{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T00:17:16Z","timestamp":1793146636389,"version":"4.5.0"},"reference-count":70,"publisher":"Public Library of Science (PLoS)","issue":"1","license":[{"start":{"date-parts":[[2023,1,18]],"date-time":"2023-01-18T00:00:00Z","timestamp":1674000000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI120765"],"award-info":[{"award-number":["R01 AI120765"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007813","name":"Center for AIDS Research, University of Washington","doi-asserted-by":"publisher","award":["P30 AI027757"],"award-info":[{"award-number":["P30 AI027757"]}],"id":[{"id":"10.13039\/100007813","id-type":"DOI","asserted-by":"publisher"}]},{"name":"University of Washington Royalty Research Fund","award":["A92723"],"award-info":[{"award-number":["A92723"]}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:p>\n                    GSK2838232 (GSK232) is a novel maturation inhibitor that blocks the proteolytic cleavage of HIV-1 Gag at the junction of capsid and spacer peptide 1 (CA\/SP1), rendering newly-formed virions non-infectious. To our knowledge, GSK232 has not been tested against HIV-2, and there are limited data regarding the susceptibility of HIV-2 to other HIV-1 maturation inhibitors. To assess the potential utility of GSK232 as an option for HIV-2 treatment, we determined the activity of the compound against a panel of HIV-1, HIV-2, and SIV isolates in culture. GSK232 was highly active against HIV-1 isolates from group M subtypes A, B, C, D, F, and group O, with IC\n                    <jats:sub>50<\/jats:sub>\n                    values ranging from 0.25\u20130.92 nM in spreading (multi-cycle) assays and 1.5\u20132.8 nM in a single cycle of infection. In contrast, HIV-2 isolates from groups A, B, and CRF01_AB, and SIV isolates SIV\n                    <jats:sub>mac239<\/jats:sub>\n                    , SIV\n                    <jats:sub>mac251<\/jats:sub>\n                    , and SIV\n                    <jats:sub>agm.sab-2<\/jats:sub>\n                    , were highly resistant to GSK232. To determine the role of CA\/SP1 in the observed phenotypes, we constructed a mutant of HIV-2\n                    <jats:sub>ROD9<\/jats:sub>\n                    in which the sequence of CA\/SP1 was modified to match the corresponding sequence found in HIV-1. The resulting variant was fully susceptible to GSK232 in the single-cycle assay (IC\n                    <jats:sub>50<\/jats:sub>\n                    = 1.8 nM). Collectively, our data indicate that the HIV-2 and SIV isolates tested in our study are intrinsically resistant to GSK232, and that the determinants of resistance map to CA\/SP1. The molecular mechanism(s) responsible for the differential susceptibility of HIV-1 and HIV-2\/SIV to GSK232 require further investigation.\n                  <\/jats:p>","DOI":"10.1371\/journal.pone.0280568","type":"journal-article","created":{"date-parts":[[2023,1,18]],"date-time":"2023-01-18T13:43:47Z","timestamp":1674049427000},"page":"e0280568","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":4,"title":["Intrinsic resistance of HIV-2 and SIV to the maturation inhibitor GSK2838232"],"prefix":"10.1371","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3202-1650","authenticated-orcid":true,"given":"Robert A.","family":"Smith","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dana N.","family":"Raugi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert 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