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Comprehensive mapping of the virus and host factors that guide the paths of HIV-1 escape from a therapeutic
Journal article   Open access   Peer reviewed

Comprehensive mapping of the virus and host factors that guide the paths of HIV-1 escape from a therapeutic

Aaron N. Gillman, Cassian M. Birler, Rohith Rao Vujjini, Mohammad Fili, Samuel A. McCarthy-Potter, Wilson Chen, Madeline M. Broghammer, Guiping Hu, Margaret J. Gartland, Manyu Prakash, …
Cell reports (Cambridge), Vol.45(7), 117558
07/28/2026
DOI: 10.1016/j.celrep.2026.117558
PMID: 42322610
url
https://doi.org/10.1016/j.celrep.2026.117558View
Published (Version of record) Open Access

Abstract

HIV-1 resistance to therapeutics can emerge through diverse mutational routes, yet the determinants guiding pathway selection in vivo remain unclear. Through comprehensive screening, we identify 18 mutations in the HIV-1 Env protein that enhance resistance to the FDA-approved small-molecule therapeutic temsavir. We then examine their occurrence in HIV-infected individuals who developed resistance on therapy. Interestingly, only a subset of the resistance-enhancing mutations emerged in vivo. On-treatment mutation frequencies correlate with their emergence rates in temsavir-untreated individuals and are governed by two parameters: (1) probability of mutation appearance, determined by the number and type of nucleotide changes required, and (2) probability of mutation persistence, determined by Env functional and immune fitness. Notably, non-neutralizing antibodies commonly elicited in HIV-infected individuals restrict emergence of multiple resistant forms, driving convergence to a narrow set of escape routes. These findings establish a quantitative framework for predicting therapeutic resistance and reveal how host immunity constrains viral evolution during treatment. [Display omitted] •Systematic screen maps multiple HIV-1 Env mutations conferring resistance to temsavir•In vivo, resistance converges on a limited set of pathways•On-treatment frequencies parallel mutation rates in untreated individuals•Emergence is governed by mutation probability, virus fitness, and immune constraints Gillman et al. systematically screen for HIV-1 Env mutations that confer resistance to the FDA-approved therapeutic temsavir (BMS-626529). They discovered that in treated individuals, resistance mutations converge to limited pathways determined by mutation probability, viral fitness, and conserved host immune pressures, providing a framework to predict evolutionary outcomes during therapy.
antiviral therapeutics BMS-626529 envelope glycoproteins fostemsavir HIV-1 selection pressures virus escape virus evolution virus fitness

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