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Raltegravir and elvitegravir-resistance mutation E92Q affects HLA-B*40:02-restricted HIV-1-specific CTL recognition.

Authors
  • Rahman, Mohammad Arif1
  • Kuse, Nozomi1
  • Murakoshi, Hayato1
  • Chikata, Takayuki1
  • Gatanaga, Hiroyuki2
  • Oka, Shinichi2
  • Takiguchi, Masafumi3
  • 1 Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan. , (Japan)
  • 2 Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan; AIDS Clinical Center, National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan. , (Japan)
  • 3 Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan. Electronic address: [email protected] , (Japan)
Type
Published Article
Journal
Microbes and infection
Publication Date
May 01, 2014
Volume
16
Issue
5
Pages
434–438
Identifiers
DOI: 10.1016/j.micinf.2014.03.003
PMID: 24657622
Source
Medline
Keywords
License
Unknown

Abstract

Interplay between drug-resistance mutations in CTL epitopes and HIV-1-specific CTLs may influence the control of HIV-1 viremia. However, the effect of integrase inhibitor (INI)-resistance mutations on the CTL recognition has not been reported. We here investigated the effect of a raltegravir and elvitegravir-resistance mutation (E92Q) on HLA-B*40:02-restricted Int92-102 (EL11: ETGQETAYFLL)-specific CTLs. EL11-specific CTLs recognized E92Q peptide-pulsed and E92Q mutant virus-infected cells less effectively than EL11 peptide-pulsed and wild-type virus-infected cells, respectively. Ex vivo ELISpot analysis showed no induction of E92Q-specific T cells in chronically HIV-1-infected individuals. Thus, we demonstrated that EL11-specific CTL recognition was affected by the INI-resistance mutation.

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