The answer may be residual immunity. According to a recent report in the journal Science, an important part of the population has Memory Cells capable of identifying the virus and ordering T Cells to attack the virus. Not because of prior immunity to Covid 19, but because they react to the lipid chains and especially to the virus anchors that connect to the AC2 receptors of the cells.
Although what was said does not imply immunity against the virus in particular, it justifies why such a high percentage of people exposed to the virus can overcome it without major problems. Covid19 as part of the Coronavirus family shares genes and lipid chains with other coronaviruses such as the one that causes the common cold. That is why people who have previously been exposed to the common cold seem to be able to fight Covid19 more efficiently.
“These are encouraging data,” says Columbia University virologist Angela Rasmussen. Although studies do not indicate whether people who clear SARS-CoV-2 infection can avoid the virus in the future, both have identified strong T-cell responses, which “bode well for the future.” Rasmussen said he develops long-term protective immunity, and the results could also help researchers create better vaccines.
Recognizing the lipid chain of the virus and not the virus itself is the strategy of the Oxford vaccine, which uses previous vaccines against other coronaviruses with Covid19 inactive RNA so that the antibodies can identify the virus anchors and thus neutralize it . Israel has pursued a similar approach by successfully isolating the most effective antibody in the fight against the virus. This approach would not be a vaccine but a therapeutic to help infected people.
Using bioinformatic tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute of Immunology, predicted which fragments of viral proteins would elicit the most potent T-cell responses. They then exposed the immune cells of 10 patients who had recovered from mild cases of COVID-19 to these viral fragments.
All patients carried helper T cells that recognized the SARS-CoV-2 peak protein, which allows the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and creates an effective immune response,” says Sette.
The results are consistent with a study published as a preprint on medRxiv on April 22 by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper protein targeting helper T cells in 15 of 18 hospitalized patients with COVID-19.
The teams also asked whether people who have not been infected with SARS-CoV-2 also produce cells that fight it. Thiel and his colleagues analyzed the blood of 68 uninfected people and found that 34% harbored helper T cells that recognized SARS-CoV-2. The La Jolla team detected this cross-reactivity in about half of the stored blood samples collected between 2015 and 2018, long before the current pandemic began. The researchers believe these cells were likely caused by a past infection with one of the four human coronaviruses that cause colds; The proteins in these viruses resemble those of SARS-CoV-2.
The results suggest that “one reason that a large part of the population can deal with the virus is that we may have little residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa. However, none of the studies attempted to establish that people with cross-reactivity do not get as sick with COVID-19.