The more we report on COVID-19, the worse it gets. This is from a recent of patients cured in Germany:
MRI center disease [cardiovascular magnetic resonance imaging] in 78 patients (78%) continuous myocardial inflammation in 60 patients (60%), regardless of pre-existing conditions, the severity and overall progression of acute disease and the time since initial diagnosis.
Nearly two-thirds of patients, even those not with pre-existing conditions, have developed myocarditis! Myocarditis isn’t serious, but it can be. Sometimes it lasts a few hours, sometimes a few months. But why does a respiratory virus cause problems in the center? The other intelligent people at UCSF mag explain:
Luckily for the evolutionary draw, [the coronavirus can] easily open the protein doors in human cells known as ACE2 receptors and, like knives, open the doors of the units. says Faranak Fattahi, PhD, a member of Sandler UCSF.
… Needless to say, SARS-CoV-2 affects cinput. After all, cinput cells are fed through ACE2 receptors, the important gateway of the virus. And, in fact, lab experiments recommend that the virus be able to enter and reflect on cultured human cinput cells, says Bruce Conklin, MD, professor of medicine and genetics expert for cinput diseases at the UCSF and Gladstone Institutes.
This, as well as immune system interactions, turns out to be to blame for many of the non-respiratory effects we have begun to see in patients with COVID-19. That’s why, increasingly, it’s not only vital to reduce COVID-19 deaths. We also want to weigh the number of cases, because even probably asymptomatic cases can cause serious disorders across the board.
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You just sent an amazing message: that quality journalism doesn’t have to respond to advertisers, billionaires or hedge funds; that the editors can basically thank the generosity of their readers. It’s so powerful. Especially in what has been called a “media extinction event,” when those seeking to benefit from the news withdraw, the Mother Jones network intervenes.
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