ArticleVirology2008
Drug-associated changes in amino acid residues in Gag p2, p7(NC), and p6(Gag)/p6(Pol) in human immunodeficiency virus type 1 (HIV-1) display a dominant effect on replicative fitness and drug response.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Gag mutations can impact virological response to dual-boosted protease inhibitor combinations in antiretroviral-naïve HIV-infected patients.Antimicrobial agents and chemotherapy · 2010Trial
- HIV-1 reverse transcriptase stability correlates with Gag cleavage efficiency: reverse transcriptase interaction implications for modulating protease activation.Journal of virology · 2023Article
- Molecular Docking-Based Screening for Novel Inhibitors of the Human Immunodeficiency Virus Type 1 Protease that Effectively Reduce the Viral Replication in Human Cells.Journal of AIDS & clinical research · 2021Article
- Easy and accurate reconstruction of whole HIV genomes from short-read sequence data with shiver.Virus evolution · 2018Article
- Gag P2/NC and pol genetic diversity, polymorphism, and drug resistance mutations in HIV-1 CRF02_AG- and non-CRF02_AG-infected patients in Yaoundé, Cameroon.Scientific reports · 2017Article
- C-Terminal HIV-1 Transframe p6* Tetrapeptide Blocks Enhanced Gag Cleavage Incurred by Leucine Zipper Replacement of a Deleted p6* Domain.Journal of virology · 2017Article
- Effects of PRE and POST therapy drug-pressure selected mutations on HIV-1 protease conformational sampling.FEBS letters · 2014Article
- Significant reductions in Gag-protease-mediated HIV-1 replication capacity during the course of the epidemic in Japan.Journal of virology · 2013Article
- Mutations in HIV-1 gag and pol compensate for the loss of viral fitness caused by a highly mutated protease.Antimicrobial agents and chemotherapy · 2012Article
- Mutational patterns in the frameshift-regulating site of HIV-1 selected by protease inhibitors.Medical microbiology and immunology · 2012Article
- Developmental regulation of P-glycoprotein activity within thymocytes results in increased anti-HIV protease inhibitor activity.Journal of leukocyte biology · 2011Article
- The role of HIV replicative fitness in perinatal transmission of HIV.Virologica Sinica · 2011Review
- A cleavage enzyme-cytometric bead array provides biochemical profiling of resistance mutations in HIV-1 Gag and protease.Biochemistry · 2011Article
- Identification of structural mechanisms of HIV-1 protease specificity using computational peptide docking: implications for drug resistance.Structure (London, England : 1993) · 2009Article
- Human immunodeficiency virus type 1 protease-correlated cleavage site mutations enhance inhibitor resistance.Journal of virology · 2009Article
- Mutation T74S in HIV-1 subtype B and C proteases resensitizes them to ritonavir and indinavir and confers fitness advantage.The Journal of antimicrobial chemotherapy · 2009Article
- Gag determinants of fitness and drug susceptibility in protease inhibitor-resistant human immunodeficiency virus type 1.Journal of virology · 2009Article
- Genetic determinants in HIV-1 Gag and Env V3 are related to viral response to combination antiretroviral therapy with a protease inhibitor.AIDS (London, England) · 2009Article
- Uncoupling human immunodeficiency virus type 1 Gag and Pol reading frames: role of the transframe protein p6* in viral replication.Journal of virology · 2009Article
- Gag mutations strongly contribute to HIV-1 resistance to protease inhibitors in highly drug-experienced patients besides compensating for fitness loss.PLoS pathogens · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Regions of HIV-1 gag between p2 and p6(Gag)/p6(Pol), in addition to protease (PR), develop genetic diversity in HIV-1 infected individuals who fail to suppress virus replication by combination protease inhibitor (PI) therapy. To elucidate functional consequences for viral replication and PI susceptibility by changes in Gag that evolve in vivo during PI therapy, a panel of recombinant viruses was constructed. Residues in Gag p2/p7(NC) cleavage site and p7(NC), combined with residues in the flap of PR, defined novel fitness determinants that restored replicative capacity to the posttherapy virus. Multiple determinants in Gag have a dominant effect on PR phenotype and increase susceptibility to inhibitors of drug-resistant or drug-sensitive PR genes. Gag determinants of drug sensitivity and replication alter the fitness landscape of the virus, and viral replicative capacity can be independent of drug sensitivity. The functional linkage between Gag and PR provides targets for novel therapeutics to inhibit drug-resistant viruses.
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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.