grow, thanks for the reference to the upcoming sym

grow, thanks for the reference to the upcoming symposium at Tulane where there are multiple abstracts which reference Leronlimab.

Here are excerpts from another abstract which look interesting (although this may require a long-term research project):

Quote:

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AAV Delivery of the CCR5-blocking monoclonal antibody Leronlimab yields long-term expression and ART-free remission from SHIV viremia

Methods: Eight SHIVsf162p3- or SHIV-AD8-EOM-infected RMs received a single intramuscular dose of AAV9 encoding macaque Fc Leronlimab with stabilizing, silencing, and half-life extending mutations (AAV9-MacLSLeron).
Animals were longitudinally monitored for CCR5 receptor occupancy (RO), plasma Leronlimab concentrations, Leronlimab-directed anti-drug antibodies (ADA), and SHIV plasma viral loads.

Results: All eight RMs achieved 100% CCR5 RO on blood CD4+ T cells with detectable free plasma Leronlimab within 4 weeks of AAV9-MacLSLeron administration. Of these, four RMs sustained complete CCR5 RO and stable
plasma Leronlimab concentrations for >1.5 years post-AAV with minimal ADA responses, which was associated with completely undetectable SHIV plasma viremia in two RMs (<15 copies/ml for >1 year), decreased SHIV plasma
viral loads in one RM, and unaffected, persistent SHIV viremia in one RM. The remaining four RMs developed robust Leronlimab-directed ADA responses within 5-15 weeks of AAV9-MacLSLeron administration, resulting in complete
clearance of Leronlimab from plasma and rapid decline in CCR5 RO. However, long-term monitoring of three such RMs revealed eventual decline of plasma ADA titers and return of blood CD4+ T cell CCR5 RO approximately 1 year
post-AAV, without subsequent rebound of ADA titers. One such macaque eventually achieved sustained 100% CCR5 RO with stable plasma Leronlimab concentrations, which was coincident with decline of SHIV plasma viral loads to undetectable levels for >1 year.

Conclusions: Overall, these data demonstrate the potential of AAV vectors for sustained antibody-based CCR5 blockade as a gene therapy approach to long-term ART-free HIV remission. However, further investigation is needed to
identify factors responsible for variability in SHIV control after complete CCR5 blockade of blood CD4+ T cells is achieved. In addition, while transgene-directed ADA remains a major obstacle for antibody-mediated therapy, the
observed re-emergence of AAV transgene product after ADA-mediated clearance highlights the need to further investigate the interplay between AAV establishment and the development of transgene-directed ADA.

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