Immunity from COVID

Last updated August 28th 2020, 9:47:20pm

There are many conflicting messages about COVID-19 immunity. The head of the World Health Organization has suggested there was no reason to think that having COVID-19 once would mean you will not get it again. At the same time, some countries are considering granting “immunity” passports to people who have already been infected. We’ve heard broad discussion of “herd immunity” (the idea that if enough people have been infected in the past, viral spread cannot take off again) but it cannot be the case that there is both no immunity and herd immunity.

The basic issue is that there is a lot of uncertainty in our understanding of immunity to COVID-19. In large part, this uncertainty arises because the virus is new — we haven’t had enough time to study it. This uncertainty cannot be immediately resolved, and reasonable experts disagree about some aspects of immunity. But this doesn’t mean we know nothing, nor does it mean that we should make statements in the extremes.

Taking into account the uncertainty, we’ll find our best understanding lies between these extremes. Basic virus science and knowledge of related viruses tells us there will be some immunity. But we don’t know nearly enough to make statements like “This person is immune” or “If 62% of your population has had the virus, herd immunity is achieved.”

To understand why we have this uncertainty, we need to step back.

What is immunity?

When a person is immune to a virus their immune systems will destroy the invading virus/bacteria and they will neither become infected nor contagious. Our immune system is the body's protection from infection and it comes in two parts.

The first is called our innate immune system and is always ready to protect from a detected foreign invader. It includes defenses like mucus, secreted chemicals that cause inflammation, and macrophages, which are pac-man like cells that eat up infected cells. This part of our immune system has no memory for a coronavirus and will not give you immunity to COVID-19.

The second, your adaptive immune system, however, is powerful enough that it can retain a memory of infection by specific invaders and protect you from future infection. This part of the immune system includes 2 classes of response: An “antibody response”, caused by B-cells, and a “cell-mediated response”, caused by T-cells. T-cells kill virus-infected cells directly, while B-cells secrete antibodies to attack and neutralize the virus.

Because this response is so destructive, it is crucial that the T-cells and antibodies are attacking the correct invader and not other molecules in your body (an incorrect distinction here is the science behind an autoimmune disease). Because of this, it takes time for your adaptive immune system to learn to distinguish a new foriegn pathogen and to kick into gear (usually 5-7 days).

Once you recover from a virus, the antibodies, B cells, and T cells can stick around. They live to fight another day! So if your body re-encounters that same virus later in your life, you are ready for it — your adaptive immune system doesn’t have to go through the learning phase again. You can see why this makes sense from an evolutionary standpoint: people wouldn’t survive very long in a high disease environment (read, all of human history) if they were immediately reinfected with viruses.

In other words, these antibodies confer some “immunity”: they protect you from getting reinfected. You can test for them to get a sense of immunity levels (see our explainer on testing for how that works).

Antibodies and immunity

Antibodies are responsible for the science behind vaccines (while T-cells play an important part in immunity, all successful vaccines to date have used antibodies). When your kids get the measles vaccines, they are getting a weakened form of the measles virus which prompts the body to produce antibodies against measles. If your children then encounter the infectious measles virus out in the world, they already have the antibodies to fight it off and will not get sick.

The basic science here is not up for debate. Just like measles, the flu, chicken pox, etc, people who get COVID-19 and recover have antibodies for at least some time. And just like with those other viruses, you can test for these antibodies with a simple blood test (Note that many coronavirus antibody tests have high false positive/negative rates).

Having these antibodies means that you have been infected with coronavirus and it likely means that you have some protection from getting infected with the virus again for some time. However, there is a tremendous amount of uncertainty around how much protection these antibodies provide,for how long, and whether all individuals (asymptomatic or symptomatic) produce an adequate amount.

Does the number of antibodies matter?

There is variation across viruses in how many antibodies you need to be “immune.” Generally speaking, higher rates of antibodies confer more protection...but the “threshold” for immunity isn’t consistent.

There is also variation across people in their degree of antibody response — some people produce more than others, and people produce different types of antibodies (remember, there’s more than one kind produced for any given virus!) in different proportions. Some of this may explain the variation in severity of the infection.

It is possible to receive a blood test to detect the quantity of COVID-19 antibodies in your blood (these tests require more blood than a typical COVID-19 antibody test), but the conclusions we can draw from the amount of antibodies detected is limited. Many studies have shown that COVID-19 antibody levels decline soon after recovery, but it is unclear whether they decline to a “baseline” level that maintains an immune response, or if this decline translates to a decrease in immunity. Some studies show that asymptomatic individuals have a smaller antibody response, but again, it is not confirmed whether this means they are less “immune” to future infections.

So...How long is immunity likely to last?

There is a lot of variation across different viruses in how long antibodies and immunity stick around. It can depend on both the virus and the individual: Chicken pox antibodies seem to confer very long term immunity; flu much less so. In the case of coronavirus, many studies have shown rapid decays in SARS-CoV-2 antibody levels within 3 months after recovery. Many scientists are quick to point out that this might not be as worrisome as it sounds, saying that some decline in antibody levels is expected because the individual is no longer sick. It’s possible that once a person fights off an infection, antibody levels decline to a low baseline level and are ramped up again upon reinfection by other parts of our adaptive immune system — or that the baseline level itself might be protective.

Despite many studies showing rapid decays in antibody levels, one study found much more moderate decays and even some increases in antibody levels after infection over a span of three months. The CDC recently updated their guidelines to say that people who have had COVID-19 do not need to quarantine or get tested for up to 3 months after recovery as long as they do not develop symptoms again, emphasizing the widespread agreement among experts that immunity to the virus persists for at least three months

Although scientists have reasonable data to work with, it’s important to note that labs often develop their own antibody test and that none can say for sure whether the antibody they are measuring offers immunity. Additionally, antibody levels don’t always correlate with immunity. Studies on immunity against Middle East Respiratory syndrome coronavirus (MERS) have shown that T-cells, another part of the adaptive immune system (the part of our immune system that sticks around) can be detectable for four years, even after antibody responses are undetectable. Memory B cells, the cells responsible for producing antibodies, have been found in survivors of the 1918 Spanish flu over 90 years after infection. If this is true for COVID-19, a second infection would likely be much milder than the first.

Other coronaviruses that infect humans with the common cold offer immunity for about one year. There is evidence that some people previously exposed to these other coronaviruses have “cross reactive” T-cells that help provide some immunity to the novel coronavirus, SARS-CoV-2. This emphasizes the possibility that T-cells created in response to SARS-CoV-2 might offer some medium-term immunity. This “medium immunity” from past exposure to coronaviruses might also help explain why COVID-19 presents itself differently in different people.

Because the novel coronavirus hasn’t been around for even a full year, it is difficult to make a comparison to other viruses. The bottom line is that this coronavirus simply has not been around long enough for scientists to make a confident statement about immunity. The best we can do is study antibody levels, look at data from other viruses, and make predictions.

Has anybody gotten Coronavirus twice?

There have been several reports of discharged patients becoming “reinfected” with the coronavirus; however, the consensus in the scientific community is that most of these involved an issue with testing and these patients were falsely told that they were free of the virus (see our conversations with experts piece on immunity for more insights).

However, four recent cases of reinfection have been confirmed by genome sequencing. In these cases, genomes on the first and second viral infections were sequenced, and there was a mismatch, confirming that the second infection was distinct from the first.

The first was a case in Hong Kong, in which a 33-year-old man originally contracted the virus in late March and then contracted it again when traveling to Europe four and a half months later. Experts emphasize that during his second infection, the man didn’t have any symptoms while during his first infection he had a cough, fever, sore throat, and headache. Milder symptoms with the second infection were also reported in the two cases in Europe. This indicates that the immune system offered some level of protection during reinfection. Experts also point out that we don’t know if the patients mounted “neutralizing antibodies” in response to the first infection. Most patients do mount a neutralizing antibody response, so without knowing these patients’ original antibody levels, there are two possibilities: 1.) These patients didn’t develop neutralizing antibodies and are outliers, or 2.) Reinfection is common after a certain amount of time but is likely to be mild/asymptomatic.

A second reinfection occurred in a 25-year-old patient in Nevada, with 48 days separating the first and second infection and led to a different finding. Unlike the case in Hong Kong, it appears that the immune system didn’t protect this person from developing symptoms during the second case. The patient recovered from the first infection after about a month, tested negative, was well for about a month, and then tested positive again after developing symptoms. During the second infection, the patient was hospitalized and put on oxygen. While this case is more worrisome than the Hong Kong case due to the apparent lack of immunity, it’s rare (think of how many cases of reinfection would’ve been detected if developing stronger symptoms the second time was common).

Taken together, all of these cases demonstrate that reinfection is possible yet none offer a generalizable finding of when, why, how often, and in which patients reinfection might occur. Many researchers hypothesize that reinfection has to do with the level of antibodies that these patients developed after the first infection, but there is no way to confirm this until more reinfection cases are reported and studied.

Antibodies are only one piece of the immunity puzzle

Scientists have focused on antibodies when they study immunity because they are easy to detect by blood and very likely are indicative of some type of immunity against COVID-19. However, the adaptive immune system (the part of our immune response that is specific to coronavirus and serves as a “memory”) also involves other components that may be able to mount a strong response even with low levels of antibodies. As mentioned above, T cells are predicted to be a critical component of long-term immunity.

One study found that coronavirus infection produces a strong T cell response, but that this response might depend on the severity of the infection. Another study found that T-cells were present in previously infected individuals even when antibody levels were undetectable.

Herd Immunity

At the population level, we do not know what share of people would need to have immunity to keep the virus out of the overall population — this is what is known as “herd immunity.” This number varies based on how infectious the virus is (aka how fast it spreads), something we also do not know perfectly. For example, measles are so infectious that you need a huge share of people to be immune (estimates suggest around 90%) in order to develop herd immunity, whereas for the flu, which spreads much less quickly, it is under 50%.

With existing viruses, we have a lot of these answers because they’ve been carefully studied. You can use lab data, or evidence across populations, to answer questions about measles immunity. They’ve existed for many years, so we can pretty confidently determine whether reinfection is possible. With a new virus, we still need to learn all of this. We cannot be certain about the answers to most of these questions in the context of the novel virus causing this pandemic.

Data from related viruses and our general analysis of the speed of COVID-19 spread suggest herd immunity may arise at around 60% infection rate. If we learn that the virus is more infectious than we now think, this percentage may go up. Currently, most people have still not been infected. In New York City around 20% of people tested positive for COVID-19 antibodies according to the CDC. So it is likely we are not very close to herd immunity against COVID-19.

Bottom Line

Putting this all together: there is a lot of uncertainty. For a bunch of reasons, it would be a mistake to come away with the impression that if you see evidence of antibodies on a simple finger prick test you are totally protected. It would also be a mistake for policymakers to get the sense that if exactly, say, 62% of their population is immune, they are good to go on opening the economy without restrictions.

On the other hand, suggesting that there is “no immunity” to COVID-19 is also misleading. It is theoretically possible that we will learn that this virus is unlike all related viruses and infection does not confer any immunity but that is incredibly unlikely. We have to make decisions based on some uncertainty here, based on the best evidence we have. As our knowledge improves, we may be able to do more with this information. So, stay tuned...