What scientists learned from the voluntary release of volunteers on COVID-19 was that almost half of them had never been infected – even when the virus had entered their noses directly. More surprisingly, these were people who had never been infected or vaccinated before. This so-called challenge trial was originally conceived as a way to speed up vaccine testing, but ended up being a window into the dynamics of the virus.
Two years into the epidemic, some estimates that about half of Americans have not yet been infected. Without a more in-depth study, it is difficult to know how many people tested positive for antigen at home, whether they had asymptomatic infections, or possibly mild infections that have gone cold without testing. But studies of challenge trials and family contacts show that some people are harder to infect. In one study, only 38% of non-vaccinated people became infected with the virus living with an infected person. This number was 25% for vaccination.
Which raises the question of who is at risk for this latest wave, powered by the Omicron submarine BA.2, which has begun to raise lawsuits in the northeastern United States. Experts quoted last week New York Times Approximately 45% of Americans had Covid-19 at the time of the Omicron wave, and it was therefore estimated that another 55% would be at risk for BA.2.
But it’s probably not that easy. Those who should be weak are not getting infected and those who should be resistant to Omicron are getting infected again. And data from challenge studies and family contacts show that there is more to it than just precaution and vaccination that differentiate those who are being infected and those who are covid-free.
An explanation that has been floated is related to the common cold-cough. Colds are caused by a whole zoo of viruses including four coronaviruses – 229E, NL63, OC43, HKU1. Published in a recent study Nature Those who remained covid-free were found to have more immune cells known as T-cells produced by past brushes with these cold-causing coronaviruses. But other studies have shown the opposite – that recent coronaviruses can make people infected with the common cold more at risk for SARS-CoV-2.
Both results are commendable. Immunity stimulated by a similar virus can help block SARS-CoV-2, or interfere with the immune response by increasing the production of antibodies that do not work perfectly against this new threat. Danny Altman, an immunologist at Imperial College London, said: “I won’t bet my house for the answer.”
To complicate matters, genes affect how our immune systems respond to any virus – specifically, a group of highly variable genes called HLA. They contain a code of proteins that allow cells to signal to the immune system that they need to be infected and killed. In infected cells, HLA proteins may attach to certain parts of the virus and display them on the outside of the cell as a target.
The HLA system is like a mission control for the way the immune system is programmed, Altman says. It is the most diverse part of the human genome. Each of us produces different HLA proteins that will target different parts of the virus – and this will induce the production of immune cells called T-cells, which will attack different parts of the same virus.
Previous studies have suggested that people with certain types of HLA genes are less likely to develop significant COVID. Another study identified genetic patterns that put some vaccinated people at risk of serious infection with Omicron. Overall, people who are more prone to one pathogen may be more resistant to others.
One reason is that evolution supports diversity for the protection of pathogens in a way that it is not for the protection of predators. Most animals will encounter the same predators over and over again, so they are more likely to pass on their genes if all of their offspring have an optimal defense – be it speed or shells, thorns or toxins. But pathogens are an ever-changing threat, so the animals that succeed in overcoming most of the genes produce immunologically diverse offspring, thus increasing the odds that at least some of them will survive the plague no matter what.
There are also external variables that affect the immune system. For example, animals under certain types of stress are more prone to infectious diseases.
It would be wonderful if half of humanity could naturally resist all forms of SARS-CoV-2, past and future, and scientists could study them to figure out how to mimic it. But it turns out that different people are at risk for different forms – those old variants break down because they run out of people susceptible to being infected, but new variants grow because they stumbled upon ways to infect the invulnerable until the last iteration.
It may even explain the mystery of why covid waves rise and fall. In early autumn 2020, some scientists suggested that human diversity could explain why the epidemic began to ebb when only a fraction of the population became infected. It’s definitely worth figuring out. The only way to effectively fight the virus is to understand it and us better.