Herd immunity without antibodies?

Herd immunity when a minority have antibodies

“Only a minority of people in Sweden have antibodies, so they can’t have herd immunity!”

That is the most common argument I’ve been hearing for why Sweden can’t have achieved herd immunity. This is in spite of the fact that the rates of hospitalizations and deaths have dropped continuously since the peak in April, and are now stable at basement levels.

The argument is also made in spite of the fact that the most recent currently available antibody data (showing that 19% in parts of Stockholm had antibodies and 7% in Sweden as a whole had antibodies) is three months old or older. And in terms of covid spread, three months is an eternity.

A study that was carried out in Japan over the summer, looking at the prevalence of antibodies among asymptomatic workers at a number of different locations around Tokyo, found that antibody levels rose from 6% to 47% over the course of the three summer months.

What conclusion can we draw? It is perfectly possible that 50% of Sweden’s population have antibodies by now, which negates the whole premise of the “only a minority have antibodies” argument. We’ll know whether that is true or not when newer antibody data becomes available from the Swedish public health authority later this year.

Apart from that, there are a few reasons why herd immunity might be achieved with only a minority of the population having antibodies, both epidemiological (to do with how the infection spreads in a population), and immunological (to do with how the immune system works).

In the rest of this article I will focus on the immunological reasons why herd immunity is possible when only a minority have antibodies. I have been receiving a lot of e-mails lately asking me about specifics of how the immune system works, so I thought it would be useful to discuss the topic in some detail. The following is a crash course in the workings of the immune system, which should help you to understand the current discussions happening in society about T-cells, antibodies, herd immunity, and whether reported cases of re-infection are real or not.

Innate immunity

The immune system consists of two fundamental parts: the innate immune system and the adaptive immune system. The innate immune system is the first part to become activated when the body encounters a new pathogen, and it consists of four parts.

The first part is physical and chemical barriers like skin, phlegm, and stomach acid, that serve to make it harder for a pathogen to get further in to the body.

The second part is immune cells that specialize in hunting down and destroying foreign invaders. These include macrophages (literally “big eaters”), which eat or wall off anything foreign that they come across, and neutrophils, which destroy bacteria.

The third part of the innate immune system is proteins, produced by the liver, that interfere with the functioning of pathogens. The most important example is the complement system, which consists of a sequence of different proteins that bind to and disable pathogens. This is the reason people with liver failure are so prone to having severe infections – they no longer have these essential proteins floating around in their bodies.

The fourth part is a collection of internal mechanisms that all cells in the body have to detect when they have been invaded, and which causes them to activate internal defences and to warn neighbouring cells that there is an infection going on. Interferon is one such signaling molecule that is released by cells when they realize that they have been invaded by viruses. It causes the infected cell to lock itself down, making it much harder for viruses to replicate inside it.

The cells, proteins, and internal mechanisms of the innate immune system are all activated in the same basic way. They recognize conserved features that are common among pathogens. An example might be a molecule called lipopolysaccharide, which is common on the surfaces of many bacteria. Another example is double-stranded RNA, which does not exist naturally in the human body, and if it is present inside a cell it is a sign that the cell has been invaded by a virus.

Since the innate immune system is always present and always active, it can react quickly. But since it needs to be able to react to many different types of pathogen (bacteria, viruses, parasites), it is not particularly effective at dealing with any single one. It is like a swiss army knife – it does lots of different jobs, but none of them extremely well. That is where the adaptive immune system comes in.

Adaptive immunity

The adaptive immune system consists of two main parts, T-cells and B-cells. B-cells make antibodies, which are proteins that can bind to pathogens and interfere with them in some way. Antibodies are similar to complement in the sense that they bind to and incapacitate pathogens, but whereas complement is always present and recognizes conserved features shared by many pathogens, antibodies are much more specific, and only appear after the body has encountered a new pathogen for the first time.

T-cells are the other part of the adaptive immune system. They can be further subdivided in to several specific types. The two main ones are T-helper cells (also known as CD4+ T-cells) and T-killer cells (also known as CD8+ T-cells).

T-helper cells are the “brain” of the adaptive immune system. They regulate the function of the other parts. Both B-cells and T-killer cells can only become fully activated after T-helper cells have been activated. That is why everyone who has antibodies by definition also has T-cells. T-helper cells are needed in order to activate B-cells.

The fact that T-helper cells are so central to the adaptive immune system is the reason HIV is such a deadly disease. The HIV virus specifically targets T-helper cells, and kills them. Without T-helper cells, the rest of the adaptive immune system cannot become activated, and so the person becomes highly susceptible to other infections. It’s not the HIV itself that kills people, it’s the fact that the immune system becomes too crippled to deal with other infections.

T-killer cells are quite different in function from T-helper cells. They are specifically designed to stop viral infections. Once they have become activated, they search out cells that have become infected by a virus and tell those cells to commit suicide. This prevents the virus-infected cells from releasing more viruses in to the body, and stops the infection in its tracks.

That is why T-killer cells are actually more central to the defence against viruses than antibodies are. T-killer cells keep viruses trapped inside infected cells, which prevents them from spreading and infecting other cells. Antibodies can only attack virus particles that are floating around outside cells – they can bind to and inactivate these virus particles, but they are only really keeping the problem at bay temporarily, because they cannot do anything about the virus particles that are multiplying inside cells. Antibodies are big molecules and have no way of crossing the cell membrane and entering cells. They always only exist outside cells. That is why antibodies are most effective at dealing with big pathogens that always exist outside cells, like most bacteria and parasites.

I mentioned before that B-cells produce antibodies. There are actually several different types of antibodies. When B-cells are first activated, they produce IgM. IgM are short lasting antibodies, generally present in the body for only a month or two at most, and they are not very specific. After a few weeks, the B-cells will usually do something known as “class switching”, where they will stop producing IgM antibodies and instead start producing other types of antibodies that are more specific. These new antibodies are generally much more long lasting than IgM.

There are four types of antibodies that can be produced after class switching. The most common antibody type is IgG, which is also the type most commonly measured in clinical antibody tests. IgG is found throughout the body.

Another important type when it comes to covid-19 is IgA, which is found primarily in areas where the body is in direct contact with the outside world, such as the lining of the respiratory tract and the gut (technically, the contents of the gut are outside the body – weird, right?). The reason IgA is important with regards to covid is that covid is a respiratory virus that is found primarily in the respiratory tract. The main difference between IgG and IgA is that IgA is hardier than IgG. It is designed to exist in harsh environments, like the respiratory tract and gut, where IgG would quickly be degraded.

Why am I talking about IgA? Because a recent study from Switzerland found that 15-20% of people who didn’t have IgG antibodies to covid-19 in their blood stream did have IgA in their respiratory tract. The reason this is important is because most antibody tests only look at IgG in the blood stream, which means that a significant number of people with antibodies to covid will be missed by standard antibody tests.

Immune memory

While the innate immune system is like a swiss army knife, the adaptive immune system is more like a very specific type of screw driver. It only does one job, but it does it very well. The adaptive immune system takes time to wake up the first time the body encounters a new pathogen, but the next time it encounters the same pathogen it reacts much more quickly, thanks to “immune memory”.

When the adaptive immune system is activated, some of the T-cells and B-cells will become memory cells. They will bide their time in the body in a state of dormancy, and the next time the body encounters the pathogen, they will quickly become activated and start mass producing clones of themselves. This usually results in the infection being dealt with before the rest of the body even realizes it has become infected.

What does this mean? That having immunity to an infection doesn’t prevent re-infection, as some people seem to think based on media reports of people having a second covid infection in spite of not having any symptoms. It just means that when re-infection happens, the adaptive immune system wakes up so quickly that the infection is dealt with before the rest of the body realizes what has happened. That is what immunity means, that the body reacts so quickly that the pathogen doesn’t have time to do damage, not that the body can’t be reinfected.

One thing to note about immune memory is that memory B-cells are dormant. This means that they are not actively producing any antibodies. So if you just look for antibodies in the bloodstream, you won’t know whether there are memory B-cells present in the body or not. What I’m getting at with this is that just because someone doesn’t have measurable antibodies any more after an infection, doesn’t mean that all the B-cells have disappeared, and doesn’t mean that the person no longer has B-cell based immunity.

A final thing to note is that T-killer cells and B-cells are activated along separate pathways (although both require T-helper cells to be activated). So it is perfectly possible for an infection to result only in T-killer cell activation, and also for an infection to only result in B-cell activation. Either pathway can result in immunity to viral infection. The more severe a viral infection is, the greater the likelihood that both pathways will be activated.

This has been shown clearly by a Swedish study that I wrote an article about a while back. In that study, more serious illness was correlated with a greater likelihood of developing both antibodies and T-cells. However there was a significant number of people who had T-cells specific for covid-19 but who didn’t develop antibodies. Those people likely have immunity to covid-19, but won’t be visible in an antibody test.


I hope this helps people understand the discussions currently going on about T-cells, antibodies, herd immunity, and whether or not people can be reinfected with covid-19, and also helps people to understand why it is perfectly possible to become infected with covid, and develop immunity, without ever developing measureable IgG-antibodies. I hope it also explains why it is perfectly possible to still have functioning immunity even if the antibodies that can be measured in the blood stream disappear after a few months.

You might also be interested in my article about why I think Sweden now has herd immunity, or my article about whether you should take fever lowering drugs when you’re sick. If you haven’t already done so, I would strongly urge you to read my guide to scientific method in medical and health science.

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32 thoughts on “Herd immunity without antibodies?”

  1. This is a great explanation of how the immune system works and why there can indeed be herd immunity without antibodies. I don’t have a science background, but I understood it so well the way you explained it. I’m learning so much from your blog with every post. Thank you for writing this.
    What you say makes a lot of sense as to why the tests are not finding antibodies, even in people that do have them! Thank you for educating us on the information we need to know to see where things are going wrong with the handling of this situation. Your posts are invaluable.

  2. This explains how the immune system works so well, and how you can definitely have herd immunity without antibodies. I don’t have a science background, but I understood it very well the way you’ve explained it. I’m learning so much from your blog. Thank you for writing this.
    I can see how even the tests that are designed to detect antibodies, are failing to, even in people who do have them! Thank you so much educating us on what we need to know in order to see where things are going wrong with the handling of this situation. Your posts are invaluable.

  3. Thank you for this very well written article. A few days ago, I was looking for just such an explanation of how the immune systems work together and found little that could be called concise, without all the ‘aren’t-I-clever’ bits. I found you via Malcolm Kendrick and this is just what I wanted. I have also found your other posts to be valuable too.

  4. That was very interesting and important information, which helps explaining a lot of the misconceptions in the msm. The fact that the immune system consists of an ”innate immune system” (Swiss knife) and an ”adaptive immun system” (specific screw driver), is critical information, if you want to understand the bigger picture of immunology.
    Also the fact that the T-cells are a much better indication of herd immunity, than the weaker and often misleading indication (or lack thereof), of lgG antibodies in the blodstream.
    Dr. Rushworth proves once more that he is one of the shining beacons on the horizon.
    Thank you.

  5. Thank you very much, Dr. Rushworth! It will take more than one reading to grasp, as does anything worth reading.

  6. Sebastian

    Earlier in the pandemic there was a hypothesis that nicotine could have some kind of protective effect against Covid19. At the time I thought , I gather that Sweden has a lot of people who regularly use SNUS so it would be interesting to know if that group of swedes were underrepresented etc in Covid19 presentations. Do you know if any data is available on that question?

  7. Great article, fascinating how the human immune system works.

    Equally interesting is to try to understand why other countries seem to be adamant to prove that the “Swedish Experiment” did not work.

  8. Immune system is very complicated and most of graduated physicians don’t understand fully as there is much “blank spaces” …. Sebastian are you graduated in immunology?

    1. Saying that two covid deaths per day is unacceptable is ignoring the facts that everybody dies, and that everybody has to die of something. What about the other 250 people who die every day in Sweden? Why are covid deaths the only deaths that matter? It makes zero sense. More people are dying of pneumonia and influenza every day in Sweden than of covid. Why is it so important to stop one specific infection but not others?

  9. Thank you, it makes sense what you are saying. It all points to one very important thing and that is to invest in the basics of population health such as alleviating poverty, promoting nutrient-rich nutrition and practicing preventive medicine – keeping 20 years ahead of any disease.

  10. Thank you for this description of the immune system and function. Very helpful. Do you know of any diagnostic tests for T cell immunity? Also, do you have any thoughts/info on coronavirus T cell cross reactivity and immunity?

    1. Hi, no-one really looks for T-cells in clinical practice, because it’s more expensive than checking for antibodies. It’s mainly used in research at this point in time. I think T-cell cross reactivity may well be a big part of the explanation why so many people seem to be immune to covid without having been infected.

  11. Thank you for all your insightful posts in general and on the swedish perspective in particular.

    Obviously there are very influential, commercial interests in covid19 and an eventual vaccine. The fearmongering and misinformation seem to have reached the journal “Nature” yesterday:


    The article is written by “science journalist Christie Aschwanden” and contains several references to scientific publications, but also many unsubstantiated claims. After citing swedish minister Lena Hallengren on the strategy followed, it is postulated that “Sweden is hardly a model of success”, and the high number of covid19-deaths is once again promoted as proof.

    What is going on, and what is your opinion?

    1. Hi Lars,
      There is a widespread campaign of disinformation, both to make covid seem much more deadly than it is, and to make natural herd immunity seem impossible without a vaccine. I think there are a lot of different motivations underlying this. The pharmaceutical companies obviously want to sell vaccines, so they have a strong vested interest in selling this idea. China wants the rest of the world to adopt severe measures that damage their economies in order to increase its relative geopolitical power. And politicians and others who heavily pushed for the lockdown earlier on don’t want to look stupid by backing down now. And then there are a lot of, as we say in Sweden ”nyttiga idioter”, i.e. people who have bought in to the propaganda.

      Even the WHO now admits the fatality rate for covid is around 0,13%, barely worse than regular flu. And the fact is that there is no excess mortality in Sweden this year, in spite of very few measures to contain the virus. Which can only mean that the vast majority of people who have died of covid would have been dead by now anyway, even without covid. In other words, covid is just replacing other things as the cause of death on death certificates, but it is not actually shortening lives.

  12. Dear Dr. Rushworth,
    I live in Uruguay. I found your blog looking for information on coronavirus. I want to thank you deeply for your time and dedication in writing about this and other topics in such a precise, clear and interesting way. In addition to being highly didactic, it is a very clear example of a deep capacity for analysis and critical thinking. In addition to learning a lot, I have been surprised that even reading irreproachable technical analysis articles, it has often made me laugh. Thank you very much.

  13. Any hints at when we might learn more recent seroprevalence data (from Sweden or other places)? The Japanese increase over summer without deaths is very interesting! Any hints at when we might learn more recent seroprevalence data (from Sweden or other places)?

  14. Sebastian,
    We are getting news in New Zealand that Sweden has made some big mistakes and cases are soaring right now. Some of us here in NZ are pinning our hopes on Sweden, showing us that there are viable alternatives to lockdown and isolation while waiting for the Magic Bullet (vaccine). If Sweden is, in fact, not working well, then we in NZ are in trouble since alternatives we are promoting will never be considered, let alone adopted by those in charge of our COVID response.

    Here is the news that appeared in our largest newspaper:

    Would you mind commenting?

    1. Hi Peter,
      As you can see from the graph you link to, there was an increase in mortality that lasted two months in the spring. Since then Sweden has been tracking in line with the average. If you look at the full year so far, Sweden is in line with the average for the preceding five years, so covid has not had any noticeable effect on overall mortality if you look at the year as a whole. The last time Sweden had a deadlier year was 2015. Personally, I don’t remember any huge deadly pandemic happening then.

    1. Hi Peter,
      That article is disingenous because it is comparing a Sweden with population 4 million to a Sweden with population 10 million. It is more correct to look at deaths per 100,000. If you do that you see that the last time Sweden had a higher death rate was 2015. At the moment, Sweden is tracking for an average year in terms for deaths per 100,000.

  15. Hello Sebastian
    Could an past infected person which already get immunity to virus to release in air degenerate ARN messenger of viruses? Imagine next scenario: the virus (ARN messenger) is catch by cell and that system have an autoimune illness and when cell start to replicate virus (ARN messenger), some how beside valid replica of virus to made a degenerate variants of virus. Mean cell have own ADN and the result of replica action could be: 1) almost same virus (ARN messenger) which is a viral agent; 2) a modified variant of virus, weak enough to be destroyed by Tcell and 3) a degenerate variant of virus which is not capable to spread ill but can stay inactive for awhile. if those 3 cases when the person exhale, the modified virus (ARN messenger) are passed by air to another person, immune system and that immune system take action on ARN messenger again. so when we have a herd of people which is in action and feedback loop with others, again and again those all immune systems are confronted with viruses somehow in natural way they reach a weak variant of virus and start to produce antigens. like a network of immune systems what are sharing information and actions against viruses until all herd got immunity? is this possible?

  16. Great overview!

    Few questions:
    1. If no antibodies doesn’t necessarily mean you have no immunity, is the opposite always true?
    Namely, high number of antibodies implies immunity?

    2. What is a reliable test, if any, for immunity?

    3. What does “asymptomatic infection” mean? Is immunity developed with asymptomatic infection?
    It seems that if you had asymptomatic infection, that your adaptive immune system wasn’t activated.

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