ArticleJournal of virology2001
Resistance to nucleoside analog reverse transcriptase inhibitors mediated by human immunodeficiency virus type 1 p6 protein.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- Amino acid insertions near Gag cleavage sites restore the otherwise compromised replication of human immunodeficiency virus type 1 variants resistant to protease inhibitors.Journal of virology · 2004Trial
- Enhanced strand transfer and mismatch extension by HIV-1C reverse transcriptase promote sequence motif duplication.Journal of virology · 2026Article
- ViReMa: a virus recombination mapper of next-generation sequencing data characterizes diverse recombinant viral nucleic acids.GigaScience · 2023Article
- Enhanced Transmissibility and Decreased Virulence of HIV-1 CRF07_BC May Explain Its Rapid Expansion in China.Microbiology spectrum · 2022Article
- Covariation of viral recombination with single nucleotide variants during virus evolution revealed by CoVaMa.Nucleic acids research · 2022Article
- The N-Terminus of the HIV-1 p6 Gag Protein Regulates Susceptibility to Degradation by IDE.Viruses · 2018Article
- PTAP motif duplication in the p6 Gag protein confers a replication advantage on HIV-1 subtype C.The Journal of biological chemistry · 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
- The PTAP sequence duplication in HIV-1 subtype C Gag p6 in drug-naive subjects of India and South Africa.BMC infectious diseases · 2017Article
- The HIV-1 late domain-2 S40A polymorphism in antiretroviral (or ART)-exposed individuals influences protease inhibitor susceptibility.Retrovirology · 2016Article
- Elucidation of the Molecular Mechanism Driving Duplication of the HIV-1 PTAP Late Domain.Journal of virology · 2016Article
- Novel tetra-peptide insertion in Gag-p6 ALIX-binding motif in HIV-1 subtype C associated with protease inhibitor failure in Indian patients.AIDS (London, England) · 2014Article
- Human immunodeficiency virus type 1 protease inhibitor drug-resistant mutants give discordant results when compared in single-cycle and multiple-cycle fitness assays.Journal of clinical microbiology · 2010Article
- Uncoupling human immunodeficiency virus type 1 Gag and Pol reading frames: role of the transframe protein p6* in viral replication.Journal of virology · 2009Article
- Non-cleavage site gag mutations in amprenavir-resistant human immunodeficiency virus type 1 (HIV-1) predispose HIV-1 to rapid acquisition of amprenavir resistance but delay development of resistance to other protease inhibitors.Journal of virology · 2009Article
- Interplay of reverse transcriptase inhibitor therapy and gag p6 diversity in HIV type 1 subtype G and CRF02_AG.AIDS research and human retroviruses · 2008Article
- Refined study of the interaction between HIV-1 p6 late domain and ALIX.Retrovirology · 2008Article
- GGA and Arf proteins modulate retrovirus assembly and release.Molecular cell · 2008Article
- Novel cytotoxic T-lymphocyte escape mutation by a three-amino-acid insertion in the human immunodeficiency virus type 1 p6Pol and p6Gag late domain associated with drug resistance.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance of human immunodeficiency virus type 1 (HIV-1) to antiretroviral agents results from target gene mutation within the pol gene, which encodes the viral protease, reverse transcriptase (RT), and integrase. We speculated that mutations in genes other that the drug target could lead to drug resistance. For this purpose, the p1-p6(gag)-p6(pol) region of HIV-1, placed immediately upstream of pol, was analyzed. This region has the potential to alter Pol through frameshift regulation (p1), through improved packaging of viral enzymes (p6(Gag)), or by changes in activation of the viral protease (p6(Pol)). Duplication of the proline-rich p6(Gag) PTAP motif, necessary for late viral cycle activities, was identified in plasma virus from 47 of 222 (21.2%) patients treated with nucleoside analog RT inhibitor (NRTI) antiretroviral therapy but was identified very rarely from drug-naïve individuals. Molecular clones carrying a 3-amino-acid duplication, APPAPP (transframe duplication SPTSPT in p6(Pol)), displayed a delay in protein maturation; however, they packaged a 34% excess of RT and exhibited a marked competitive growth advantage in the presence of NRTIs. This phenotype is reminiscent of the inoculum effect described in bacteriology, where a larger input, or a greater infectivity of an organism with a wild-type antimicrobial target, leads to escape from drug pressure and a higher MIC in vitro. Though the mechanism by which the PTAP region participates in viral maturation is not known, duplication of this proline-rich motif could improve assembly and packaging at membrane locations, resulting in the observed phenotype of increased infectivity and drug resistance.
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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.