After more than two years of the COVID-19 pandemic, most Americans have some immunity against the virus either by vaccination or infection or a combination of both. But there have been a few rare cases where some unvaccinated people have managed to dodge the virus despite being repeatedly exposed to it. This raised the question of whether it is possible that some people are simply immune or resistant to COVID-19 without having the virus or a vaccine.
Scientists have been trying to understand whether such resistance to COVID-19 exists and how it would work. Researchers say studying these cases could help develop new vaccines and therapeutics against the disease, which is currently over 990,000 American lives.
“It was hard to talk about it in public because you say something and then people say, ‘Oh, that must be me, because I haven’t been infected yet,’ when in fact, you know, you might were not infected. because you just got lucky so far,” Shane Crotty, a virologist and professor at the La Jolla Institute of Immunology, told Yahoo News.
Crotty said he and other experts are cautious about the topic because it is still being studied and there are no clear answers yet.
“Risking a life-threatening illness because you think about something you don’t really know is dangerous. Most of us [scientists] tried to be very careful. … Look, this is not something we know, but these are opportunities,” he added.
A simple potential explanation is that some of those who didn’t get COVID were just lucky, Crotty said. It could also be that their behavior, such as wearing a mask properly or avoiding certain situations that would put them at risk of contracting the disease, might have protected them.
“We rarely know if it’s not a family member that we contracted COVID from, so it’s possible you just haven’t been exposed or have been exposed in small amounts,” said Katherine Troisi, an infectious disease epidemiologist at the University of Texas School of Public Health. Health in Houston reported Yahoo News. “The other explanation, which I think is probably relevant for most of these cases, is that you had it. We know that many cases are asymptomatic. You are not sick, so you don’t know you had it,” she said.
But scientifically, Crotty said, there are two possible explanations that could explain why some people may have much greater resistance to SARS-CoV-2, the virus that causes COVID-19, than others. One idea is that some people can clear the virus quickly before it reaches detectable levels, due to existing immunity to other coronaviruses, such as those that cause the common cold.
There are over 200 types of cold viruses, four of which are coronaviruses, accounting for about 30% of all cold infections. According to the Centers for Disease Control and Preventionmost people become infected with one or more of these seasonal coronaviruses at some point in their lives.
“The basic idea is that there are T-cell responses that some people elicit in response to certain coronaviruses they have had before that can provide a degree of protection that other people simply don’t have.” Crotty said.
T cells are an important part of the immune system that helps us fight off certain viruses. While antibodies, such as those from a vaccine or a previous infection, attack the virus when it enters the body, T cells act as another line of defense after the virus has entered the body, preventing the virus from multiplying and causing severe illness. Scientists call these T cells, which appear to be effective against different types of coronaviruses, “cross-reactive.”
Crotty and colleagues among the first to publish a study on this topicback in May 2020. Scientists analyzed blood samples from people who had been infected with SARS-CoV-2 and then compared them with blood samples from people who had never been infected with the virus.
“All the labs around the world have shown that these cross-reactive T cells do exist, and they exist in about 50% of people, depending on how you measure them,” Crotty said.
Another study of medical professionals in England published in November last year, contained similar conclusions. The study evaluated a group of British healthcare workers during the first wave of the pandemic who were exposed to the virus but did not become ill with COVID-19. The researchers found that the presence of cross-reactive memory T cells in some participants contributed to “quick clearance from SARS-CoV-2 and other coronavirus infections.”
But, according to Crotty, this is something that scientists need to continue to study. “There is no study that just nailed it to the nails, because this is a very complex study,” said the professor. He and his team are determined to find some answers; they have registered people who have never been infected and have never been vaccinated, and they plan to follow them for a long time.
These T-cell response studies will play an important role in the development of new COVID-19 vaccines, he said. In fact, there are already different groups scientists are working on vaccines that specifically target T cells.
Our current vaccines are designed to train B cells, a type of white blood cell, to produce antibodies that recognize and bind to proteins found on the surface of the virus, such as the spike protein, which is the part of the virus that helps it attach to cells. When antibodies are present, the virus cannot infect the cell. But the main problem has been that the spike protein of the coronavirus often mutates, which gives the virus the advantage of being able to evade any antibodies that no longer recognize it.
Some experts believe that T-cell vaccines may be more effective because these cells are able to recognize other parts of the virus that may not mutate at the same rate as the spike protein. Vaccines that target T cells may also provide longer-term protection against severe forms of the disease, as studies have shown that antibodies wane several months after vaccination.
Another possible explanation for COVID-19 resistance is that some people may have innate immunity, meaning that there are genetic factors that protect them from SARS-CoV-2 infection.
Neville Sanjana, assistant professor of biology at New York University and principal lecturer at the New York Genome Center, is studying potential genetic factors behind COVID-19 resistance. He says one interesting point that may provide some answers is the virus entry mechanism, which in the case of SARS-CoV-2 is a specific protein that allows the virus to infect human cells, called the angiotensin-converting enzyme 2, or ACE2 receptor. .
Sanjana says mutations in the ACE2 receptor make it harder for the virus to enter. Resistance to these types of mutations has already been demonstrated against other viruses such as HIV.
“We know that there is an entry receptor similar to the one we identified for SARS-CoV-2, but it is a different gene,” he said. “For HIV, the virus that causes AIDS, the entry receptor is CCR5, and we know that there are people in whom a natural mutation gets rid of CCR5 … and this makes them practically immune,” he added.
In addition to studying possible entry receptor mutations, scientists are studying other genetic variations in the human genome, Sanjana said.
“There are about 20,000 genes in the human genome, and we really don’t know which of these genes can influence key cells, such as cells in the epithelium of our respiratory tract or in our lungs, which we think are the pathway for SARS-CoV to enter. . -2,” he said, adding that some of these genes could make people more or less vulnerable to COVID-19.
A joint project called COVID Human Genetic Effort is studying thousands of people around the world looking for genetic variations that may explain why some people never get COVID-19, and why some people get so sick while others don’t.
Sanjana said these studies are important for developing next-generation therapies.
“Most of the therapeutics that we have, be it remdesivir or paxlovid, act on the virus. They target the virus. They target viral genes,” he said. “You can imagine that if you understood what key host genes are… we could develop other treatments that target those genes.”
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