Great question, and one I wondered also.
The PR referred to the once canceled Dr. Sacha late-breaking study on SIV PrEP study. I imagine they decided if LL can prophylactically prevent new infection, it could perhaps also prevent re-infection from latent reservoir. They thought that once the latent reservoir reactivated but found nowhere to go (due to LL block), it would either peter out and be gone from the body for good (a sterilizing cure) or more likely go back into dormancy (a functional cure).
But the above is just a guess. I agree with you, that if they "cured" SIV with LL and myeloablation and HSCT, they would be shouting it from the rooftops and have it published a long time ago. Didn't NP announce the "HIV cure" possibility and trial several months ago - like 4 or 5?
Abstract of "sterilizing" protection in macaques (I used to work with these little guys, hah almost called them "buggers"
:
https://cattendee.abstractsonline.com/meeting...Session/24
The PR referred to the once canceled Dr. Sacha late-breaking study on SIV PrEP study. I imagine they decided if LL can prophylactically prevent new infection, it could perhaps also prevent re-infection from latent reservoir. They thought that once the latent reservoir reactivated but found nowhere to go (due to LL block), it would either peter out and be gone from the body for good (a sterilizing cure) or more likely go back into dormancy (a functional cure).
But the above is just a guess. I agree with you, that if they "cured" SIV with LL and myeloablation and HSCT, they would be shouting it from the rooftops and have it published a long time ago. Didn't NP announce the "HIV cure" possibility and trial several months ago - like 4 or 5?
Abstract of "sterilizing" protection in macaques (I used to work with these little guys, hah almost called them "buggers"
: https://cattendee.abstractsonline.com/meeting...Session/24
Quote:BACKGROUND: Adherence remains a challenge to the success of pre-exposure prophylaxis (PrEP) in preventing HIV acquisition. Thus, new approaches are urgently needed. The primary use of the CCR5 coreceptor by mucosally transmitted virus, together with the resistance to infection observed in CCR5-delta 32 homozygous people, suggests that CCR5-blocking reagents might be effective PrEP agents. Leronlimab is a CCR5-specific monoclonal antibody with excellent safety and adherence profile used in over 800 HIV+ people. We hypothesize that leronlimab can protect from the sexual transmission of HIV.
METHODS: To determine if subcutaneous leronlimab at the lowest and highest doses tested in clinical trials (10 mg/kg or 50 mg/kg in rhesus macaques via allometric scaling) could prevent sexual transmission of SHIV, we conducted a study in macaques using low-dose intra-rectal SHIVSF162P3 challenges. Three groups of six macaques received either no treatment or leronlimab at 10 mg/kg weekly or 50 mg/kg bi-monthly. We monitored longitudinally for plasma viremia, CCR5 occupancy, cell-associated virus, and anti-SHIV immune responses.
RESULTS: Following eight weekly challenges, all animals treated with 50 mg/kg were protected from acquisition, while all control animals became infected (p=0.0005). Four animals treated with 10 mg/kg were fully protected, while two animals were infected following the last two challenges (p=0.001). Of these two infected animals, one developed anti-leronlimab antibodies resulting in rapid leronlimab clearance, while the other maintained CCR5 occupancy with the lowest longitudinally viral loads. Colon and duodenum biopsies taken from the protected animals after completion of all challenges showed complete CCR5 occupancy and absence of cell-associated viral DNA and RNA. Following leronlimab uncoating from CCR5, protected animals remained aviremic and lacked anti-SHIV immune responses for at least six weeks before sacrifice, indicating sterilizing protection from rectal SHIV acquisition.
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