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Research shows interstitial macrophages are unexpectedly the primary target for SARS-CoV-2 in the lungs, leading to severe COVID-19, suggesting new therapeutic targets. Credit: SciTechDaily.comthat causes COVID-19, is not the one previously assumed to be most vulnerable. What’s more, the virus enters this susceptible cell via an unexpected route. The medical consequences may be significant.
In an uninfected interstitial macrophage, the nucleus and outer cell membrane are intact. In an infected interstitial macrophage, the nucleus is shattered, copious newly made viral components clump together, and the cell broadcasts inflammatory and scar-tissue-inducing chemical signals .
A collaboration ensued. Krasnow and Blish and their associates obtained fresh healthy lung tissue excised from seven surgical patients and five deceased lung donors whose lungs were virus-free but for one reason or another not used in transplants.
The two kinds of SARS-CoV-2-susceptible lung-associated macrophages are positioned in two different places. So-called alveolar macrophages hang out in the air spaces within the alveoli. Once infected, these cells smolder, producing and dribbling out some viral progeny at a casual pace but more or less keeping a stiff upper lip and maintaining their normal function.
But that’s not all. In contrast to alveolar macrophages, infected interstitial macrophages pump out substances that signal other immune cells elsewhere in the body to head for the lungs. In a patient, Krasnow suggested, this would trigger an inflammatory influx of such cells. As the lungs fill with cells and fluid that comes with them, oxygen exchange becomes impossible. The barrier maintaining alveolar integrity grows progressively damaged.
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