Extracellular nef protein activates signal transduction pathway from ras to mitogen-activated protein kinase cascades that leads to activation of human immunodeficiency virus from latency

Minoru Tobiume, Koh Fujinaga, Satoko Suzuki, Satoshi Komoto, Tetsu Mukai, Kazuyoshi Ikuta

研究成果: Article査読

18 被引用数 (Scopus)

抄録

We previously reported that viral antigen expression was markedly up-regulated by stimulation with extra-cellular Nef, similar to the effects of tumor necrosis factor (TNF)-α and phorbol myristate acetate, in model cells for HIV-1 latency. In this study, we examined the molecular mechanism of this novel Nef function. Flow cytometry revealed specific binding of Nef on the surface of latently infected cells. Furthermore, activation of Ras in the cells was detected after treatment with Nef, indicating the involvement of Ras in Nef-mediated activation of HIV-1 from latency. This was also confirmed by the observations that HIV-1 long-terminal repeat-luciferase (LTR-Luc) activity was significantly up-regulated by introduction of the active Ras into uninfected cells, and that LTR-Luc activity observed in Nef-treated cells was specifically inhibited by introduction of a dominant negative Ras. In addition, PD98059 inhibited the activation of HIV-1 by Nef, but not by TNF-α. Thus, Nef-mediated reactivation of HIV-1 in latent model cells occurs by signal transduction from Ras to mitogen-activated protein kinase cascades.

本文言語English
ページ(範囲)461-467
ページ数7
ジャーナルAIDS Research and Human Retroviruses
18
6
DOI
出版ステータスPublished - 2002

All Science Journal Classification (ASJC) codes

  • Immunology
  • Virology
  • Infectious Diseases

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