Back in November of 2020, during the first wave of the COVID-19 pandemic, I was teaching an in-person microbiology laboratory. One of my students had just been home to see his parents, and they all came down with COVID-19. I suspect that was when I was exposed to the virus. I was in the SARS-CoV-2 monitoring program and was being tested weekly for signs of the virus. Sure enough, I got a notice from the program that I was COVID-positive. I dutifully went into isolation, nervously waiting for symptoms to appear. They never did. Neither my wife nor daughter, who were living with me, contracted the virus or showed symptoms. Scientists suspected that some people just didn't get that sick from the virus, and they hypothesized that these individuals may have a genetic background that makes them more resistant.
A research study by Augusto et al. uncovers the first evidence that may explain the difference in susceptibility. It turns out that part of the warning system our body uses is a protein called HLA (also known as MHC molecules -- HLA is the name given to these proteins in humans). A small portion of the protein being expressed in human cells is chopped up, and parts of it are put into HLA and then displayed on the surface. The immune system, namely T-cells, will check these HLA molecules. If it's all host protein the T-cell just moves along. If on the other hand, a virus has infected the cell, the immune system reacts. I will let the authors of the study take it from there.
This version of HLA [in resistant humans] is good at grabbing the bits of other coronaviruses — the ones that cause seasonal colds — that look the most like SARS-CoV-2. So if you’ve got this HLA and you’ve been exposed to those viruses (which most people have), when SARS-Cov-2 shows up, your body doesn’t need time to make specifically targeted T cells to fight it off. They’re already there.
These results may lead to other effectives treatments.