Since President Trump claims to be immune to COVID-19 and there are isolated reports of reinfection, what is the truth about immunity to COVID-19?
To date, there have been six cases of COVID-19 reinfection with various other unverified accounts from around the world. Although this is a relatively small proportion of the millions of people known to be infected, should we be concerned? To solve this puzzle, we must first consider what we mean by immunity.
How immunity works
When we are infected with any pathogen, our immune system responds quickly, trying to contain the threat and minimize any harm. Our first line of defense is against immune cells known as innate cells. These cells are usually not enough to eliminate the threat, this is where a more flexible “adaptive”; immune response comes into play – our lymphocytes.
Lymphocytes are of two main types: B-lymphocytes, which form antibodies, and T-lymphocytes, which include cells that directly kill embryonic invaders.
Because antibodies are easily measured in the blood, they are often used to indicate a good adaptive immune response. However, over time, the level of antibodies in our blood drops, but this does not necessarily mean a loss of protection. We store some lymphocytes that know how to deal with the threat – our memory cells. Memory cells are extremely durable, patrol our body and are ready to take action when needed.
Vaccines work by creating memory cells without the risk of a potentially fatal infection. In an ideal world, building immunity would be relatively easy, but it’s not always that simple.
Although our immune system has evolved to fight a huge variety of pathogens, these microbes 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 fight.
Infections that come from animals – zoonotic diseases – are also difficult for our immune system because they can be completely new. The virus that causes COVID-19 is a zoonotic disease that originates from bats.
COVID-19 is caused by beta-coronavirus. Some beta-coronaviruses are already common in the human population – the most common cause of colds. Immunity to these cold-causing viruses is not as strong, but immunity to more serious conditions, Mers and Sars, is more stable.
To date, data on COVID-19 show that antibodies can be detected three months after infection, although, as with Sars and Mers, antibodies gradually decrease over time.
Of course, the level of antibodies is not the only indicator of immunity and does not tell us about T-lymphocytes or cells of our memory. The virus that causes COVID-19 is similar in structure to Sars, so perhaps we can be more optimistic about a longer-lasting protective response – time will tell. So how do we bother reporting COVID-19 re-infection?
How can we worry?
Several reports of reinfection of COVID-19 do not necessarily mean that immunity does not occur. Testing problems can be caused by some reports, as the “virus” can be detected after infection and recovery. Tests look for viral RNA (the genetic material of the virus), and viral RNA that cannot cause infection can be expelled even after the person has recovered.
Conversely, false-negative results occur when the sample used in the test does not contain enough viral material to detect – for example, because the virus is at a very low level in the body. Such obvious negative results can be explained by cases when the interval between the first and second infection is short. Therefore, it is extremely important to use additional measures, such as viral sequencing and immune indicators.
Reinfection, even with immunity, can occur, but it can usually be moderate or asymptomatic, as the immune response protects against the worst consequences. Accordingly, most of the tested cases of reinfection did not report no symptoms or moderate symptoms. However, one of the last tested cases of reinfection – which occurred only 48 days after the initial infection – actually had a more serious reaction to reinfection.
What can cause worse symptoms a second time? One possibility is that the patient is not responding to a reliable adaptive immune response for the first time, and that their initial infection was largely restrained by an innate immune response (first line of defense). One way to monitor this is to evaluate the antibody response, as the type of antibody detected can tell us something about the time of infection. But, unfortunately, the results of antibodies were not analyzed at the first infection of the patient.
Another explanation is that different viral strains caused infections with subsequent effects on the immune system. Genetic sequencing has indeed shown differences in viral strains, but it is not known whether this equates to altered immune recognition. Many viruses share structural features, allowing the immune response to a single virus to protect against a similar virus. It is suggested to take into account the absence of symptoms in young children, who often catch colds from beta-coronaviruses.
However, a recent study, which has not yet been reviewed, has shown that protection against coronaviruses that cause cold does not protect against COVID-19. In fact, antibodies that recognize such viruses can be dangerous – explaining the rare phenomenon of aggravation of antibody-dependent disease (ADE). ADE occurs when antibodies exacerbate viral infection of cells with potentially life-threatening consequences.
It should be emphasized, however, that antibodies are only one indicator of immunity, and we have no data on either T lymphocytes or memory cells in these cases. In these cases, the need for standardized approaches to obtain critical information to reliably assess the risk of reinfection is emphasized.
We are still learning about the immune response to COVID-19, and each new piece of data helps us figure out the puzzle of this complex virus. Our immune system is a powerful ally in the fight against infection, and only by unlocking it can we finally hope to defeat COVID-19.
Shina Kruikshenk, Professor of Biomedical Sciences, University of Manchester.
This article was originally published by The Conversation. Read the original article.