because of regulatory capture

      When you consider that India has only had 252 deaths per million of population (according to Worldometer today) you realise that they are doing much better than most of the wealthy European countries and the U.S.

      I think it is important to realise that in India about 2,000 die a day from diarrhea
      This article from 2017 in the Hindustani Times:
      “Diarrhoeal dieases are one of the biggest causes of under-5 deaths, killing between 800,000 and one million children, hospitalising 900,000 and causing 327,000 visits to clinics each year. Adding Rotavirus vaccine to India’s universal vaccination programme in 2016 to protect children against the leading cause of severe diarrhoea in young children, helped lower numbers rapidly”.

      So covid-19 has in no way had a catastrophic impact in India. The last thing India needs is to have any distraction from their other public health problems. The current spate of infections from the “Delta” virus has now turned the corner and is in rapid decline and deaths will follow in due course.

      This is a result of the normal and natural course of a pandemic virus.

      Governments in the Western world should stop terrorising us with tales about variants and India.

      1. Yes, India has its real, deep, sanitary problems associated ex-colonial and other underprivileged.

        But saying
        “So covid-19 has in no way had a catastrophic impact in India.”
        Is a deeply scientifically flawed observation, calling a statistic that this thread has pretty much called into question at every turn. I mean no polarity here yet calling no catastrophic impact? I won’t challenge this further as at this point it has become opinionated, which tends to degenerate (as we see in some comments).

    2. According to World-o-Meters data, the epidemic is nearly over in India. The current population fatality rate is 261 per million. Covid19 is not killing many people in India compared to other causes. Western media is lying to promote fear.

    3. Well, India has had the good sense to fight over antiviral treatments and it shows in their statistics, which show a decline in cases since physicians are allowed to use antivirals in India because doctors stood up to the national association.

  41. I am glad to have a reasonably believable answer to this question. That answer might make it possible for actuaries and economists to calculate more accurately the health risks of letting asymptomatic and untested people work versus the economic and societal costs of making everybody stay home, shutting down the whole economy, with food and supplies delivered to homes by FEMA workers in hazmat suits. Uncaring as it may seem to those who would die as a result of the first scenario, the overall cost of the second scenario would be catastrophic. Since it is mostly older people (I fit into that category) who are at greatest risk from the virus, isn’t it time for us seniors to take on our special responsibility, by protecting ourselves as we see fit and take our chances while letting younger generations go on with their lives? What if we were old Inuits in winter and food was scarce? Would we snatch scraps away from babes?

    1. I find this comment a bit besides the point of this discussion, though very much to the point, at the heart of the evaluation of this ‘situation’. The importance of the question being discussed here depends highly on the weight given to what has been called – correctly in my view – a ‘casedemic’ (I will not use the word ‘plandemic’). Once we stop using pcr en antigen tests on this scale and return to a regular practice of diagnozing, the question of a-/pre-/symptomatic spread looses its importance. Especially in the situation we’re in – very low virulence – with a unacceptable high number of false positives.

  42. Perhaps this is an oversimplification, but logic says symptomatic covid is caused by a combination of sufficient viral load plus susceptibility (higher age, comorbidities, level of immune functioning, etc)

    And positive tests in asymptomatic cases would indicate a high level of immune function in those individuals, so the virus is present but prevented from developing a high enough load to render the individual symptomatic.

    So asymptomatic individuals would not be expressing high viral loads to begin with, making it generally less likely they would spread covid infection.

    1. Some viruses have the ability to hide from the immune system or disable the immune system, but at some point everyone will develop symptoms or clear the virus.

      The idea of asymptomatic superspreaders is ludicrous.

  43. Sebastian

    It would seem that there is a grey area that encompasses asymptomatic with viral load at very low levels to pre-symptomatic with higher levels that progresses to mild symptoms that resolve quickly.

    Have you read the following paper from the JAMA open network?
    Household Transmission of SARS-CoV-2 – A Systematic Review and Meta-analysis
    Madewell et al

    Would it be correct to deduce that if the symptomatic secondary attack rate was 18.0% and the asymptomatic or pre-symptomatic secondary attack rate was 0.7% that there is actually a 25 times difference in infectivity? And then by deduction: In the real world (outside the household context which would have less ventilation and reduced social distancing) would it be likely that asymptomatics and pre-symptomatics would only be responsible for significantly less than 4% of all infections?

    I believe that hospitals in the UK were probably responsible for 40% of infections so the figure would probably drop further by at least half

    1. As mentioned higher up in this thread, the estimate from that meta-analysis isn’t based on looking at studies that actually compared symptomatic and asymptomatic spread. One estimate comes from one group of studies and the other comes from a different group with different methodologies, so putting the two together and calling it a meta-analysis is problematic.

  44. Grand discussion. I think Sebastian summarises well, even this discussion.

    “When taken together, I think these two studies show that people with asymptomatic covid-19 can and do spread the disease, and the best estimate from both studies is that those with symptomatic disease are about three to four times more infectious than those with asymptomatic disease. That is not a huge difference. Even though people with symptoms are a couple of times more infectious than people without symptoms, those without symptoms could still be causing more infections overall.” Well said.

  45. Is it possible that innate immune response (symptomatic) vs adaptive immune response (asymptomatic) is a function of how much live vs killed virus we are exposed to? So lets say a herd animal encounters a new virus it’s innate immune response kicks in, it separates itself from the herd, then when symptoms subside it rejoins the herd. At this point it is shedding both live and killed virons, with live % decreasing with time. As more and more animals get sick and recover spreading killed virons around the herd, the initial immune response can shift from innate only to adaptive only. Maybe viruses don’t mutate to become less severe over time it only looks that way as the shift from innate to adaptive takes place.

  46. So Sebastian, regarding the answer on my earlier question, if you can get Covid multiple times even when you have antibodies, (i know one who could have had it 3 times then (?) and asymptotic infected spreads the virus, then there is no hope to get back to a “normal” world. The “lockdowns and other measures will continue a long time. Also it is of absolute no benefit to vaccinate younger (under lets us say 50-55 years of age) healthy people, since they still can get Covid and spread the virus even if they are asymptotic. I would prefer the explanation that the PCR test is picking up “remnants” of the virus and that the you are unlikely to get covid multiple times.

  47. Having 0,2% positives in summer doesn’t necessarily mean that the false positive rate is 0,2% or less. I’ve read reports about some PCR tests reacting also to other viruses than SARS-CoV 2 (SARS1, regular coronaviruses, animal coronaviruses and even influenza). If that’s the case then the false positive rate can be <0,2% in summer but way higher in winter.

  48. Very sad to read this analysis and the many comments. It seems to me that some pressure may have been applied as the emphasis has gently shifted from the optimistic towards the so called “Follow The Science” camp?

    As a Doctor, Sebastian, I’m sure you can appreciate the distress these types of open ended and inconclusive analysis can cause. I for one can no longer include this Blog as a Favourite source of Medical opinion or discussion.

    On the one hand we were originally told that Sars Cov2 was a relatively weak virus that most people would only suffer mild consequences from, NOW you and others are suggesting that YES this is a Deadly virus that will kill many of its victims. eg: over 70’s up to a 25% mortality rate? And Children have to be injected so they do not kill Granny or their Teacher(s)

    The much maligned PCR test is now stated to have a false positive rate of less than 0.2%, but surely the real point is what it is detecting – Alive or Dead? Why do you “Swerve Away From” the Ct value issue, surely its very relevant to the studies.

    Sorry to be negative, but we always looked up to Sweden as having the correct policy, now it seems you have capitulated.

  49. Studies about asymptomatic spread seems to be inconsistent. My intuition is that asymptomatic spread i overestimated. Due to the world wide stigmatization of covid-19 “Don’t kill your gran” my guess is that most people would lie even for themselves if they are asked about symptoms when they face the fact that they have spread the disease. The only way to avoid such an overestimation is to make randomized trials. Fohm ( has made 6 studies where randomly selected people where invited to make a test and report symptoms. The number of people that were infected was limited but there was in principle none that did not have any symptoms. If asymptomatic spread was significant they should have at least caught some cases in these trials. Have such studies been made in different parts of the world and what do they indicate if they exist?

    1. The problem with that study is that they include pretty much any symptom imaginable and count it as a covid symptom, including stomach pain, muscle soreness, nose bleeds, and rashes. Almost everyone on the planet will have experienced some little twinge somewhere within the last two weeks. That doesn’t mean everybody has covid. Only around 65% of participants actually had the classic symptoms, which aligns with studies elsewhere finding that 50-70% are symptomatic.

  50. I have serious doubts about this issue. Both Mike Yeadon and Beda Stadler who had really solid scientific careers argue that it is not possible or in worst case scenario irrelevant or rare. They say that in order to pass a virus to someone one must have a significant viral load in the upper airways, but if you have that is not possible to have no symptoms. Yeadon adds that is mostly trough cough and sneezing that your able to pass it by, otherwise your breathing carries mostly carbon dioxide and moister. Stadler asks: If you have a significant number of virus how do you produce them? They are produced by viral replication and cell destruction that inevitably leads to pain.

    On other hand I follow Denis Rancourt, specialist in nano-particles, to whom masks are absolutely useless, but he claims that one of the reasons is that the infectious dose is very small. Wonder if this contradicts Yeadon and Stadler and gives strength to asymptomatic transmission theory. (By the way, contrary to Sebastian Rusworth, Rancourt believes that current load of respiratory diseases is not different from previous years and that the causes for all this mass hysteria are the fact that USA do not want to loose their leading position and are therefore trying to isolate China economically who threatens their global dominance (please see interview with Nils)).

    In any case it seems to me that there has been a consensus in last decades that viral respiratory diseases are not transmitted by people without symptoms and therefore if someone wants to claim that this is something completely new, those have the burden to produce robust scientific evidence to prove it, witch so far to my knowledge has not been the case.

    I would had the following questions?:
    -If a virus gets in to you what is the time frame that you either neutralize it or the virus is able to replicate to some extent and cause you symptoms
    -Is it possible that the virus gets in to you and does not attempt to enter your cells? Is it possible that a certain amount of virus will walk around undetected without causing an immunitary reaction and are able to remain in your airways for a long time.


  51. There is so much research, studies and opinions on whether asymptomatic spread is relevant.

    My two cents is this:

    The common cold is a corona virus, just like this COVID-19 disease; yet we do not have a cure for the common cold after thousands of years, nor do we have vaccine for it, and most importantly, nor do we treat asymptomatic people who HAVE or HAD the common cold as if they are vectors/spreaders

  52. > This intuition is based on the fact that the virus has spread so rapidly and successfully around the world

    While I agree with this in principle, if China had been shown to deliberately infect the rest of the world, would you still think the same way?

    Do you remember numerous videos “hug me I am Chinese not a virus”? There are plenty more on youtube.

  53. Just found this…

    “A persistently replicating SARS-CoV-2 variant derived from an asymptomatic individual”

    “The SARS-CoV-2 GZ69 strain, isolated in May from an asymptomatic healthcare worker, showed an unprecedented capability of replication in Vero E6 cells in the absence of any evident cytopathic effect. Vero E6 subculturing, up to passage 4, showed that SARS-CoV-2 GZ69 infection was as productive as the one sustained by the cytopathic strain AP66. Whole genome sequencing of the persistently replicating SARS-CoV-2 GZ69 has shown that this strain differs from the early AP66 variant in 9 nucleotide positions (C2939T; C3828T; G21784T; T21846C; T24631C; G28881A; G28882A; G28883C; G29810T) which lead to 6 non-synonymous substitutions spanning on ORF1ab (P892S; S1188L), S (K74N; I95T) and N (R203K, G204R) proteins.”

    With no cytopathicity, maybe the immune response will be diminished and covid progression less likely? Maybe covid will tend towards producing the effects of colds like some other coronaviruses?

  54. Correct me if I’m wrong, but how can you differentiate between a false positive test and an asymptomatic Covid case? If someone tests +ve on PCR (a questionable method for diagnosis to begin with) and that person has zero symptoms how can we know that this is an error with the test or an “asymptomatic” case?

  55. If I can summarize:
    First question: ‘Can asymptomatic people spread covid-19?’ the answer to the seems to be YES. And there is data to support this (in addition to spread by pre-symptomatic people).
    Regarding the second question, how does this differ from spread by symptomatic people? Maybe less, we don’t know.
    The most important lesson seems to be that it can be dangerous to ignore asymptomatic spread.

      1. David: None of your links are real-life studies, it is models & recommendations, except for link no. 4 which is a review of studies of probabilities.

        That is not evidence of the existence of asymptomatic transmission.

        The study from BMJ concludes the opposite of your claim: ‘ The absence of strong evidence that asymptomatic people are driver of transmission is another good reason for pausing the roll out of mass testing in schools, universities, and communities.’

        Your last link in JAMA is a strange model, which has been beautifully debunked by biologists Weinstein & Heying here:

      2. So I guess that we don’t have to worry, the evolutionary biologists are on the way… with the ivermectin!

        The Bret lost me at ‘the thing that causes symptoms are the same thing that causes infection’ and ‘it would be surprising to have a high rate of asymptotic transition’. How does he get to this assumption?
        Would the model be that difference if infectiousness of asymptotic people is not 75%, but only 50%? Wouldn’t this still mean that they are infective?

        What about these:,,,
        Never mind

      3. David: Your latest four links contain no evidence of asymptomatic transmission.

        The first three papers just assume asymptomatic transmission exists, because the PCR-test identifies many people without diease as ‘positive’. Asymptomatic people are not infected, however – they are just PCR-positive, either because the sensitive PCR-test picked up old viral debris, contaminated swaps, or they are technically false positives.

        Study no. 3 is based on the cirkular JAMA-model, which Weinstein & Heying concluded is ‘garbage’.

        Study no. four, from France concludes: ‘We identified pre-symptomatic transmission in 40% of this cluster, but no transmission from asymptomatic to symptomatic cases.’

      4. Thank you – I understand now. Do you think that there is >25% false positives?

    1. What about asymptomatic spread of influenza?

      What about asymptomatic spread of other coronaviruses?

      What about asymptomatic spread of other ILI’s?

      Tunnel vision.

      1. Wouldn’t it be nice if sick people just stayed home and didn’t go to work/school?
        Some diseases (such as MERS) aren’t infections before symptoms (or what we recognize as symptoms) – and some are. Interesting, severely symptomatic patients are infect fewer people – as they don’t feel good and stay home (and maybe in bed).

        What about asymptomatic spread of HIV?

      2. Also, no evidence exists for person-to-person transmission of influenzavirus. A set of army-experiments in 1918 demonstrated that it was not possible to induce healthy volunteers with influenza.

        The supervisor of these experiments, Dr. Milton Rosenau, wrote in Jama 1919:

        ‘We entered the outbreak with a notion that we knew the cause of the disease, and were quite sure we knew how it was transmitted from person to person. Perhaps, if we have learned anything, it is that we are not quite sure what we know about the disease.’

    2. It depends on your definition of ‘false positives’. Most people define it as the technical ‘built-in’ fault rate that is present in all medical tests. That rate is, I think, in the range between 0,1 and 1,0% of all tests taken, depending on the sample.

      You could however also call the asymptomatic ‘cases’ false positives as these people are obviously not sick. That rate is much higher.

      1. The definition is ‘a result that shows something is present when it really is not’ (Webster). That is the definition used in analytics. As some countries have had positive test rates of <0.5%, I can't see any proof for anything over 0.2% false positives.
        You can't 'also call the asymptomatic ‘cases’ false positives'. That's a question of interpreting the results, that's a different question.

        I would estimate that there are more 'false negatives', due to low viral loads or problems with sample preparation or sampling. But I don't have any data

  56. A pediatrician has said that she has been around covid patients for over a year and has consistently tested negative with PCR and serology tests. She thinks that it’s due to cross immunity from other coronaviruses to which she has been exposed heavily from her work. Maybe mucosal IgA immunity.

    Maybe the best treatment for grandma and grandpa is to see the grandkids regularly.

    1. Maybe – but one thing we do ‘know’ is that children don’t spread as much as grownups (or didn’t with the previous variants).
      Wouldn’t older people have immune systems that have already been exposed to all kinds of viruses? Isn’t that part of the problem, having ‘over active’ immune systems?

      1. All the asymptomatic ‘cases’ fall in the PCR-false positive category: ‘showing something is present when it really is not’, i.e. a disease, Covid-19.

      2. Now you are not only claiming that asymptomatic people can’t spread (even the evolutionary biologists did say that, just didn’t accept the stated rate of infectiousness) but that there are any asymptomatic cases in the first case. How do you get to that conclusion? What about extremely mild symptoms?
        Regardless of symptom severity, peek shedding is often before symptom onset (
        You can’t really compare to influenza to Covid-19, and expect them to behave the same (

  57. Sebastian – I have read several posts of yours which were very enlightening, but the arguments in this one, about ‘healthy people can spread disease’ is not convincing at all.

    Not only is it counter intuitive and illogical that people without disease should be able to spread disease, it has also been revealed that the virus is airborne (i.e. not only transmitted by ‘droplets’) – so it is a huge mistake to assume that only person-to-person transmission is possible.

    The ‘asymptomatic spread’-argument goes like this: ‘Ah – so this symptomatic patient could not have gotten the infection from anywhere else than at his meeting with this asymptomatic person, and so asymptomatic transmission exists…’

    Wrong! The virus is airborne and can linger in tiny particles in the air in unventilated buildings & rooms for days, some scientists even suggest for weeks. That means you can enter an empty room (fx. in an army camp) and breathe in the virus. With no ‘asymptomatic carrier’ present.

    The reason the science of the airborne status of virusses has not been fully appreciated in the mainstream seems to be that it shows that all lockdowns, restrictions, social distancing and ‘test & trace’ are completely useless. Keeping people who are sick isolated and ventilating indoors would have done the trick much, much better.

    Please read:

    1. With respect, the logic of all false positives being asymptomatic is a mistake itself. There are false positives in symptomatic cases, too. These are flu symptoms. Everyone of us I am confident knows someone who had a “flu”, got tested for cov19, got positive results, but never actually had covid19. There are more who did actually have it I am also confident. Part of the challenge of this thread is “speaking in absolutes”. False pos happens in both asymp and symptomatic cases. Being a carrier of a bug (sarscov2) is not the same as having the “dis-ease” (covid19). There are latent spreaders of many bugs. And the bug need not only spread human to human. Viral load in interaction with one’s immune system determins “disease and it symptoms”. Low viral load can mean “yup, pos, yup carrier, nope no symptoms, yup, potential spreader.

  58. But aren’t the asymptomatic ones those that are needed to establish herd immunity, because they move around and are less infectious? Thus spreading less virus but in a greater radius . Thus infecting more people but giving those people the chance to handle the infection quite well? Herd immuity is reached respectively maintained because asymptomatic people are holding up a level of minor infections over time. Thus updating their surroundings with every new variant. You can’t copy such updates via injections in such a density over time. Only if all vaccinated people are one and the same and the injections work equal in everybody and are repeated every week (?), month (?), year (?).

    1. If asymptomatic carriers induce asymptomatic infections, that would be great – almost like an infectious vaccine (talk about lack up consent!). But we don’t have anything to back that up – I think that asymptomatic transition is detected when someone has symptoms.

    2. The asymptomatics are those who are immune to the disease. There is no logical reason to believe that these people transmit disease, and no real life evidence to support it. The whole thing relies on a ‘ridiculous assumption’, as Beda Stadler says.

      The theory that healthy people spread disease is an old dream among disease & fear mongers in the pharma and medical establishments, and it has strong support from those invested in tests. It is a way of transforming huge numbers of healthy people into customers of the medico industry. That is why much energy is used and many model studies is trying to establish ‘asymptomatic transmission’ as a medical fact.

      1. Respectfully, the logic of “asymptomatic are immune” is false negative itself.

        A). We all are asymptomatic for an incubation time. All of us.
        B) Some of us bloom mildy, some bloom severly, and everywhere in between.
        C) The interactive factors are 1. Viral load with 2. An individual’s immune system (genes).

        The same amount of sarscov2 virons contracted by two different people can and do produce different “disease results” for two different people. Take a 10yr old and an 85yr old, for example. The 10yr old can absorb and cary that load (and spread it) without anyone knowing (never feeling bad enough to get tested). Even a 40yr old can. While the 85yr old might suffer. There it is. Viral load. The factor of highest significance to severity of infection, 2nd to the genetic immune system it encounters, are the key factors. Very basic logic, virology, and present knowledge tells us: yes it’s possible to carry, be asymptomatic (we all are for a time), and spread it, and NOT become immune to it, and possibly test negative or positive or false in either direction. But simple Virology says, yes, you can be an asymptomatic carrier and spreader the liklihood is directly related to viral load. (Consider: main spread and deaths in confined places like rest homes and ships and homes with several ill people where viral load skyrockets). Discussing this void of the variable of viral load is guarenteed to draw spurious conclusions. Add viral load and accepted, known Virology to it, and is clear. At least to me.

      2. From the evidence so far, the asymptomatic don’t spread covid significantly. And most of us have learned the difference between “presymptomatic” and “asymptomatic”. Asymptomatic people _never_ show symptoms. They obviously are immune. The immunity may be due to cross-reactivity from mucosal IgA, which hasn’t been looked at much so far.

        People with high viral load who are asymptomatic can only spread a virus if the virus doesn’t cause much apoptosis, which has only been found in one SARS-COV-2 variant so far of the covid strains. (Localized, heavy apoptosis triggers an immune reaction, with symptoms.)

  59. Thank. Later phase of a flu disease (all 48 patients) is often post “infectious” stage to my limited knowledge. Do you have “early stage” study to confirm that early stage, usually less contagious, is as benign? Some statistical power would also be appreciated, also. An anova with n=48 has very low statistical power. Not one I would rely on.

  60. With respect, the thread is about spread of the disease sars-cov2. We all know people who have had it, didn’t know it, and likely spread it. They didn’t know it because their symptoms were very mild. Likely due to low viral load and a strong immune system. But they were carriers and could spread. They later tested positive and thus classified as asymptomatic. 1. Viral load is more determinant than most any other variable. 2. All Virology tells us that depending on viral load AND the host immune system, the disease (and the appearance of symptoms) evolves on a case by case basis. We are holding a discussion not addressing this (the determinant viral load precursors of disease impact), and using post incubation, Llikely non-infectious (late stage data) case sample of 41 (statistical power at embarrassing low levels) to refute 70 years of virological science. This is a mistake of logic and science.

    1. With respect, virological science doesn’t assert asymptomatic spread of ILIs. That remains an open question. We know that there are diseases like chickenpox that spread pre-symptomatically and that AIDS can develop from an HIV infection that initially shows no symptoms, but eventually does show symptoms. Influenza has asymptomatic infections, but the data is sparse about asymptomatic spread of influenza.

      1. Thanks. From what I see, we still are not addressing viral load. We (myself included) are speculating as follows:

        1. We hannot “proven” that asymptomatic spread happens.
        2. We know the amount of virons is strongly positively correlated with severity of symptoms, moderated by the immune system of the host.
        3. We don’t know the range of the amount of virons that guarantees disease symptoms (depends on the person).
        4. Virology is clear that it is the presence of virons that IS sarscov2 and those can spread on surfaces (not only p2p).
        5. It is clear a person (or a thing like a door handle) who is asymptomatic can carry the virons.

        Ergo, if we can catch a dose of sarscov2 virons from an asymptomatic door handle, we can catch it from any other “host”, especially one who spreads it by breathing.

        That’s the science to which I humbly refer.

      2. I see no reason to think that viral load correlates with severity of symptoms. Possibly the more severe symptoms are due to pathological immune response after viral load has cleared. And maybe the pathological immune response is due to inadequate vitamin D.

        There are so few studies that culture virus, it is impossible to find much reliable data; most are based on PCR alone, which perhaps may only represent an uninfectious person.

        Hence, the notion of spread by door handles is simply speculation. We have seen cases where spread has occurred indoors with long exposure. Presumably, the length of exposure correlates with risk because the disease spread was by aerosols. It was seen on buses where no door handles were involved.

        It seems to me that virus clears in about 8 days post symptom onset, based on studies using viral culturing. Have you seen any studies using viral culturing which show a longer time to viral clearance?

  61. With respect, if you are attempting to stand on the ground of 70 years of scientific data and reasoning ‘ We all know people who have had it, didn’t know it, and likely spread it’ has no place – this is a belief, not a fact.

    It is my belief that SARS-CoV2 is a ‘bioweapon’ and understanding quite who released it and to what ends it was released is THE single most important question facing humanity and central to the whole COVID debate, but one that few seem to be attempting to answer. Why is this? It is either for profit, or control – most likely the latter. The over driven role of asymptomatic spread has enabled this ‘pandemic’ to roll on beyond its sell by date – but folk like to pick over insignificant discussion points, as is happening here, whilst missing the real point – freedom is being usurped, democracy is being superseded by a new political system, a new financial and political system based on totalitarianism and technocratic control is being moved in to place. You should not give a sh## about asymptomatic spread. It is not important. Period. Take your head out of your ass and wake up FFS.

  62. theasdgamer: no, I don’t know culture-based duration studies in support or not. This article draws attention to viral load.

    My reasoning was/is based on broader work and evidence, and operating on the view that sarscov2 is in fact like most other flu/respiratory viruses.

    For example, closed, circulating (poorly ventilated) environments are the deadliest/most severe. Virus replicates in hosts, slowly overwhelming them or not, and virons themselvs have some half life on non-biological surfaces. Symptoms of viron uptake are not necessarily instant (like say “pepper spray is”).

    These are pretty much “facts of viral life” and its spread and uptake.

    Because of the individual, unique, interaction patterns of “load and immune system” combined with delays in symptoms, we need to, as you are trying to do, combine viral & epidemiological reasoning and data.

    An individual’s human immune “state” at any time is capable of thwarting-off an amazing variety if biological infections, even types never before encountered. The more familiar, the quicker and more potent usually the immune response. The less familiar, the tougher it is, especially if it is a high viron count invasion of a fast replicating microbe, like pox. These are well understood facts of biological viral microbial life and defense, and the genetic adaptations of “both sides” aka microbial life being spread and organismic life defending against the invaders.

    So, reasoning from there, and the difficulty of “ruling-out” what we know happens in viral microbial life and survival, the hypothesis that “asymptomatic carriers don’t spread” the microbe, makes the “null hypothesis to test” that asymptomatic spread is the normal state. To reject the null hypothesis means we have to prove they don’t spread, not the other way around. Simply because viral life, and most all viral knowledge indicates both load and non-contact spread of virus IS the normal.”

    100 years ago the null hypothesis was that (bacterial) infection could not spread between patience by surgeons and nurses. (Like (unfortunately) we pose the null hypothesis that asymptomatic spread is “not proven” today). Then, we tested that infection could spread via surgeons and the intervention was hygiene washing. The null hypothesis then was: infection does not spread by hand.

    However, today, we take as normal that infection spreads with poor hygiene. If we were to question this, today, in science, we would establish the null hypothesis as “bacterial infection DOES spread via poor hygiene” and test accordingly.

    My position is: we do know load plays a role. We have undeniable epidemiological evidence (circulation of high concentration virons) as most deadly/severe. We know the virus can spread via air and surface contact. We cannot possibly gather enough demonstrable evidence beyond this to “test” right or wrong because of the unique load/immunesystem interactions at individual levels with the basic track testing we deploy. So, for me, the natural assumption is that this virus is indeed like all others. Spreadable by people and surfaces, and the success of vaccines in slowing spread is confirming this (aka not rejecting the null hypothesis that the virus is indeed LIKE 99% of all other viruses). Thoughts?

    1. My position is that PCR testing _by itself_ only shows exposure. We cannot know the degree of viral load at any given time from PCR testing. The match between detectable RNA and virions is certainly not 1:1 and we have no idea what it is for any given person. Perhaps some people are slow to clear RNA and also have few symptoms and low levels of virus, but they accumulate high levels of RNA. We just don’t know. Do you see how this undercuts the studies on which you rely?

      I have seen the CDC study that asserts that transmission is seldom by surface contact. And the Bazant study showed that transmission occurs to people distant from index cases in enclosed spaces. These look to be reliable.

      Raoult and Heneghan have established that culturing virus is essential to know viral load and for transmission studies. Otherwise we are merely thrashing about in quicksand.

  63. For further clarification: I mean that some people can be infected with, for them, a “manageable load of sarscov2 virons” that their immune system successfully fights off perhaps without them even thinking they caught it, yet they carry it and spread it along the way.

    The thought that asymptomatic.spread is rare, when the spread of the virus is rampant, seems highly counter logical, counter intuitive, statistically unlikely, counter to 99% of what we understand about microbial infection spread, and the success of vaccines now supports the opposite, as predicted it would.

    1. Covid is likely spread by mild cases primarily, in my view. Just a cough with no fever. Maybe through casual sex, which actually occurs quite often in nursing homes. Those randy seniors!

      1. This is often the case – more severe cases feel sick and usually stay home (cutting down of opportunity). transition seem to be correlated to the presymptomatic stage and/or mild symptoms

  64. Ha! Funny. Randy seniors.

    You consider mild cases, to be symptomatic? This is where we differ. I consider mild cases to be un-reported by and large (large statistical support that people are avoiding hospitals), then by the time the whole inadequate test and trace system catches up, they are recorded randomly, with “guily” parties not wanting to think they might have spread the stuff. Behavioral reporting around contagious disease in retrospect for carriers skews heavily to “gee, I had know idea”.

    Novel idea. It’s not the ventilation systems but rather casual sex among navy personnel on ships. But it is funny…

  65. David, what’s the (our) assumption about mild cases? At what point, and how many are “non-help-seeking” mild cases not registered as cov19, by registered as asymptomatic? Mild symptoms being likely “flue-like” lasting a few days? Then later they get tested positive for antibodies (trace exercise), and they genuinely report “I didn’teven know I had it?” Do they get registered as “mildly symptomatic or asymptomatic”. I ask because the frequency of asymptomatic itself, as a statistic, seems greatly subject to error. As irrelevant as that sounds, this thread is about “spread from asymptomatic cases” which basically must ultimately rely on retrospective self-reports. Such data tend to be prone to error. I am not trying to be contentious or confrontational. But how many “mild cases” are out there that get (erroneously) classified as asymptomatic due to simple human memory and descriptive error?

    To me this points to unreliability of the stats. Leading to us assuming (null hypothesis) sarscov2 does not spread from asymps. When the nature of all microbial life is indeed to spread from host to host. We find ourselves now saying the same strain causes symptoms in one but not another person, and because of THAT asymps don’t spread. I just cannot get my logical head around that. Thoughts?

    1. What’s your point?
      Are the statistics perfect? No – From what I understand, most people assume that cases are under counted, with most of them asymptomatic. I would think that lost of people have mild cases, and don’t go get tested/treatment. But I would also assume that this is relative to different countries, and their testing methodology and capacity (it seems that Sweden is among the worst, only catching 1/3 of all cases). The best ‘track-and-trace’ systems can only track <70% of cases, so who knows how many asymptomatic transitions there are. This is even more complicated by the fact the rates of transmission is effected by living conditions (home life, environmental conditions etc.). It also seems that not all people transmit at the same rate.
      Don't forget that you can't call a case 'asymptomatic' tell they have 'recovered' (or no longer test for the various), so it's only in hindsight. So when s person test positive but (still) doesn't have symptoms, you don't know what way it will go.
      My 'guess' is that asymptomatic cases are less infectious, but how much I don't know. Even an infectiousness of 25% could contribute significantly to total transitions, due to the increased opportunity.
      Your logic has nothing to do with biology – only with your narrative from your own knowledge. I think that a major question is – what do you want the cost to be if you're wrong?

  66. David. Thank you. Not sure you understand me. Wrong about what? To be clear, are you interpreting me to say asymps. don’t transmit? Or asymps do transmit? And should we worry? Or not?

    You asked: what’s my point? My point is I assume asymp tramission happens. I further believe we don’t have any good reliable stats on asymp cases. I further draw attention to biology aka microbial spread is the normal, irrespective of whether or not a person shows symptoms. I therefore believe we should assume asymp transmission happens because to assume it does not is more risky than not to.

  67. This is an info sheet for health care professionals in British Columbia on how to interpret PCR (NAT) results:

    This is the last paragraph (note, NAT=PCR):

    Ultimately, for COVID-19 testing, there is currently no gold standard, and the overall clinical sensitivity and specificity of NAT in patients with COVID-19 infection is unknown (i.e., how well NAT results correlate with clinical infection, “true positivity” or “true negativity” rate).

    This was published in April, 2020 and has never been amended.

    I conclude that everybody is driving in the dark on a foggy night with the lights off.

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