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Impact of human leukocyte antigen-B*51-restricted cytotoxic T-lymphocyte pressure on mutation patterns of nonnucleoside reverse transcriptase inhibitor resistance.

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Impact of human leukocyte antigen-B*51-restricted cytotoxic T-lymphocyte pressure on mutation patterns of nonnucleoside reverse transcriptase inhibitor resistance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gatanaga, Hiroyuki Ode, Hirotaka Hachiya, Atsuko Hayashida, Tsunefusa Sato, Hironori Takiguchi, Masafumi Oka, Shinichi
Description	Country affiliation: Japan Author Affiliation: Gatanaga H ( AIDS Clinical Center, International Medical Center of Japan, Tokyo, Japan. higatana@imcj.acc.go.jp)
Abstract	OBJECTIVE: The objective of this study is to determine the impact of human leukocyte antigen (HLA)-B51-restricted cytotoxic T-lymphocyte (CTL) pressure on the development of nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance. DESIGN: The prevalence of HIV-1 harboring an escape mutation, I135X, in a major epitope of HLA-B51-restricted CTL located in reverse transcriptase is increasing worldwide. We analyzed the effects of escape mutations on the emerging mutation patterns of NNRTI resistance. METHODS: Monoclonal HIV-1 sequences harboring each of the escape mutations, including I135L (HIV-1I135L), I135V (HIV-1I135V), I135T (HIV-1I135T), and I135R (HIV-1I135R) in reverse transcriptase, and a wild-type monoclonal HIV-1 (HIV-1WT) were cultured in the presence of increasing concentrations of efavirenz. Induced mutations during culture passages of the culture were analyzed. RESULTS: E138K emerged during the cultural passages of HIV-1I135V, HIV-1I135T, and HIV-1I135R, but not during the passages of HIV-1WT. The combination of I135T, the most frequent escape mutation, and E138K (HIV-1I135T/E138K) conferred significant resistance to efavirenz, nevirapine, and etravirine. The HIV-1I135L/E138K and HIV-1I135R/E138K were significantly resistant to nevirapine and etravirine, respectively, though each solo of escape mutations and E138K did not confer significant resistance to NNRTI. Computational analysis indicated that I135T and E138K cooperatively extend the gap between the binding site of reverse transcriptase and NNRTI. CONCLUSION: HLA-B*51-restricted CTL can induce novel mutation patterns of NNRTI resistance by selecting escape mutations. The spread of CTL escape variants may alter the mutation patterns of drug resistance.
File Format	HTM / HTML
ISSN	02699370
Issue Number	5
Volume Number	24
e-ISSN	14735571
Journal	AIDS
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2010-03-13
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Immunology Drug Resistance, Viral Genetics Hiv Infections Immunology Hiv-1 Immune Evasion Mutation Reverse Transcriptase Inhibitors Therapeutic Use T-lymphocytes, Cytotoxic Drug Therapy Drug Effects Hla-b Antigens Humans Immunodominant Epitopes Molecular Sequence Data Viral Load Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Immunology and Allergy Immunology

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