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As President Trump claims he is immune to COVID-19 and isolated reports of reinfection emerge, what is the truth about immunity to COVID-19?
To date, there have been six published cases of COVID-19 reinfection, with several other unverified accounts from around the world. Although this is a comparatively small fraction of the millions of people known to have been infected, should we be concerned? To unravel this puzzle, we must first consider what we mean by immunity.
How immunity works
When we become infected with any pathogen, our immune system responds quickly to try to contain the threat and minimize any damage. Our first line of defense is immune cells, known as innate cells. Usually these cells are not enough to eliminate a threat, which is where a more flexible “adaptive” immune response comes into play: our lymphocytes.
Lymphocytes come in two main varieties: B lymphocytes, which make antibodies, and T lymphocytes, which include cells that directly kill invading germs.
Since antibodies are easily measured in the blood, they are often used to indicate a good adaptive immune response. However, over time, the levels of antibodies in our blood decrease, but this does not necessarily mean that protection is lost. We retain some lymphocytes that know how to deal with the threat: our memory cells. Memory cells are remarkably long-lived, patrolling our bodies, ready to spring into action when needed.
Vaccines work by creating memory cells without the risk of a life-threatening infection. In an ideal world, it would be relatively easy to create immunity, but it is not always that simple.
Although our immune system has evolved to deal with a wide variety of pathogens, these germs have also evolved to hide from the immune system. This arms race means that some pathogens such as malaria or HIV are very difficult to treat.
Infections that have been spread by animals (zoonotic diseases) are also challenging for our immune systems because they may be entirely new. The virus that causes COVID-19 is a zoonotic disease that originates in bats.
COVID-19 is caused by a betacoronavirus. Several betacoronaviruses are already common in the human population, the most familiar as a cause of the common cold. Immunity to these cold-causing viruses is not as strong, but immunity to the most serious conditions, Mers and Sars, is more durable.
Data to date on COVID-19 shows that antibodies can be detected three months after infection, although, as with Sars and Mers, the antibodies gradually decline over time.
Of course, antibody levels are not the only indication of immunity and do not tell us anything about T lymphocytes or our memory cells. The virus that causes COVID-19 is structurally similar to Sars, so perhaps we can be more optimistic about a more durable protective response; time will tell. So how concerned should we be about reports of reinfection with COVID-19?
How worried should we be?
The handful of reports of reinfection cases with COVID-19 does not necessarily mean that immunity is not being produced. Problems with the tests could explain some reports because “viruses” can be detected after infection and recovery. The tests look for viral RNA (the genetic material of the virus), and viral RNA that cannot cause infection can be removed from the body even after the person has recovered.
In contrast, false negative results occur when the sample used in the tests contains insufficient viral material to be detected, for example, because the virus is at a very low level in the body. These apparent negative results may explain cases where the interval between the first and second infection is short. Therefore, it is very important to use additional measures, such as viral sequencing and immune indicators.
Re-infection, even in immunity, can occur, but would generally be mild or asymptomatic because the immune response protects against the worst effects. Consistent with this is that the majority of verified cases of reinfection reported little or no symptoms. However, one of the last verified cases of reinfection, which occurred just 48 days after the initial infection, actually had a more severe response to reinfection.
What could explain the worst symptoms the second time around? One possibility is that the patient did not develop a robust adaptive immune response the first time and that his initial infection was largely contained by the innate immune response (the first line of defense). One way to control this would be to assess the antibody response, as the type of antibody detected can tell us something about the time of infection. But sadly, the antibody results were not analyzed in the recent patient’s first infection.
Another explanation is that different viral strains caused the infections with a subsequent impact on immunity. Genetic sequencing showed differences in the viral strains, but it is not known if this amounts to impaired immune recognition. Many viruses share structural characteristics, which allow immune responses to one virus to protect against a similar virus. This has been suggested to account for the absence of symptoms in young children who frequently get colds caused by betacoronavirus.
However, a recent study, which has yet to be peer-reviewed, found that protection against cold-causing coronaviruses did not protect against COVID-19. In fact, antibodies that recognize similar viruses can be dangerous, which explains the rare phenomenon of antibody-dependent intensification of disease (AME). AD occurs when antibodies enhance viral infection of cells with life-threatening consequences.
However, it must be emphasized that antibodies are only an indicator of immunity and we have no data on T lymphocytes or memory cells in these cases. What these cases emphasize is the need for standardized approaches to capture critical information for a robust assessment of the threat of reinfection.
We are still learning about the immune response to COVID-19, and each new information is helping us unravel the puzzle of this challenging virus. Our immune system is a powerful ally in the fight against infection, and only by unlocking it can we hope to defeat COVID-19.
Sheena Cruickshank, Professor of Biomedical Sciences, University of Manchester.
This article was originally published by The Conversation. Read the original article.
