How To Think About Immunity to COVID-19

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This is what immunity is not: You are an organism walking down the street, and you are immune to the rare virus squirrelpox. A squirrelpox virus is walking on the same sidewalk towards you. It sees you, and goes, “that one’s immune to me,” and quickly crosses the street, going nowhere near you. Beause you are immune.

This is what immunity often is: You have built up an immunity to a common cold virus. Somebody infected with that virus sneezes on you and now that virus is in you. It begins to reproduce and do its thing, and you develop cold symptoms. However, your adaptive immune system has seen this virus before, so it quickly mounts a defense, so even though you do get a cold, you fight it off quickly and in five days you feel fine.

Lots of times, though, immunity works like this: You have an immunity to a certain disease. Perhaps you had that disease earlier in your life and your adaptive immune system developed a strategy to attack this pathogen next time it comes around. Perhaps you got a vaccine that prompted your adaptive immune system to develop a strategy to attack this pathogen next time it comes around. The virus goes in you — the virus does in fact infect you, it does not “cross the street” to avoid you. But your body is so ready for it that the counter attack is fast and effective, and before you can either develop symptoms or start passing the disease on to someone else, your body’s immune system has literally killed it.

An acquired or induced immunity can be called “100%” and it can be “life long” but it is never able to actually keep the disease out, and it is likely that few, if any, adaptive immune system build-ups last for the entire life of a person who lives a long time. Some immunity does not stop you from getting sick but does cause you to get better faster, and some immunity doesn’t last that long.

Much of the misunderstanding about immunity comes from the fact that our understanding of immunity comes from two distinct diseases: Polio and influenza. Polio vaccine is famous because its invention and deployment was historic and significant. Polio vaccine confers a strong immunity, one that is seen as life long and complete. Even this is not so simple, but if you believe what I just said about polio vaccination and immunity you would be in the ballpark. Influenza immunity is often discussed because it is at the center of the anti-vax debate, everyone gets the flu now and then (or so it seems) and the so-called “flu vaccine” is supposedly only “60% effective” or thereabouts, and thus, being imperfect, is the focus of rage on the internet as though it was a candidate for office.

If polio is an outlaw gunslinger in the old west, and the polio vaccine is Marshal Dillon, then influenza is all the underground crime organizations imagined in fiction and the flu vaccine is a competent but underfunded police agency.

When we say that the influenza vaccine is 50% effective in a give year in the US, as an example, what that can mean is that there are five kinds of flu circulating at various proportions in the population, and there are three kinds of vaccine in the shot you get; maybe two of those vaccines are nearly 100% effective in immunizing a person against two of the circulating influenza viruses, one of the viruses is untouched by the vaccine but doesn’t get you that sick, and one of the vaccines is for a virus that never really showed up, and the leftover viruses are the ones doing most of the damage. Or something along those lines. The outcome is, across the population, that the average vaccinated person in the population under consideration would have their chance of getting the flu if exposed is half what it would have been were they not vaccinated. So, 50% effective that year. Some other year these parameters may be very different, and the “vaccine” (a mix of different vaccines in one shot) is different. And, each vaccine may itself have a higher or lower level of effectiveness.

And that is the simple version of the story.

Immunity is not a folk concept. It is a medical concept. The fact that many people believe that immunity is the inability of a disease to affect a person, which is 100% wrong in every way, is not relevant to anything but people’s misunderstanding of the concept.

When we hear that there is a certain possible reinfection rate of COVID-19 in China or Japan, this does not mean that people don’t get immunity once they have the disease, or that COVID-19 has special powers. One health expert misstated that since we don’t know for sure what acquired immunity to COVID-19 looks like, we can’t assume that it is long term. That is balderdash. It is very likely long term (if “long” is years) because that is what normally happens. This statement is like looking at the first new car off the line of a new make and model and saying, “since we’ve never actually seen one of the drive, we have to assume there is a good chance none of these cars will work.” There may be a few recalls in the future of this make and model car, but it will work.

We can assume normalcy, we can assume biology to do what biology does. Bill O’Reilly does not know how tides work, but someone else does. Normally, adaptive immunity occurs, and lasts for a good time. Normally, immunity to certain kinds of viruses can be less than 100%, so there is some getting sick, and normally, a subset of people don’t develop much of an immunity because their own immune system simply fails at that task. COVID-19 will ultimately be found to match normal biological expectations, though we don’t know the details yet, and we won’t for some time. The fact that normal biological expectations do not form the basis of folk thinking about this disease, or pathogens and immunity in general, does not make Covid-19 a preternatural force, or an unknowable thing.

Still, remain hiding in your house until the all clear.

There is another level of thinking about immunity that I won’t go into detail about right now, but I’ll mention. We often, rightly, think of immunity at the population level, even though it does, truly, work at the individual and molecular level. Assume a particular vaccine, or exposure, typically provides ~100%) immunity in individuals. If 10% of the population have that immunity at the start, the disease will act like nobody is immune, as far as we’d be able to see. Often, natural (genetic?) immunity at low levels exist in a population, and can only be discovered by intensive research over a long time. If, on the other hand, 90% of the people in a population are ~100% immune, the disease may be so unable to get a foothold that it is like it isn’t there. The point is, the appearance of a diseases behavior seems to range from 0% (there ain’t none) to 100% (it’s everywhere!) on the surface, but this outcome is a function of a much smaller range of actual immunity values, like the 10-90% just noted, or more likely, closer to 0-70%. Putting this another way, a population gets very close to “immune” at the population level as the proportion of individuals who can’t get and pass on the pathogen rises over about half. This is called herd immunity. It will take several cycles of COVID-19 infection to achieve natural herd immunity, most likely, unless a vaccine is found. But once that happens, the disease is likely to stay around at low levels then occasionally come back and be menacing, but not as bad as it is now, on occasion.

So, let’s get that vaccine going!

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24 thoughts on “How To Think About Immunity to COVID-19

    1. 742 cases as of morning of April 3, 2020 – not that low. 18 states have a lower number of cases than Minnesota.

      But I would say it is because we are in the middle of the country. So less traffic from infected cases from outside the USA. Less population density than New York city is a factor also.

    2. Those states with lower number of cases have much lower populations. Of states with similar population, only Alabama is close to Minnesota’s number, and even that is about 1300 cases, 60% higher.

  1. “So less traffic from infected cases from outside the USA”

    Only an idiot thinks “those foreigners” are driving this.

    Oh, it’s rickA. Idiot, bigot and racist.

    1. Dean,
      do you think Andrew Cuomo is an idiot, bigot and racist?

      [New York City is a world-renowned tourist destination and the most visited destination in the US. As such, Cuomo said that contagious people from countries that had earlier coronavirus outbreaks traveled to the city and spread the virus.
      “We have international travelers who were in China and who were in Italy and who were in Korea and who came here,” Cuomo said Wednesday. “And I have no doubt that the virus was here much earlier than we even know. And I have no doubt that the virus was here much earlier than it was in any other state. Because those people come here first.”

      President Donald Trump implemented a series of travel restrictions to try to stop that spread. On February 2, the US implemented strict travel restrictions on those who had recently been to China. And on March 11, Trump said he was suspending travel from two dozen European countries, including Italy.
      Still, those moves were too late to stop the virus from reaching New York because of its heavy travel, Caplan said.
      New York’s heavy travel “sort of made the virus arrive here earlier,” he said. “It started here faster.”]

      Dr. Arthur Caplan is a CNN medical analyst and the head of the Division of Medical Ethics at NYU’s School of Medicine.

    2. snape, if you can’t keep up don’t bother. rickA’s comments over the years have cemented his characteristics: liar, science denier, racist, bigot, and more.

      something like you.

  2. One health expert misstated that since we don’t know for sure what acquired immunity to COVID-19 looks like, we can’t assume that it is long term. That is balderdash. It is very likely long term (if “long” is years) because that is what normally happens.


    1. This recent review article, “IMMUNE RESPONSES TO COVID-19 AND POTENTIAL VACCINES: LESSONS LEARNED FROM SARS AND MERS EPIDEMIC,” Prompetchara E, Ketloy C, Palaga T, – Asian Pacific Journal of Allergy and Immunology 38(1):1-9 (March 2020) – addresses many of the topics and issues discussed above.

      The authors are immunologists and infectious disease experts at Chulalongkorn University (Bangkok), Thailand’s (and one of Asia’s) foremost biomedical research center.

      Although SARS-CoV-2 has some especially scary features that we are rapidly learning more about (e.g., CNS involvement), there’s no evidence to suggest that long-term immunity, at least to current strains, will not occur after recovery from Covid-19.


      “In general, the Th1 type immune response plays a dominant role in adaptive immunity to viral infections. Cytokine microenvironment generated by antigen-presenting cells dictate the direction of T cell responses. Helper T cells orchestrate the overall adaptive response, while cytotoxic T cells are essential in killing of viral infected cells. Humoral immune response, especially production of neutralizing antibody, plays a protective role by limiting infection at later phase and prevents reinfection in the future. In SARS-CoV, both T and B cell epitopes were extensively mapped for the structural proteins, S, N, M and E protein.”

      “SARS-CoV infection induces seroconversion as early as day 4 after onset of disease and was found in most patients by 14 days. Long-lasting specific IgG and neutralizing antibody are reported as long as 2 years after infection. For MERS-CoV infection, seroconversion is seen at the second or third week of disease onset. For both types of coronavirus infections, delayed and weak antibody response are associated with severe outcome. A limited serology details of SARS-CoV-2 was reported. In a preliminary study, one patient showed peak specific IgM at day 9 after disease onset and the switching to IgG by week 2. Interestingly, sera from 5 patients of confirmed COVID-19 show some cross-reactivity with SARS-CoV, but not other coronaviruses. Furthermore, all sera from patients were able to neutralize SARS-CoV-2 in an in vitro plaque assay, suggesting a possible successful mounting of the humoral responses. Whether the kinetic/titer of specific antibody correlates with disease severity remains to be investigated.”

      “T cell response in SARS-CoV was extensively investigated. In one study using 128 convalescent samples, it was reported that CD8+ T cell responses were more frequent with greater magnitude than CD4+ T cell responses. Furthermore, the virus-specific T cells from the severe group tended to be a central memory phenotype with a significantly higher frequency of polyfunctional CD4+ T cells (IFN?, TNF?, and IL-2) and CD8+ T cells (IFN?, TNF? and degranulated state), as compared with the mild-moderate group. Strong T cell responses correlated significantly with higher neutralizing antibody while more serum Th2 cytokines (IL-4, IL-5, IL-10) were detected in the fatal group. For the epitope mapping, most responses (70%) were found against the structural proteins (spike, envelope, membrane, and nucleocapsid). In MERS-CoV infection, early rise of CD8+ T cells correlates with disease severity and at the convalescent phase, dominant Th1 type helper T cells are observed. In an animal model, airway memory CD4+ T cells specific for conserved epitope are protective against lethal challenge and can cross-react with SARS-CoV and MERS- CoV. As neutrophils play a destructive role in all infections, the protective or destructive role of Th17 in human coronavirus infection remains unanswered.”

      “Current evidence strongly indicated that Th1 type response is a key for successful control of SARS-CoV and MERS-CoV and probably true for SARS-CoV-2 as well. CD8+ T cell response, even though crucial, needs to be well controlled in order not to cause lung pathology. Because most epitopes identified for both viruses concentrate on the viral structural proteins, it will be informative to map those epitopes identified with SARS-CoV/MERS-CoV with those of SARS-CoV-2. If overlapping epitopes among the three viruses can be identified, it will be beneficial for application in passive immunization using convalescent serum from recovered SARS or MERS patients. For T cell epitopes, it will help in designing cross-reactive vaccine that protect against all three human coronaviruses in the future.“

  3. Roger D. Seheault is a pulmonologist and critical care specialist at UC-Riverside and Loma Linda University medical schools. By days he attends to ICU patients – many with Covid-19 – and, almost nightly, creates outstanding videos on various aspects of the pandemic. Some of these videos are quite basic, while others provide fairly rigorous primers on immunology and basic biochemistry. His explanations and graphics are straightforward, and they always include primary journal citations.

    I highly recommend his videos.

  4. A useful read for those who don’t understand the problems in developing vaccines and much else on this complex topic:

    Deadliest Enemy: Our War Against Killer Germs.

    Took some time arriving but worth it so that I can pass on to others.

    Shame that the POTUS will not be able to read and understand a work such as this, that is America’s tragedy, the populace has been persuaded to elect one totally unsuited to the post. The founding fathers would be rolling in their graves.

    “We don’t know at what point that bone-chilling figure was presented to Donald Trump. What we do know is that on the same day, 6 March, the president of the United States was taking a tour of the Atlanta offices of the federal disease control agency, the Centers for Disease Control and Prevention (CDC).

    He was in ebullient mood. He had just heard on Fox News that the latest tally of coronavirus cases in the country was 240, with 11 deaths. Trump and his favourite TV channel were as one in their interpretation of those figures – things were going great, there was really nothing to worry about.

    Source: “How science finally caught up with Trump’s playbook – with millions of lives at stake”

  5. Also from The Guardian:

    When the definitive history of the coronavirus pandemic is written, the date 20 January 2020 is certain to feature prominently. It was on that day that a 35-year-old man in Washington state, recently returned from visiting family in Wuhan in China, became the first person in the US to be diagnosed with the virus.

    On the very same day, 5,000 miles away in Asia, the first confirmed case of Covid-19 was reported in South Korea. The confluence was striking, but there the similarities ended.

    In the two months since that fateful day, the responses to coronavirus displayed by the US and South Korea have been polar opposites.

    One country acted swiftly and aggressively to detect and isolate the virus, and by doing so has largely contained the crisis. The other country dithered and procrastinated, became mired in chaos and confusion, was distracted by the individual whims of its leader, and is now confronted by a health emergency of daunting proportions.

    Within a week of its first confirmed case, South Korea’s disease control agency had summoned 20 private companies to the medical equivalent of a war-planning summit and told them to develop a test for the virus at lightning speed. A week after that, the first diagnostic test was approved and went into battle, identifying infected individuals who could then be quarantined to halt the advance of the disease.

    Some 357,896 tests later, the country has more or less won the coronavirus war. On Friday only 91 new cases were reported in a country of more than 50 million.

    The US response tells a different story. Two days after the first diagnosis in Washington state, Donald Trump went on air on CNBC and bragged: “We have it totally under control. It’s one person coming from China. It’s going to be just fine.”

    1. More from the Guardian:

      Donald Trump was warned at the end of January by one of his top White House advisers that coronavirus had the potential to kill hundreds of thousands of Americans and derail the US economy, unless tough action were taken immediately, new memos have revealed.

      The memos were written by Trump’s economic adviser Peter Navarro and circulated via the National Security Council widely around the White House and federal agencies. They show that even within the Trump administration alarm bells were ringing loudly by late January, at a time when the president was consistently downplaying the threat of Covid-19.

      The memos, first reported by the New York Times and Axios, were written by Navarro on 29 January and 23 February. The first memo, composed on the day Trump set up a White House coronavirus task force, gave a worst-case scenario of the virus killing more than half a million Americans.

      According to the Times, it said: “The lack of immune protection or an existing cure or vaccine would leave Americans defenseless in the case of a full-blown coronavirus outbreak on US soil. This lack of protection elevates the risk of the coronavirus evolving into a full-blown pandemic, imperiling the lives of millions of Americans.”

      The second memo went even further, predicting that a Covid-19 pandemic, left unchecked, could kill 1.2m Americans and infect as many as 100m.

      This was not the first time Trump and his White House team were warned that the virus had the potential to devastate the US and needed to be dealt with quickly and firmly. Senior scientists, epidemiologists, and health emergency experts in the US and around the world delivered that message clearly early on in the crisis, only for Trump to continue belittling the scale of the threat which he compared falsely to the dangers of seasonal flu.

      There are signs that ministers in the UK are trying to rewrite history and blame NHS England and the Civil Service for the lack of preparedness in tackling a pandemic which was known to be coming even if the agent of harm was not known. If it had not been a Coronavirus it could have been another strain of influenza and one of those latter will strike us yet.

      ‘Deadliest Enemy: Our War Against Killer Germs’ provides a very important overview of all the issues involved in preparing for and combating such an outbreak.

  6. Lionel and Greg,

    Thanks again to you both for bringing this new book to my attention. It’s not yet out in hard copy (at least in the U.S., it must be pre-ordered), but it is available in audiobook format and on Kindle. I started reading it yesterday – I’m not quite sure why I’m SUCH a glutton for punishment; after all, I’ve got an entire bookshelf, plus a Kindle, stuffed with excellent books on the topic.

    In the end, last night at least, I put down Osterholm and re-read Camus’ “The Plague.” Whereas I generally recommend that people start with Paul Ewald, I now think perhaps the best primer is Albert …

    1. Thanks again to you both for bringing this new book to my attention. It’s not yet out in hard copy…

      Strange. The book ‘Deadliest Enemy: Our War Against Killer Germs’ was published in 2017 and I got hold of a copy (hardback) here in the UK without trouble.

  7. This very frequently updated YouTube channel is an excellent COVID-19 resource in general, and yesterday’s nice 12-minute video states the case against the likelihood of SARS-CoV-2 re-infection, by means of a simple review of some basic biology and a summary of a new South Korean study:


    The presenter is Roger Seheult, MD, a pulmonologist/critical-care doc (and sleep-medicine specialist) treating COVID-19 patients in ICUs in southern California.

    1. It was worthless rickA. There was nothing there. That was pointed out to you, with detailed explanation, a couple times. The fact that you are too fucking stupid to understand it doesn’t mean other people are in the same boat.

  8. As an aside, all of this vociferous support for Sweden’s supposed ‘herd immunity’ approach to Covid-19 (which it wasn’t really) has mostly melted away as the death toll has mounted there. Last week Sweden’s per capita death toll was the highest in the world, surpassing the UK which, as Ian Sinclair pointed out yesterday, was certainly a herd immunity approach until it was pointed out that 200,000 to 400,000 people would die to reach the herd immunity threshold. And by the time the incompetent Conservative regime reacted with a lockdown, it was too late to prevent tens of thousands of people from dying unnecessarily.

    As for Sweden, despite models predicting that 25% of the people in Stockholm had been infected by Covid in early May, the more reliable figure looks like around 13%, or not much different from data obtained in France, Spain and Italy. And outside of Stockholm the infection rates are much lower than that.

    Herd immunity only works when a vaccine is available. Period. I am therefore flabbergasted when one of Sweden’s chief epidemiologists, Johan Giesecke, argues for a herd immunity approach saying that lockdowns only postpone deaths until later. But ‘later’ may mean a vaccine is available! It is a bit like saying that it is no use trying to put out a fire now as a house will probably burn down later – at a time when I may have bern able to better fireproof the house.

    1. How about keeping schools open to have the kids get infected, as close to 100% as you can get?
      Their parents will be more affected, but they can try and avoid for a few weeks.

  9. The answer is:

    How about keeping schools open to have the kids get infected, as close to 100% as you can get

    (Rings in) “Alex, what is “What’s the dumbest effing idea the clowns on the right have to offer?””

    That is the correct.

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