Interferons, then, can make or break a host’s fate. Researchers have found that people whose interferons are weak or laggy after catching the coronavirus are far more likely to get very seriously sick. Others experience similar problems when their immune system churns out misguided antibodies that attack and destroy interferons as they try to ferry messages among cells. Interferons also play a very dramatic role in counteracting the viruses that cause dengue and yellow fever. Those pathogens are rapidly wrangled by rodent interferons and never make those animals sick, Morrison told me. In people, though, the microbes have cooked up ways to muffle the molecules—a big reason they cause such debilitating and deadly disease.
Coronaviruses in general are pros at interferon sabotage. Among the most powerful is MERS, which “just shuts down everything” in the interferon assembly line, says Susan Weiss, a coronavirologist at the University of Pennsylvania. That essentially ensures that almost no interferons are released, even when gobs of virus are roiling about, a dismantling of defenses that likely contributes to MERS’ substantial fatality rate. Weiss doesn’t think SARS-CoV-2 is likely to copy its cousin in that respect anytime soon. The virus does have some ability to gum up interferon production, but it would take a lot more, she told me, to silence the system as MERS has.
Still, SARS-CoV-2 seems to be taking its own small, tentative steps toward interferon censorship. For months, several groups of researchers, CU Anschutz’s Santiago among them, have been studying how well the virus can invade and replicate inside of cells that have been exposed to interferons. Recent variants such as Delta and Omicron, they’ve found, seem to be better at infiltrating those reinforced cells compared with some versions that preceded them—a hint that this resistance might be helping new iterations of the virus sweep the globe and cause repeated rounds of disease.
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