Your Immune System May Hold the Key to How Badly the Corona Virus Will Effect Your Body
One of the Biggest fears about contracting the COVID-19 virus is how sick will it make me, and could it kill me. The mystery lies with in your own immune system.
An international team of researchers found that in some people with severe COVID-19, the body goes rogue and attacks one of its own key immune defenses instead of fighting the coronavirus.
Separate research suggests that youths fare better than adults thanks to a large supply of “first responder” immune cells that lesson in the body with age.
“We have the knowledge and capability of really boosting many aspects of the immune system. But we need to not use the sledge hammer.”
Warned Dr. Betsy Herold of New York’s Albert Einstein College of Medicine. Adding to the complexity, people’s wildly varying reactions also reflect other factors, such as how healthy they were to begin with and how much of the virus, or “dose” they were exposed to.
There are two main arms of the immune system. Innate immunity is the body’s first line of defense. As soon as the body detects a foreign intruder, key molecules, such as interferon's and inflammation-causing cytokines, launch a wide-ranging attack.
Innate immune cells also alert the slower-acting “adaptive” arm of the immune system, the germ-specific sharpshooters, to gear up. B cells start producing virus-fighting antibodies, the proteins getting so much attention in the vaccine research.
Usually when a virus invades the cells, proteins called Type I interferon's spring into action, defending the cell by interfering with viral growth. But new research shows those crucial molecules were essentially absent in a subset of people with severe COVID-19.
An International Project Uncovered Two Reasons.
In blood from nearly 1,000 severe COVID-19 patients, researchers found 1 in 10 had what are called auto-antibodies. Antibodies that mistakenly attack those needed virus fighters. Surprising, autoimmune disorders tend to be more common in women, but 95% of these COVID-19 patients were men.
In another 660 severely ill patients, the same team found 3.5% had gene mutations that didn’t produce Type I interferon's.
Each of those silent vulnerabilities was enough to tip the balance in favor of the virus early on, said Dr. Jean-Laurent Casanova, an infectious disease geneticist at Rockefeller University in New York, who co-leads the COVID Human Genetic Effort.
Certain interferon's are used in potential vaccines and are under study as a possible COVID-19 treatment; the auto-antibody discovery adds another factor to consider.
The coronavirus that causes COVID-19 is new to humans. But Sette’s team studied blood samples that were stored in freezers before the pandemic and found some harbored memory T cells that recognized a tiny portion of the new virus in laboratory tests.
The new coronavirus has cousins that cause as many as 30% of common colds, so researchers believe those T cells could be remnants from past colds.
But despite the speculation, “we don’t know yet” that having those T cells makes any difference in who gets seriously sick with COVID-19, noted Rory de Vries, co-author of a study in the Netherlands that also found such T cells in old blood.
All these findings beg for a deeper understanding of the myriad ways some people can be more susceptible than others. “We need to look quite broadly and not jump into premature conclusions about any one particular facet of the immune system,” said Stanford University immunologist Bali Pulendran.
He also has found some innate immune cells “in a state of hibernation” in seriously ill adults and next is looking for differences before and after people get sick.
But, “it’s not just all about the immune system,” cautioned Dr. Anita McElroy, a viral immunity expert at the University of Pittsburgh Medical Center who’s closely watching the research. A way to tell in advance who’s most at risk? “We’re a long, long way from that.”