As everyone now knows, Covid-19 is caused by the SARS-CoV-2 virus. Like other viral infections, SARS-CoV-2 stimulates the human immune system and usually provides what we call “acquired immunity” – the amazing ability to fight off future attacks of the same pathogen or closely related. However, what is widely known but misunderstood is that it is reversible with SARS-CoV-2, despite the fact that it stimulates acquired immunity. Here I look at the science of such transplants.
The immune response to SARS-CoV-2
First, it is important to understand how the normal adaptive immune response to SARS-CoV-2 works. When an antigen like the coronavirus novel affects an individual, white blood cells called lymphocytes, make up natural killer cells, T cells, and B cells. B cells are important because they form, secrete, and carry antibodies. Antibodies are proteins that have the special ability to lock down certain molecules on the surface of a pathogen such as a virus. For example, the spike protein “S” protruding from the surface of the SARS-CoV-2 virus can be identified by antibodies. When an antibody locks on the spike protein “S”, the virus cannot reproduce in a cell.
Scanning electron micrograph of lymphocyte.
US National Cancer Institute
Antibodies, also known as immunoglobulins, come in five main types called IgA, IgD, IgE, IgG, and IgM. The two most relevant are IgG and IgM. IgG is the most common antibody and accounts for most of the antibody-based immune response. IgM is often the first antibody to respond to the presence of antigen.
Schematic shows time and scale of antibody response starting from the time of infection … [+]
Post et al. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0244126
From the early days of Covid-19 we know that most ill patients put up visible IgG and IgM responses within three weeks of first showing symptoms. However, some patients do not develop an antibody response at all. Why? One study found that these “non-seroconverters” (i.e. individuals who did not produce levels of potential antibodies) appeared to exhibit disease more quickly, although they were less severe.
Indeed, a broad spectrum of disease in SARS-CoV-2, ranging from asymptomatic diseases to severe respiratory disease, leads one to assume that those with milder disease may be less likely to respond. provide effective. A study comparing 26 completely asymptomatic cases with 188 symbolic cases found evidence that was consistent with this hypothesis, although with the relatively small sample size it was impossible to draw definitive conclusions. (In this study, 85% of asymptomatic cases developed a visible antibody response compared with 94% of symbolic cases.)
From these and other studies, it is now widely acknowledged that while most people with SARS-CoV-2 develop antibodies, not everyone does. . Those are less likely to be as vulnerable to a second exposure to the virus as they were the first time. This is one way to redefine.
Defensive defense
A second reason for relapse is related to declining immunity. As our immune system successfully fights infection, there is a decrease in the level of circulating antibodies – a sign that a person ‘s immune system is functioning in a healthy way. Then, on second sight, immune memory cells (B cells, T cells, and “natural killer” cells) can be reactivated for a faster response. What is of concern about SARS-CoV-2 and its ability to redefine is that persistent immunity after the first infection may not be the same. In an interesting paper published on March 23 this year in The Lancet, researchers at Duke-NUS School of Medicine and the Singapore National Center for Infectious Diseases concluded that functional immunity to SARS-CoV-2 is highly individualized. Following 164 people living in Singapore for six to nine months after a positive diagnosis of Covid-19 disease, a machine learning algorithm placed individuals in one of five sets: (1) those who did not secreted antibodies (12%) ;; (2) “rapid decline” group (27%); (3) “slow-moving” group (29%); (4) a “continuous” group (32%) with little change in overall antibody levels; (5) and a “response delay” group (2%) that showed an increase in antibodies over time. All patients classified to specific subsets submitted blood samples up to 180 days after Covid-19 symptoms. The suggestion of this study that continued immunity to the coronavirus novel must be “individually tested” is a clear demonstration of what we still need to learn.