期刊
JOURNAL OF VIROLOGY
卷 84, 期 11, 页码 5842-5845出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01907-09
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资金
- National Institute of Allergy and Infectious Diseases (NIAID) [R01 AI052778, U19 AI076981]
- La Jolla Foundation
- Swiss National Science Foundation
- CONRAD
- World Health Organization
- International Partnership for Microbicides
Resistance of human immunodeficiency virus type 1 (HIV-1) to small-molecule CCR5 inhibitors is well demonstrated, but resistance to macromolecular CCR5 inhibitors (e.g., PSC-RANTES) that act by both CCR5 internalization and receptor blockade had not been reported until recently (3). The report of a single simian-human immunodeficiency virus SHIVSF162-p3 variant with one V3 and one gp41 sequence change in gp160 that conferred both altered replicative fitness and resistance to PSC-RANTES was therefore surprising. We introduced the same two mutations into both the parental HIV-1(SF162) and the macaque-adapted SHIVSF162-p3 and found minor differences in entry fitness but no changes in sensitivity to inhibition by either PSC-RANTES or the small-molecule allosteric inhibitor TAK-779. We attribute the earlier finding to confounding fitness effects with inhibitor sensitivity.
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