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Do you think they monitored and captured data surrounding those points? When those events occured, What caused those events to occur? What the sickness was? How high did HIV viral load climb to? Would they also have been measuring biomarkers at the time? What type of labs do you think they might have been measuring? CRP, ESR, WBC? IL-1, Interferon Gamma?

How do you think HIV was able to replicate during these events if leronlimab was still attached to ccr5?

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At that time I doubt they were looking at biomarkers since they weren't necessary for approval. They were looking at CCR5 occupation, viral suppression, causes of any SAEs and AEs and possibly CD4 T-cell counts.

Cytodyn would have the actual numbers for the virological suppression failure points what we know is they were they were over 200 copies per milliliter in two subsequent tests.

I can see two different reason for a rise in the HIV virus caused by another immunological challenge. It could be a sharp rise in CCR5 expression caused by another virus which 700mg of leronlimab was not enough to cover. It could also be that another virologic challenge releases HIV from reservoirs. HIV can also achieve replication by cell to cell fusion but it seems uncommon.

Of note, maraviroc has shown to increase the release of HIV from reservoirs. Which goes along with my notion that HIV release from reservoirs is increased when there is less active HIV in the body. Back in 2019 I proposed that if leronlimab could always achieve near 100% receptor occupancy that in 15 years the viral reservoirs could be depleted achieving a cure. With the FDA hold shutting down the HIV extension trial now we'll never find out. I would still like to know if the HIV viral load continued to decrease over time. I know in some patients 1/2 copy per milliliter was achieved which is astounding.