[gingerbread-man]

Speaking only for myself, I found this article to be particularly difficult to comprehend. If there are any physicians or molecular biologists who could more plainly summarize the authors' conclusions, I would greatly appreciate it.

From what I can gather: — SARS-CoV-2 uses ACE2 in the alveolar epithelium as an entry receptor. ACE2 may also be involved in regulating cytokine activity and in viral replication. — "Pro-inflammatory cytokines have a central role in the progression of COVID-19 infection." — Anti-cytokine therapy may help reduce pulmonary inflammation in C19 patients. — ACE2 is also present in the leydig (testosterone producing) cells of male rats. — Long-term smokers express higher levels of ACE2 in their lungs. COPD patients are more likely to have low testosterone levels. And low testosterone has been linked to increased Pro-inflammatory cytokine activity. ——> Maybe testosterone reduces inflammation and, by extension, mortality, in COVID-19 patients? (I still do not really understand how the production of ACE2 in the leydig cells is related to this.)

Or, on the high-testostetone side: — Androgen receptors activate the transcription of TMPRSS2, a transmembrane serine protease found primarily in prostate epithelium. — "TMPRSS2 activity is regarded as essential for viral spread and pathogenesis in the infected hosts." ——> Elevated testosterone in some young men may increase TMPRSS2 activation, and be a common cause in the relatively small number of severe cases in that age group.