Induction of heat-shock protein 70 by prostaglandin A1 inhibits HIV-1 Vif-mediated degradation of APOBEC3G

Ryuichi Sugiyama, Makoto Abe, Hironori Nishitsuji, Yuko Murakami, Hiroaki Takeuchi, Hiroshi Takaku

研究成果: Article査読

5 被引用数 (Scopus)

抄録

Previous studies have demonstrated that cyclopentenone prostaglandins (cyPGs) inhibit human immunodeficiency virus type 1 (HIV-1) replication in various cell types. This antiviral activity has been associated with the induction of heat-shock protein 70 (HSP70) in infected cells. We investigated a new role of prostaglandin A1 (PGA1) in the replication of HIV-1 in non-permissive cells. Because overexpression of HSP70 blocks the viral infectivity factor (Vif)-mediated degradation of APOBEC3G (A3G) via the ubiquitin-proteasome pathway, we examined the effects of PGA1 on A3G and HIV-1 replication. The induction of HSP70 synthesis by PGA1 blocked Vif-mediated A3G degradation and enhanced the incorporation of A3G into both wild-type and Vif-deficient viruses. Furthermore, we determined the viral titer of HIV-1 particles produced from PGA1-treated 293T cells. The induction of HSP70 synthesis by PGA1 significantly reduced the viral titer in the presence of A3G. Additionally, the p24 Gag antigen levels were dramatically reduced in non-permissive cells treated once or repeatedly with PGA1. Thus, we showed that PGA1 inhibits HIV-1 replication, at least in part, by blocking Vif-mediated A3G degradation.

本文言語English
ページ(範囲)307-311
ページ数5
ジャーナルAntiviral Research
99
3
DOI
出版ステータスPublished - 01-09-2013
外部発表はい

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Virology

フィンガープリント 「Induction of heat-shock protein 70 by prostaglandin A<sub>1</sub> inhibits HIV-1 Vif-mediated degradation of APOBEC3G」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

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