As President Trump claims he is immune to COVID-19 and separate reports have emerged of replenishment, what is the truth about COVID-19 immunity?
To date, there have been six published cases of COVID-19 reconsideration, along with various unverified accounts from around the world. Although it is a comparable fraction of the millions of people who are known to be infected, should we be concerned? To choose 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 to try to contain a threat and reduce any damage. Our first line of defense comes from immune cells, known as natural cells. These cells are not usually sufficient to eliminate a threat, in which the presence of a more flexible “adaptive”; immune response is played with – our lymphocytes.
Lymphocytes are derived from two main variations: B lymphocytes, which produce antibodies, and T lymphocytes, which include cells that directly kill germy invaders.
As antibodies are easily measured in the blood, it is often used to indicate a good flexible immune response. However, over time, the levels of antibodies in our blood decrease, but this does not mean that protection is lost. We keep some lymphocytes that know how to deal with the threat – our memory cells. Memory cells are fully alive, patrolling our body, ready to act when needed.
Vaccines work by creating memory cells without the risk of getting a deadly infection. In an ideal world, it would be easy to create immunity, but you are not always that straightforward.
Although our immune system has evolved to deal with a large variety of pathogens, these germs have also evolved to be secreted from the immune system. This arms race means that some pathogens such as malaria or HIV are very difficult to deal with.
Infections destroyed from animals –– zoonotic diseases –- are also challenging for our immune system because they can be a complete novel. The virus caused by COVID-19 is a zoonotic disease, caused by bats.
COVID-19 is caused by a betacoronavirus. Many betacoronaviruses are common in the human population – most familiar as a cause of the common cold. Immunity to colds caused by viruses is not that strong but immunity to more severe conditions, Mers and Sars, is more robust.
Data to date on COVID-19 show that antibodies can be detected three months after infection, although, as in Sars and Mers, antibodies gradually decrease over time.
Of course, antibody levels are not just an indication of immunity and do not tell us about T lymphocytes or our memory cells. The virus that causes COVID-19 is similar in structure to Sars, so perhaps we can be more optimistic about a more robust protective response – time will tell. So how much should we worry about reports of re-attachment to COVID-19?
How much should we worry?
Small case reports on the reintegration of COVID-19 do not mean that immunity does not occur. Test issues may report for some reports because the “virus” can be detected after infection and recovery. Tests look for viral RNA (virus genetic material), and viral RNA that cannot cause infection can be shed from the body even after the person has recovered.
Conversely, false negative results occur when the sample used in the test contains insufficiently detected viral material – for example, because the virus is at a very low level in the body. Such apparent negative results can lead to cases where the gap between the first and second infections is short. It is very important, therefore, to use additional measures, such as viral sequencing and immune indicators.
Disinfection, even in immunity, can occur, but it will usually be mild or asymptomatic because the immune response is protected against the worst effects. Corresponding to this are the most proven cases of replenishment reported either no or mild symptoms. However, one of the most recently verified cases of reinfection – which occurs only 48 days after the initial infection – actually has a more severe response to re-emergence.
What could account for worse symptoms in the second hour? One possibility is that the patient did not mount a stable flexible immune response for the first time and that their initial infection was more content with the natural resistance response (the first line of defense). One way to monitor this is to assess the antibody response because the type of antibody detected can tell us something about the time of infection. But unfortunately, antibody results were not evaluated in the first infection of the recent patient.
Another explanation is the various viral strains caused by infections that have subsequent immunity effects. Sequence of genetics has shown differences in viral strains, but it is not known whether it is matched to altered immune recognition. Many viruses share structural features, enabling immune responses to a virus to protect against a similar virus. It has been suggested to consider the lack of symptoms in young children who are often cold caused by betacoronaviruses.
However, a recent study, which has not yet been peer reviewed, found that protection against the causes of cold coronavirus does not protect against COVID-19. In fact, antibodies that recognize similar viruses can be dangerous – referring to the rare phenomenon of antibody-dependent disease enhancement (ADE). ADE occurs when antibodies enhance the viral infection of potentially life-threatening cells.
It should be emphasized, however, that antibodies are only an indicator of immunity and we have no data on either T lymphocytes or memory cells in these cases. The emphasis of these cases is a need for standardized techniques to obtain critical information for rigorous reassessment threat analysis.
We still know about the immune response to COVID-19, and each piece of new data helps us select the puzzle of this challenging virus. Our immune system is a strong ally in the fight against infection, and just by unlocking it we can expect to defeat COVID-19.
Sheena Cruickshank, Professor of Biomedical Science, University of Manchester.
This article was originally published by The Conversation. Read the original article.