SOCS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag

Akihide Ryo, Naomi Tsurutani, Kenji Ohba, Ryuichiro Kimura, Jun Komano, Mayuko Nishi, Hiromi Soeda, Shinichiro Hattori, Kilian Perrem, Mikio Yamamoto, Joe Chiba, Jun Ichi Mimaya, Kazuhisa Yoshimura, Shuzo Matsushita, Mitsuo Honda, Akihiko Yoshimura, Tatsuya Sawasaki, Ichiro Aoki, Yuko Morikawa, Naoki Yamamoto

研究成果: Article査読

61 被引用数 (Scopus)

抄録

Human immunodeficiency virus type 1 (HIV-1) utilizes the macromolecular machinery of the infected host cell to produce progeny virus. The discovery of cellular factors that participate in HIV-1 replication pathways has provided further insight into the molecular basis of virus-host cell interactions. Here, we report that the suppressor of cytokine signaling 1 (SOCS1) is an inducible host factor during HIV-1 infection and regulates the late stages of the HIV-1 replication pathway. SOCS1 can directly bind to the matrix and nucleocapsid regions of the HIV-1 p55 Gag polyprotein and enhance its stability and trafficking, resulting in the efficient production of HIV-1 particles via an IFN signaling-independent mechanism. The depletion of SOCS1 by siRNA reduces both the targeted trafficking and assembly of HIV-1 Gag, resulting in its accumulation as perinuclear solid aggregates that are eventually subjected to lysosomal degradation. These results together indicate that SOCS1 is a crucial host factor that regulates the intracellular dynamism of HIV-1 Gag and could therefore be a potential new therapeutic target for AIDS and its related disorders.

本文言語English
ページ(範囲)294-299
ページ数6
ジャーナルProceedings of the National Academy of Sciences of the United States of America
105
1
DOI
出版ステータスPublished - 2008 1 8
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ASJC Scopus subject areas

  • General

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