Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is likely to be androgen mediated
Carlos Gustavo Wambier, Andy Goren, Carlos Gustavo Wambier, Andy Goren
No abstract availableKeywords: 5-α reductase; ACE2; COVID-19; SARS-CoV-2; TMPRSS2; androgen receptor; androgenetic alopecia; angiotensin converting enzyme 2; antiandrogen therapy; dutasteride; finasteride; human skin; retinoids; transmembrane protease serine 2.
Figures
Androgen-mediated COVID-19.
References
- Shi Y., Yu X., Zhao H., Wang H., Zhao R., Sheng J. Host susceptibility to severe COVID-19 and establishment of a host risk score: findings of 487 cases outside Wuhan. Crit Care. 2020;24(1):108.
- Hoffmann M., Kleine-Weber H., Schroeder S. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020:1–10.
- Heurich A., Hofmann-Winkler H., Gierer S., Liepold T., Jahn O., Pohlmann S. TMPRSS2 and ADAM17 cleave ACE2 differentially and only proteolysis by TMPRSS2 augments entry driven by the severe acute respiratory syndrome coronavirus spike protein. J Virol. 2014;88(2):1293–1307.
- Lucas J.M., Heinlein C., Kim T. The androgen-regulated protease TMPRSS2 activates a proteolytic cascade involving components of the tumor microenvironment and promotes prostate cancer metastasis. Cancer Discov. 2014;4(11):1310–1325.
- National Institutes of Health TMPRSS2 transmembrane serine protease 2 [Homo sapiens (human)] Gene ID: 7113. Updated March 13, 2020. Available at:
Source: PubMed