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 |
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| 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. |
| doi_str_mv | 10.1073/pnas.0704831105 |
| format | Article |
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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. 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.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0704831105</identifier><identifier>PMID: 18172216</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>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</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2008-01, Vol.105 (1), p.294-299</ispartof><rights>Copyright 2008 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jan 8, 2008</rights><rights>2008 by The National Academy of Sciences of the USA 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c614t-d5ff15f7daf055b5350879c497e1e1ff367dea57bc8285f88845caf6ac05dfaf3</citedby><cites>FETCH-LOGICAL-c614t-d5ff15f7daf055b5350879c497e1e1ff367dea57bc8285f88845caf6ac05dfaf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/105/1.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25451077$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25451077$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,315,729,782,786,805,887,27931,27932,53798,53800,58024,58257</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18172216$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ryo, Akihide</creatorcontrib><creatorcontrib>Tsurutani, Naomi</creatorcontrib><creatorcontrib>Ohba, Kenji</creatorcontrib><creatorcontrib>Kimura, Ryuichiro</creatorcontrib><creatorcontrib>Komano, Jun</creatorcontrib><creatorcontrib>Nishi, Mayuko</creatorcontrib><creatorcontrib>Soeda, Hiromi</creatorcontrib><creatorcontrib>Hattori, Shinichiro</creatorcontrib><creatorcontrib>Perrem, Kilian</creatorcontrib><creatorcontrib>Yamamoto, Mikio</creatorcontrib><creatorcontrib>Chiba, Joe</creatorcontrib><creatorcontrib>Mimaya, Jun-ichi</creatorcontrib><creatorcontrib>Yoshimura, Kazuhisa</creatorcontrib><creatorcontrib>Matsushita, Shuzo</creatorcontrib><creatorcontrib>Honda, Mitsuo</creatorcontrib><creatorcontrib>Yoshimura, Akihiko</creatorcontrib><creatorcontrib>Sawasaki, Tatsuya</creatorcontrib><creatorcontrib>Aoki, Ichiro</creatorcontrib><creatorcontrib>Morikawa, Yuko</creatorcontrib><creatorcontrib>Yamamoto, Naoki</creatorcontrib><title>SOCS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><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.</description><subject>Acquired Immunodeficiency Syndrome - therapy</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biological Sciences</subject><subject>Cell Line</subject><subject>Cell Membrane - metabolism</subject><subject>Cytokines</subject><subject>Enzymes</subject><subject>Gene Products, gag - metabolism</subject><subject>HIV</subject><subject>HIV 1</subject><subject>HIV Infections - metabolism</subject><subject>HIV-1 - metabolism</subject><subject>Human immunodeficiency virus</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Infections</subject><subject>Jurkat Cells</subject><subject>Microscopy, Electron</subject><subject>Microscopy, Electron, Transmission</subject><subject>Muramidase - 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PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2008-01-08</date><risdate>2008</risdate><volume>105</volume><issue>1</issue><spage>294</spage><epage>299</epage><pages>294-299</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>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.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>18172216</pmid><doi>10.1073/pnas.0704831105</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2008-01, Vol.105 (1), p.294-299 |
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| language | eng |
| recordid | cdi_proquest_miscellaneous_70193132 |
| source | MEDLINE; JSTOR Archive Collection A-Z Listing; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| 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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