期刊
JOURNAL OF VIROLOGY
卷 82, 期 16, 页码 8210-8214出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00444-08
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资金
- NCRR NIH HHS [K24 RR016482] Funding Source: Medline
- NIAID NIH HHS [U01 AI068636, T32 AI007387, K24 AI051966, P30 AI060354, R37 AI553537, K24 AI-51966] Funding Source: Medline
Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.
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