期刊
VIROLOGY
卷 442, 期 1, 页码 51-58出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2013.03.026
关键词
HIV-1; Maraviroc; Resistance; T-cell; Macrophage; Tropism; Env; gp120
类别
资金
- Australian National Health and Medical Research Council [1006534]
- Australian National Health and Medical Research Council (NHMRC) Level 2 Biomedical Career Development Award
- Australian Research Council (ARC) Future Fellowship (FT2)
- Australian NHMRC Postdoctoral Training Fellowship
- Iranian Ministry of Health and Medical Education
- NHMRC Practitioner Fellowship
Human immunodeficiency virus type 1 (HIV-1) resistance to CCR5 antagonists, including maraviroc (MVC), results from alterations in the HIV-1 envelope glycoproteins (Env) enabling recognition of antagonist-bound CCR5. Here, we characterized tropism alterations for CD4+ T-cell subsets and macrophages by Envs from two subjects who developed MVC resistance in vivo, which displayed either relatively efficient or inefficient recognition of MVC-bound CCR5. We show that MVC-resistant Env with efficient recognition of drug-bound CCR5 displays a tropism shift for CD4+ T-cell subsets associated with increased infection of central memory T-cells and reduced infection of effector memory and transitional memory T-cells, and no change in macrophage infectivity. In contrast, MVC-resistant Env with inefficient recognition of drug-bound CCR5 displays no change in tropism for CD4+ T-cell subsets, but exhibits a significant reduction in macrophage infectivity. The pattern of HIV-1 tropism alterations for susceptible cells may therefore be variable in subjects with MVC resistance. (C) 2013 Elsevier Inc. All rights reserved.
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