8 min read
This story originally appeared in The Conversation
By Sheena Cruickshank, University of Manchester
US President Donald Trump claims he is immune to COVID-19, but it is known that isolated cases of reinfection have occurred. Which of the two hypotheses applies to immunity to COVID-19?
To date, there have been six cases of COVID-19 reinfection worldwide, with a few more pending. Should we be concerned even though we are only a small percentage of the millions of people infected? To answer this question, we would first have to consider what we mean by that immunity.
How does immunity work?
When we become infected with a pathogen, our immune system reacts quickly to contain the threat and minimize damage. Our first line of defense corresponds to the immune cells known as innate cells. Usually these cells are not enough to eliminate the threat, and this is where a more flexible and “adaptive” immune response comes into play: I’m talking about lymphocytes.
There are two main types of lymphocytes: B lymphocytes, which are responsible for producing antibodies, and T lymphocytes, which comprise the cells responsible for killing invading germs.
Because the presence of antibodies in the blood can be measured, this data is often used to determine the extent to which an immune system is providing an adequate and adaptive response. Over time, our blood antibody levels decrease. However, this does not mean that we will lose protection completely, as we will retain some lymphocytes that know how to deal with the threat (our memory cells). Memory cells have a remarkably long lifespan, they patrol from our bodies and are ready to take action if necessary.
The job of vaccines is to create memory cells without causing a life-threatening infection. In an ideal world, creating immunity would be relatively easy, but it’s not always an easy process.
Although our immune systems have evolved to deal with a wide variety of pathogens, germs have evolved to trick you too. In this gun escalation logic, this means that some pathogens such as malaria or HIV are very difficult to fight.
Infections of animal origin (zoonotic diseases) also pose a challenge to our immune system as they can pose a completely new threat to the immune system. COVID-19 is a zoonotic disease because the virus that causes it comes from bats.
COVID-19 is caused by a beta coronavirus, and these beta coronaviruses are very common in human populations (the most well known is responsible for the common cold). Immunity to viruses that cause colds is usually poor, but that to viruses that are responsible for more serious diseases like MERS or SARS is more permanent.
So far, the data on COVID-19 show that the antibodies can be detected up to three months after infection. However, similar to MERS and SARS, the antibodies gradually decrease over time.
Of course, antibody levels are not the only indicator of immunity and say nothing about T lymphocytes or our memory cells. Given that the virus that causes COVID-19 is structurally similar to that of SARS, it may be possible to be more optimistic about the duration of the immune response … although this will only be known in time. To what extent should we be concerned with information about reinfection cases?
How worried should I be?
The handful of confirmed COVID-19 reinfection cases do not necessarily imply that such patients have not developed immunity. Behind some of these cases there may have been problems with the tests so that the virus could have been detected after infection and recovery. The tests detect viral RNA (the genetic material of the virus). And viral RNA, although it can no longer cause infections, can remain in the patient’s body even after the disease has been overcome.
This creates false negative results when the sample analyzed in the test does not contain enough viral material to be detected (e.g. because the body has very low indicators of the presence of the virus). These seemingly negative results can occur in cases where the interval between the first and second infection is short. For all of these reasons, it is extremely important to check other values such as virus sequencing or immune indicators.
Re-infection (or even immunity) is possible. It is normal, however, that in this case the new infection is mild or asymptomatic, as the immune response protects against the worst effects. This is supported by the fact that in the best established cases of reinfection, patients either had mild symptoms or were asymptomatic. It is true, however, that in one of the most recent cases of reinfection credited (and which occurred only 48 days after the initial infection) the patient had more severe symptoms.
And what could explain the more severe symptoms during the second infection? One possibility would be that the patient had not developed a robust adaptive response for the first time and, therefore, that the first infection was largely contained by their innate response (the first line of defense). One way to check this would have been to score the immune response based on the type of antibody being produced, as this could have given us information about the times of infection. Unfortunately, the antibodies were not tested during the patient’s first infection.
Another explanation would be that the infections were caused by different strains of the virus, which affected the immune response. Genetic sequencing has shown the existence of various strains of the virus, but it is not known whether this changes how the immune system recognizes it. And the fact is that many viruses share certain structural properties, which enables an immune response generated by a particular virus to protect against a similar one. This hypothesis has been mixed up to explain the lack of symptoms in young children who commonly feel cold from betacoronavirus.
However, a recent study (which has yet to be evaluated by peers) has shown that the defenses created by the coronaviruses responsible for colds do not protect against COVID-19. In fact, it can be dangerous for antibodies to recognize similar viruses as this explains the rare phenomenon of antibody dependent infection (ADE). It is a phenomenon that occurs when antibodies promote viral infection with potentially fatal effects.
However, it should be emphasized that antibodies are only one of the indicators of immunity and that in these cases of reinfection we have no information about T lymphocytes or memory cells. It appears from these cases that the criteria for collecting the required information need to be standardized in order to obtain a more accurate assessment of the risk of re-infection.
We continue to learn about the immune response to COVID-19, and each new piece of information helps us add another piece to the puzzle of such a difficult virus to fight. Our immune systems are powerful ally in fighting infection, but only by fine-tuning can we hope to defeat this disease.
This article is republished by The Conversation under a Creative Commons license. Read the original article.