ArticleScience advances2025
Elucidating the mechanism by which HIV-1 nucleocapsid mutations confer resistance to integrase strand transfer inhibitors.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Mechanisms of HIV-1 assembly, release and maturation.Nature reviews. Microbiology · 2026Review
- The hidden reservoir of INSTI resistance: large scale sequence analysis identifies prevalent Gag NC mutations compromising dolutegravir and cabotegravir efficacy.Science China. Life sciences · 2026Article
- Non-integrase mechanisms for dolutegravir resistance.Retrovirology · 2026Review
- Article
- Effect of TAR hairpin stabilization on HIV-1 reverse transcription.Journal of virology · 2026Article
- Review
- Real-world Prevalence of Nonintegrase INSTI Resistance-Associated Mutations and Virological Outcomes in People Who Have Recently Acquired HIV-1 in the United Kingdom.The Journal of infectious diseases · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Persons with HIV (PWH) receiving integrase (IN) strand transfer inhibitors (INSTIs) have been reported to experience virologic failure (VF) in the absence of resistance mutations in IN. We previously reported that mutations in the viral nucleocapsid (NC) are selected in the presence of the INSTI dolutegravir (DTG). Here, we show that these NC mutations accelerate the kinetics of viral DNA integration, suggesting that they limit the window of time available for INSTIs to block viral DNA integration. We find that in primary peripheral blood mononuclear cells, HIV-1 acquires mutations in the viral envelope glycoprotein, NC, and occasionally IN during selection for INSTI resistance. Notably, the selected NC and IN mutations act in concert to reduce the susceptibility of the virus to INSTIs. These results provide insights into the mechanism by which HIV-1 escapes the inhibitory activity of INSTIs and underscore the importance of genotypic analysis outside IN in PWH experiencing VF on INSTI-containing drug regimens.
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Registered trials
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