Emergence of Resistant Human Immunodeficiency Virus Type 1 in Patients Receiving Fusion Inhibitor (T-20) Monotherapy

By Xiping Wei, J. Decker, Hongmei Liu, Zee Zhang, R. Arani, J. Kilby, M. Saag, Xiaoyun Wu, G. Shaw, J. Kappes. Antimicrobial Agents and Chemotherapy, 2002

1,677 citations recorded by the source corpus.

Subfields: Epidemiology, Infectious Diseases, Virology

View Paper: https://www.semanticscholar.org/paper/b0e055ba097b2e3e875b768a45fa979766fdecd2

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In Virology

1. Beatrice H. Hahn
2. Paul M. Sharp

Citations in the corpus

• HIV-1 antiretroviral drug therapy. (2012, background): “Monotherapy with enfuvirtide resulted in viral load rebounds after 14 days with resistance which mapped to determinants in the HR1 domain (G36D, I37T, V38A, V38M, N42T, N42D, N43K) (Wei et al. 2002).”
• Antibody neutralization and escape by HIV-1 (2003, background): “As a result, the composition of plasma virus provides a sensitive indicator of biologically relevant selection pressures acting on virus and virus-producing cell”
• HIV Enters Cells via Endocytosis and Dynamin-Dependent Fusion with Endosomes (2009, neutral): “J.C. Kappes and X. Wu ( Wei et al., 2002 )) and CEMss cells (donated by Dr. P. Nara) were obtained from NIH AIDS Research and Reference Reagent Program and were grown in DMEM and RPMI-1640, respectively, supplemented with 10% Fetal Bovine Serum (FBS) and penicillin-streptomycin.”
• Deciphering Human Immunodeficiency Virus Type 1 Transmission and Early Envelope Diversification by Single-Genome Amplification and Sequencing (2008, methodology): “Full-length rev/env cassettes (including parts of the first exon of the tat gene; the entire vpu, rev, and env genes; and parts of the nef gene) were amplified by nested PCR from plasma-derived viral cDNA as previously described (5, 50 , 51).”
• Human immunodeficiency virus reverse transcriptase and protease sequence database (2003, background): “A wide range of mutations in gp41 contributing to T-20 resistance, most occurring between residues 36–45, have been reported, but mutations outside of this region also appear to contribute to drug resistance (7,8); (ii) integrase sequences.”