Reply to thread

Message: [QUOTE="pj, post: 3482661, member: 2524"] Here's a scientist's comment on Losartan for coronavirus: AT1R blocker losartan is being tested based on a proposal that it will upregulate the SARS-CoV-2 receptor ACE2, preventing loss of ACE2 function which may be protective against the acute respiratory distress syndrome that is one cause of death by SARS and COVID-19 (Pubmed 32129518) ([URL="http://www.startribune.com/university-of-minnesota-to-testthree-drugs-for-covid-patients/568766632/"]www.startribune.com/university-of-minnesota-to-testthree-drugs-for-covid-patients/568766632/[/URL]) – This only deals with lung injury secondary to viral replication, not the virus itself. – This comes from an old hypothesis (2005) that SARS lethality was due to downregulation of ACE2 ([URL="http://www.nature.com/articles/nrd1830"]www.nature.com/articles/nrd1830[/URL]) whose validity I’m not too confident about, since it was based on injecting massive amounts of viruses into mice (who are pretty different from humans in their cardiovascular regulation). – Others have suggested that upregulating the receptor for the virus with losartan might increase susceptibility to the initial infection; this probably doesn’t matter either because a virus particle isn’t going to care if the cell it’s sitting on has 100 or 300 receptor molecules when it’s stuck on the surface and has time to swim around ([URL="http://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30116-8/fulltext"]www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30116-8/fulltext[/URL]). – I think it’s better to concentrate on specific antiviral medications and not worry about the complex ACE2/AT1R pathway. [/QUOTE]

Verification: First name of men's bb coach