Yes Figgs,
The question that requires asking & answering
Yes Figgs,
The question that requires asking & answering is why is it that this phenomenon is observed when Leronlimab is introduced & bound to the CCR5 receptors, but when HIV or CCL5 RANTES is bound in mass quantity, the same increase in CCR5 & CD4 is not observed?
I believe the answer has to do with the fact that Leronlimab is not a cyto or chemokine. LL has no communication potential whatsoever.
It is only a blocker and it says nothing. RANTES is ahemokine & does speak, but not when LL is around. Almost like putting earplugs on CCR5 cannot hear anything while LL is bound to it.
In the case of HIV,
Once HIV binds to CCR5, it is only a matter of time that CD4 cell is dead & destroyed by the same HIV which bound to the CCR5 receptor on its surface. As the virus enters the CD4 cell it hijacks the replication machinery and soon the cell plus the CCR5 receptors on its surface are all destroyed by the HIV virus. more than likely, the CD4 cell undergoes apoptosis, so then, how can CD4 cells increase in number when their CCR5 receptors are bound to buy HIV?
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