Quote:reacting like a CCR5-Delta 32 patient
Yes that is what Dr. Sacha said in the cc, leronlimab turns cells into delta-32. And they I believe they used that to cure HIV in monkeys. I don't believe there are ccr5 delta 32 donors like with humans, so they used leronlimab to simulate a ccr5 delta 32 donor and it worked from what I gather.
When that gets published it will be big news imo. NP said end of year but this week said end of year or 1st quarter. I'm not sure if this is the CROI, if it is, it will not be released until March 10th.
There is one big difference though, it blocks hiv, binding to similar location, being competitive with hiv and rantes(ccl5). But it allows ccl3 and ccl4 to continue to bind. ccr5 delta 32 people have a couple issues, with some viruses like the flu, they have a higher death rate. But the paper I posted earlier, didn't have the same issue with ccr5 antagonists, shown with mice studies as with ccr5 deficient mice, which had the same flu issue. The issue was without ccr5 for ccl3 and ccl4 to bind, they bound to other receptors which caused the issue. So leronlimab, I believe will give the best of both worlds blocking rantes, but allowing ccl3 and ccl4 to continue working, which is why the safety data is much better that other ccr5 antagonists. This ccl5, rantes, is what some cancers use to recruit t-cells, a layer of protection around them. So blocking that is one reason this should work well with cancer, removing that layer of protection.
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