論文

査読有り
2014年3月

Lack of Association between Intact/Deletion Polymorphisms of the APOBEC3B Gene and HIV-1 Risk

PLOS ONE
  • Mayumi Imahashi
  • Taisuke Izumi
  • Dai Watanabe
  • Junji Imamura
  • Kazuhiro Matsuoka
  • Hirotaka Ode
  • Takashi Masaoka
  • Kei Sato
  • Noriyo Kaneko
  • Seiichi Ichikawa
  • Yoshio Koyanagi
  • Akifumi Takaori-Kondo
  • Makoto Utsumi
  • Yoshiyuki Yokomaku
  • Takuma Shirasaka
  • Wataru Sugiura
  • Yasumasa Iwatani
  • Tomoki Naoe
  • 全て表示

9
3
開始ページ
e92861
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1371/journal.pone.0092861
出版者・発行元
PUBLIC LIBRARY SCIENCE

Objective: The human APOBEC3 family of proteins potently restricts HIV-1 replication APOBEC3B, one of the family genes, is frequently deleted in human populations. Two previous studies reached inconsistent conclusions regarding the effects of APOBEC3B loss on HIV-1 acquisition and pathogenesis. Therefore, it was necessary to verify the effects of APOBEC3B on HIV-1 infection in vivo.
Methods: Intact (I) and deletion (D) polymorphisms of APOBEC3B were analyzed using PCR. The syphilis, HBV and HCV infection rates, as well as CD4(+) T cell counts and viral loads were compared among three APOBEC3B genotype groups (I/I, D/I, and D/D). HIV-1 replication kinetics was assayed in vitro using primary cells derived from PBMCs.
Results: A total of 248 HIV-1-infected Japanese men who have sex with men (MSM) patients and 207 uninfected Japanese MSM were enrolled in this study. The genotype analysis revealed no significant differences between the APOBEC3B genotype ratios of the infected and the uninfected cohorts (p = 0.66). In addition, HIV-1 disease progression parameters were not associated with the APOBEC3B genotype. Furthermore, the PBMCs from D/D and I/I subjects exhibited comparable HIV-1 susceptibility.
Conclusion: Our analysis of a population-based matched cohort suggests that the antiviral mechanism of APOBEC3B plays only a negligible role in eliminating HIV-1 in vivo.

リンク情報
DOI
https://doi.org/10.1371/journal.pone.0092861
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000333675600093&DestApp=WOS_CPL
ID情報
  • DOI : 10.1371/journal.pone.0092861
  • ISSN : 1932-6203
  • Web of Science ID : WOS:000333675600093

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