How COVID-19 sends some bodies to war with themselves
MANY COVID-19 PATIENTS MAY BE DYING FROM THEIR IMMUNE RESPONSE TO THE VIRUS, NOT FROM THE VIRUS ITSELF. CAN SCIENCE FIGURE OUT HOW TO SAVE THEM?
Story continuesEarly in her career, Navarro-Millán worked at the University of Alabama at Birmingham, where most of her patients had lupus, an autoimmune disease that can affect various parts of the body, including the kidneys, blood and even the brain. Its sufferers are especially prone to cytokine storms, which are often triggered by viral infections. What Navarro-Millán saw now in her Covid-19 patients wasn’t, she thought, all that different from what she encountered in Alabama.
After her patient provided his consent, Navarro-Millán gave him the anakinra. His improvement was rapid. When she had first seen him, he was wearing nasal tubes that dispensed oxygen; by the next morning, his condition had deteriorated, and he needed a rebreather mask to get more oxygen. He received his first anakinra injection that day; the morning after, his breathing became less labored and he no longer needed the mask. Nose tubes were sufficient.
This proposed fix is something of a paradox. It posits that the best way to help some patients survive Covid-19 may not be to fortify the immune system, so that it can fight the virus with greater ferocity, but to subtly suppress the counterattack, so that the patient avoids self-destruction. The notion is controversial, not least because differentiating an appropriate immune response from a self-harming one can be difficult.
THERE IS A natural tension between what physicians themselves sometimes describe as the art and the science of medicine. Medicine’s bedrock, its science, consists of treatments and protocols that have been tested rigorously and proven to work . But in daily practice, as they try to help patients, none of whom are the same, doctors sometimes move slightly beyond what has been proven, particularly when established practices prove ineffective or when it’s unclear what really ails a patient.
Officials at Temple University Hospital in Philadelphia early on established a protocol for Covid-19 patients centered on aggressive immunomodulation. Roberto Caricchio, the head of rheumatology there, told me that the hospital, which serves a high-risk, mostly African-American and Hispanic population, immediately began giving steroids in low doses to everyone who tested positive for Covid-19 and who needed oxygen.
One possible explanation for these divergent results is that suppressing the immune system in mildly ill patients actually delays, rather than helps, their recovery. For those who are beating back the virus just fine on their own, the treatment might hinder that process.
If an overexuberant immune response is a major contributor to these conditions, as many suspect, then it’s paramount to come up with methods to combat them by calming the immune system. That has proved to be easier said than done. “In both sepsis and ARDS, we haven’t made the strides we wish we could have,” says Nuala Meyer, a critical-care physician and scientist at the University of Pennsylvania’s medical school.
Retrospective parsing of old studies can’t definitively prove that something works. Only large, well-designed trials that follow patients after treatment can. But these reanalyses hint at the existence of smaller groups within the broader syndromes that may respond to drugs directed at the immune system.
One hypothesis follows from the animals’ adaptations to flight. Flapping wings requires immense amounts of energy, causing bat cells to spew out large quantities of a metabolic byproduct called reactive oxygen species, which might be thought of as cellular exhaust. In other animals, that cellular waste, which bears some resemblance to a viral infection, might trigger overwhelming inflammation — a cytokine storm. But bats have evolved ways to keep that inflammation in check.
Adults experience less inflammation and, as they enter old age, have a harder time mounting that interferon response at all, a problem called immune senescence. This deficiency may be why older people get so much sicker from Covid-19, Thomas told me. Aging immune systems may find themselves playing catch-up, increasing the chances that they will overdo it later and damage the self.
The Covid-19 pandemic has already prompted many physicians to bend in this direction. So few tools exist to reliably eliminate the virus from our bodies that they have, out of necessity, turned to the idea of prodding the immune system in various ways. They have shifted their focus in a manner that Ayres has long argued is necessary: from eradicating the pathogen to helping the patient survive the pathogen. They are, in a way, pinning their hopes on innate tolerance mechanisms.
Or maybe the studies would have produced better results had they been designed differently. Thomas Yadegar, who thinks tocilizumab can be a lifesaver, if used in the right way, surmises that one study didn’t employ stringent-enough criteria for choosing its study patients. Navarro-Millán thinks the trials tried to treat patients too late in the course of the disease. She likened these efforts to trying to cure Stage 4 metastatic cancer — probably doomed from the start.
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