ArticleJournal of virology2011
Second-site compensatory mutations of HIV-1 capsid mutations.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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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Who cites it
33 citing papers in PubMed.
- Different mechanisms for human rhinovirus survival in the presence of deleterious amino acid substitutions at virion protein-protein or RNA-protein interfaces.Journal of virology · 2026Article
- Pharmacokinetics, Pharmacodynamics, Efficacy and Drug Resistance Selection of Injectable Long-Acting Lenacapavir Pre-Exposure Prophylaxis (PrEP) Against HIV.CPT: pharmacometrics & systems pharmacology · 2026Article
- Pharmacokinetics, pharmacodynamics, efficacy and drug resistance selection of injectable long-acting lenacapavir pre-exposure prophylaxis (PrEP) against HIV.medRxiv : the preprint server for health sciences · 2025Article
- HIV-1 adapts to lost IP6 coordination through second-site mutations that restore conical capsid assembly.Nature communications · 2024Article
- HIV-1 capsid stability enables inositol phosphate-independent infection of target cells and promotes integration into genes.PLoS pathogens · 2023Article
- Article
- Elucidating the Basis for Permissivity of the MT-4 T-Cell Line to Replication of an HIV-1 Mutant Lacking the gp41 Cytoplasmic Tail.Journal of virology · 2020Article
- Intrinsic curvature of the HIV-1 CA hexamer underlies capsid topology and interaction with cyclophilin A.Nature structural & molecular biology · 2020Article
- Genome-Wide Mutagenesis of Hepatitis C Virus Reveals Ability of Genome To Overcome Detrimental Mutations.Journal of virology · 2020Article
- Authentication Analysis of MT-4 Cells Distributed by the National Institutes of Health AIDS Reagent Program.Journal of virology · 2019Article
- Functional Rescue of Cataract-Causing αA-G98R-Crystallin by Targeted Compensatory Suppressor Mutations in Human αA-Crystallin.Biochemistry · 2019Article
- Article
- Epistasis detectably alters correlations between genomic sites in a narrow parameter window.PloS one · 2019Article
- CCR5 Inhibitors and HIV-1 Infection.Journal of AIDS and HIV treatment · 2019Article
- Evolutionary footprint of epistasis.PLoS computational biology · 2018Article
- Inhibition of HIV-1 Maturation via Small-Molecule Targeting of the Amino-Terminal Domain in the Viral Capsid Protein.Journal of virology · 2017Article
- Analysis of quinolinequinone reactivity, cytotoxicity, and anti-HIV-1 properties.Bioorganic & medicinal chemistry · 2016Article
- Functional and Structural Characterization of Novel Type of Linker Connecting Capsid and Nucleocapsid Protein Domains in Murine Leukemia Virus.The Journal of biological chemistry · 2016Article
- Analysis of HIV-1 Gag protein interactions via biotin ligase tagging.Journal of virology · 2015Article
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The human immunodeficiency virus (HIV) capsid (CA) protein assembles into a hexameric lattice that forms the mature virus core. Contacts between the CA N-terminal domain (NTD) of one monomer and the C-terminal domain (CTD) of the adjacent monomer are important for the assembly of this core. In this study, we have examined the effects of mutations in the NTD region associated with this interaction. We have found that such mutations yielded modest reductions of virus release but major effects on viral infectivity. Cell culture and in vitro assays indicate that the infectivity defects relate to abnormalities in the viral cores. We have selected second-site compensatory mutations that partially restored HIV infectivity. These mutations map to the CA CTD and to spacer peptide 1 (SP1), the portion of the precursor Gag protein immediately C terminal to the CTD. The compensatory mutations do not locate to the molecularly modeled intermolecular NTD-CTD interface. Rather, the compensatory mutations appear to act indirectly, possibly by realignment of the C-terminal helix of the CA CTD, which participates in the NTD-CTD interface and has been shown to serve an important role in the assembly of infectious virus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.