One of the tragic ironies of disease-causing infections is that, in many cases, it’s not the offending virus or bacteria that kills. At least not directly. It’s the immune system’s response to a pathogen — or, more accurately, its over-response — that ultimately causes internal destruction and death.
The novel coronavirus seems to play by these rules. One of the defining features of life-threatening and life-ending Covid-19 disease is the now-infamous “cytokine storm,” a surge of inflammation-summoning molecules that, in an attempt to eradicate the infection, ends up mutilating the tissues of the lungs, heart, kidneys, or other organs. Like burning down a house to rid it of rats, the immune system’s remedy can be worse than the threat.
So far, SARS-CoV-2 has sickened more than 30 million people worldwide. Its death toll has exceeded 1 million. But a large percentage of those infected — by most estimates, somewhere around 40% to 45% of carriers — seem to endure the virus without symptoms or lingering effects.
Unlike “disease resistance,” which refers to all of the body’s methods of killing and expunging a threat, disease tolerance describes a host’s ability to put up with or even accommodate an intruder.
It’s often assumed that these people possess immune systems that are more adept at killing or clearing the germ. But that doesn’t seem to be the whole story.
Studies on people with Covid-19 have found that viral load, or the amount of virus detectable in the body, usually peaks during the first week of symptoms and steadily declines thereafter, regardless of whether a person quickly recovers or grows critically ill. There also doesn’t seem to be a correlation between maximum viral load and disease severity; asymptomatic carriers appear to be walking around with just as much of the virus in their body as sick carriers.
These sorts of findings have prompted some researchers to ask whether attempts to help…