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

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...

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Veröffentlicht in:Proceedings of the National Academy of Sciences - PNAS 2008-01, Vol.105 (1), p.294-299
Hauptverfasser: Ryo, Akihide, Tsurutani, Naomi, Ohba, Kenji, Kimura, Ryuichiro, Komano, Jun, Nishi, Mayuko, Soeda, Hiromi, Hattori, Shinichiro, Perrem, Kilian, Yamamoto, Mikio, Chiba, Joe, Mimaya, Jun-ichi, Yoshimura, Kazuhisa, Matsushita, Shuzo, Honda, Mitsuo, Yoshimura, Akihiko, Sawasaki, Tatsuya, Aoki, Ichiro, Morikawa, Yuko, Yamamoto, Naoki
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container_title Proceedings of the National Academy of Sciences - PNAS
container_volume 105
creator Ryo, Akihide
Tsurutani, Naomi
Ohba, Kenji
Kimura, Ryuichiro
Komano, Jun
Nishi, Mayuko
Soeda, Hiromi
Hattori, Shinichiro
Perrem, Kilian
Yamamoto, Mikio
Chiba, Joe
Mimaya, Jun-ichi
Yoshimura, Kazuhisa
Matsushita, Shuzo
Honda, Mitsuo
Yoshimura, Akihiko
Sawasaki, Tatsuya
Aoki, Ichiro
Morikawa, Yuko
Yamamoto, Naoki
description 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.
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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. 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subjects Acquired Immunodeficiency Syndrome - therapy
Antibodies
Biochemistry
Biological Sciences
Cell Line
Cell Membrane - metabolism
Cytokines
Enzymes
Gene Products, gag - metabolism
HIV
HIV 1
HIV Infections - metabolism
HIV-1 - metabolism
Human immunodeficiency virus
Human immunodeficiency virus 1
Humans
Immunoblotting
Infections
Jurkat Cells
Microscopy, Electron
Microscopy, Electron, Transmission
Muramidase - chemistry
Particle production
Plasmids - metabolism
Proteins
RNA Processing, Post-Transcriptional
RNA, Small Interfering - metabolism
Signal Transduction
Small interfering RNA
Suppressor of Cytokine Signaling 1 Protein
Suppressor of Cytokine Signaling Proteins - metabolism
Suppressor of Cytokine Signaling Proteins - physiology
T lymphocytes
Virions
Virology
Virus Replication
Viruses
title SOCS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag
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