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Posted On: 05/13/2021 7:15:21 AM
Post# of 148908
In that specific case they're talking about COVID-19 variants which is nonsensical in that context because COVID-19 doesn't bind to CCR5. Leronlimab may have the ability to reduce COVID-19 viral replication but that runs through it's downregulation of the mTORc1 pathway.
With HIV the 7 contact points for CCR5 and the one for the N terminus are so exacting that I would expect any genomic change would render that HIV variant non-viable.
Now we come to CCR5 binding chemokines. It's a key that fits a specific lock and after millions of years of evolution any mutations are at a competitive disadvantage.
One claim made by Cytodyn that I now think may possibly be untrue is that leronlimab selectively blocks chemokines. Being large molecule it never really made sense to me and I've never seen any testing for it.
With HIV the 7 contact points for CCR5 and the one for the N terminus are so exacting that I would expect any genomic change would render that HIV variant non-viable.
Now we come to CCR5 binding chemokines. It's a key that fits a specific lock and after millions of years of evolution any mutations are at a competitive disadvantage.
One claim made by Cytodyn that I now think may possibly be untrue is that leronlimab selectively blocks chemokines. Being large molecule it never really made sense to me and I've never seen any testing for it.
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