I am looking forward to Dr. Sacha publication on the HIV “cure” (I think this is the way NP named it) as it relates to Leronlimab (or CCR5 for that matter). The information below in blue is copy-and paste from some articles in the subject (for general info. purposes):
There are two reports of cures so far: Timothy Ray Brown, known as the 'Berlin patient' who received two stem cell transplants in 2006 (ha was being treated for leukemia). His donor had double copies of a CCR5-delta-32 gene mutation that resulted in missing CCR5 co-receptors on T cells, most HIV strains use this venue to infect cells. Also, professor Gupta of University College London presented a case of a man ‘London patient‘ who has no remaining detectable HIV a year and a half after undergoing a bone marrow stem cell transplant to treat lymphoma. His donor had a double CCR5-delta-32 mutation as well.
There is another case of long-term HIV remission: in Dusseldorf, a man underwent a procedure in February 2013 to treat acute myeloid leukemia. He remained on antiretroviral therapy with undetectable viral load until November 2018. This patient stopped antiretroviral therapy in November 2018, still has undetectable HIV and is undergoing continued monitoring.
The problem here is that these patients had cancer, stem cell transplantation is risky and this procedure will not be an option for people suffering of HIV only (not cancer).
Generally speaking, HIV-1 enters host cells by binding to a CD4 receptor and then interacting with either CCR5, or the CXC chemokine receptor (CXCR4). Having two identical alleles (alternative form of a gene) for a 32-bp deletion (delta32/delta32) confers high resistance against HIV-1 acquisition.
I have to say here that this is pure speculation from somebody that is not trained in medicine like me. I am just pointing to the fact that the upcoming paper of Dr. Sacha can be a depiction and opening of a very large market: that of possible HIV cure (CCR5-delta-32 “like” interaction). This, of course is a looooong way ahead (and, of course, might not come to fruition at all), but, as far as we are concerned, a paper depicting the mechanisms of action of this therapeutic possibly in relation to Leronlimab’s flavor of CCR5 receptor interaction will bring lots of exposure to our CYDY. Also, this mechanism might well be correlated to the PrEP mode of action (efforts already under way in Thailand).
Again, I am here simply speculating and there are much more suitable people to talk about this, but, as I mentioned before, can’t wait to read Dr. Sacha’s article.
There are two reports of cures so far: Timothy Ray Brown, known as the 'Berlin patient' who received two stem cell transplants in 2006 (ha was being treated for leukemia). His donor had double copies of a CCR5-delta-32 gene mutation that resulted in missing CCR5 co-receptors on T cells, most HIV strains use this venue to infect cells. Also, professor Gupta of University College London presented a case of a man ‘London patient‘ who has no remaining detectable HIV a year and a half after undergoing a bone marrow stem cell transplant to treat lymphoma. His donor had a double CCR5-delta-32 mutation as well.
There is another case of long-term HIV remission: in Dusseldorf, a man underwent a procedure in February 2013 to treat acute myeloid leukemia. He remained on antiretroviral therapy with undetectable viral load until November 2018. This patient stopped antiretroviral therapy in November 2018, still has undetectable HIV and is undergoing continued monitoring.
The problem here is that these patients had cancer, stem cell transplantation is risky and this procedure will not be an option for people suffering of HIV only (not cancer).
Generally speaking, HIV-1 enters host cells by binding to a CD4 receptor and then interacting with either CCR5, or the CXC chemokine receptor (CXCR4). Having two identical alleles (alternative form of a gene) for a 32-bp deletion (delta32/delta32) confers high resistance against HIV-1 acquisition.
I have to say here that this is pure speculation from somebody that is not trained in medicine like me. I am just pointing to the fact that the upcoming paper of Dr. Sacha can be a depiction and opening of a very large market: that of possible HIV cure (CCR5-delta-32 “like” interaction). This, of course is a looooong way ahead (and, of course, might not come to fruition at all), but, as far as we are concerned, a paper depicting the mechanisms of action of this therapeutic possibly in relation to Leronlimab’s flavor of CCR5 receptor interaction will bring lots of exposure to our CYDY. Also, this mechanism might well be correlated to the PrEP mode of action (efforts already under way in Thailand).
Again, I am here simply speculating and there are much more suitable people to talk about this, but, as I mentioned before, can’t wait to read Dr. Sacha’s article.
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