I already knew the Timothy Ray Brown story before posting the links yesterday.

However, I started wondering why doctors didn't just replicate the same bone marrow transplant with other HIV/AIDS patients using the same kind of donor having the CCR5-Delta 32 mutation.

Well, it turns out that:

Quote:

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Brown, the "Berlin patient", suffered from graft-versus-host disease and leukoencephalopathy – both transplant complications that are potentially fatal. This means that the procedure should not be performed on others with HIV, even if sufficient numbers of suitable donors could be found.

As of 2017, six more people also appear to have been cleared of HIV after getting graft-versus-host disease ; only one of them had received CCR5 mutant stem cells, so it appears that when a transplant recipient has graft-versus-host disease the transplanted cells may kill off the host's HIV-infected immune cells.[

Link: https://en.wikipedia.org/wiki/Timothy_Ray_Brown

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After reading the first paragraph, I thought that maybe leronlimab's potential role was to make this type of procedure safer by removing the risk of GvHD fatality.

However, the second paragraph suggested something else was happening.

And after watching yesterday's video again, my layman's understanding is that if leronlimab is administered during the transplant process, the remaining HIV cannot bind to any CCR5, and ultimately can't replicate. And without being able to replicate, it is eliminated from the body.

Does this square with anyone else's understanding?

Video Link Excerpt: https://youtu.be/TwdjWhWV1nc?t=431