HIV Pol inhibits HIV budding and mediates the severe budding defect of Gag-Pol
The prevailing hypothesis of HIV budding posits that the viral Gag protein drives budding, and that the Gag p6 peptide plays an essential role by recruiting host-cell budding factors to sites of HIV assembly. HIV also expresses a second Gag protein, p160 Gag-Pol, which lacks p6 and fails to bud from...
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| Veröffentlicht in: | PloS one 2012-01, Vol.7 (1), p.e29421-e29421 |
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| creator | Gan, Xin Gould, Stephen J |
| description | The prevailing hypothesis of HIV budding posits that the viral Gag protein drives budding, and that the Gag p6 peptide plays an essential role by recruiting host-cell budding factors to sites of HIV assembly. HIV also expresses a second Gag protein, p160 Gag-Pol, which lacks p6 and fails to bud from cells, consistent with the prevailing hypothesis of HIV budding. However, we show here that the severe budding defect of Gag-Pol is not caused by the absence of p6, but rather, by the presence of Pol. Specifically, we show that (i) the budding defect of Gag-Pol is unaffected by loss of HIV protease activity and is therefore an intrinsic property of the Gag-Pol polyprotein, (ii) the N-terminal 433 amino acids of Gag and Gag-Pol are sufficient to drive virus budding even though they lack p6, (iii) the severe budding defect of Gag-Pol is caused by a dominant, cis-acting inhibitor of budding in the HIV Pol domain, and (iv) Gag-Pol inhibits Gag and virus budding in trans, even at normal levels of Gag and Gag-Pol expression. These and other data support an alternative hypothesis of HIV budding as a process that is mediated by the normal, non-viral pathway of exosome/microvesicle biogenesis. |
| doi_str_mv | 10.1371/journal.pone.0029421 |
| format | Article |
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HIV also expresses a second Gag protein, p160 Gag-Pol, which lacks p6 and fails to bud from cells, consistent with the prevailing hypothesis of HIV budding. However, we show here that the severe budding defect of Gag-Pol is not caused by the absence of p6, but rather, by the presence of Pol. Specifically, we show that (i) the budding defect of Gag-Pol is unaffected by loss of HIV protease activity and is therefore an intrinsic property of the Gag-Pol polyprotein, (ii) the N-terminal 433 amino acids of Gag and Gag-Pol are sufficient to drive virus budding even though they lack p6, (iii) the severe budding defect of Gag-Pol is caused by a dominant, cis-acting inhibitor of budding in the HIV Pol domain, and (iv) Gag-Pol inhibits Gag and virus budding in trans, even at normal levels of Gag and Gag-Pol expression. These and other data support an alternative hypothesis of HIV budding as a process that is mediated by the normal, non-viral pathway of exosome/microvesicle biogenesis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0029421</identifier><identifier>PMID: 22235295</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Amino acids ; Base Sequence ; Biology ; Biosynthesis ; Budding ; Carbohydrates ; Defects ; DNA, Viral - genetics ; DNA, Viral - metabolism ; Drug resistance ; Exosomes - virology ; Fusion Proteins, gag-pol - metabolism ; Gag protein ; Genomes ; HEK293 Cells ; HIV ; HIV - metabolism ; HIV - physiology ; Human immunodeficiency virus ; Humans ; Hypotheses ; Localization ; Medicine ; Peptides ; Proteases ; Proteins ; Virus Release ; Viruses</subject><ispartof>PloS one, 2012-01, Vol.7 (1), p.e29421-e29421</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Gan, Gould. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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HIV also expresses a second Gag protein, p160 Gag-Pol, which lacks p6 and fails to bud from cells, consistent with the prevailing hypothesis of HIV budding. However, we show here that the severe budding defect of Gag-Pol is not caused by the absence of p6, but rather, by the presence of Pol. Specifically, we show that (i) the budding defect of Gag-Pol is unaffected by loss of HIV protease activity and is therefore an intrinsic property of the Gag-Pol polyprotein, (ii) the N-terminal 433 amino acids of Gag and Gag-Pol are sufficient to drive virus budding even though they lack p6, (iii) the severe budding defect of Gag-Pol is caused by a dominant, cis-acting inhibitor of budding in the HIV Pol domain, and (iv) Gag-Pol inhibits Gag and virus budding in trans, even at normal levels of Gag and Gag-Pol expression. These and other data support an alternative hypothesis of HIV budding as a process that is mediated by the normal, non-viral pathway of exosome/microvesicle biogenesis.</description><subject>Amino acids</subject><subject>Base Sequence</subject><subject>Biology</subject><subject>Biosynthesis</subject><subject>Budding</subject><subject>Carbohydrates</subject><subject>Defects</subject><subject>DNA, Viral - genetics</subject><subject>DNA, Viral - metabolism</subject><subject>Drug resistance</subject><subject>Exosomes - virology</subject><subject>Fusion Proteins, gag-pol - metabolism</subject><subject>Gag protein</subject><subject>Genomes</subject><subject>HEK293 Cells</subject><subject>HIV</subject><subject>HIV - metabolism</subject><subject>HIV - physiology</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Localization</subject><subject>Medicine</subject><subject>Peptides</subject><subject>Proteases</subject><subject>Proteins</subject><subject>Virus Release</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkk1v1DAQhiMEoqXwDxBEQgJx2MUfiZ1ckKoK2pUqivjo1ZrE46xX2XgbO1X77_Gy6WqDekA-2Bo_89oz8ybJa0rmlEv6aeWGvoN2vnEdzglhZcbok-SYlpzNBCP86cH5KHnh_YqQnBdCPE-OGGM8Z2V-nHy7WFyn312b2m5pKxt8ug1Ug9a2a1LodLpGbSGgT8MSU4-32OP-XqPBOqTOpOfQzKLMy-SZgdbjq3E_SX5__fLr7GJ2eXW-ODu9nNWipGGWYWY0FFBoYJqikIwwWVVSFEYXmakk1DU1hHCAquSYU2OIQG64znUGOeMnydud7qZ1Xo2t8IpyFmvOKZORWOwI7WClNr1dQ3-vHFj1N-D6RkEfbN2i4hwEl1hSqfPMlFUlZCF1qUXFNQFJo9bn8bWhiu2osQs9tBPR6U1nl6pxt4qznGRcRIEPo0Dvbgb0Qa2tr7FtoUM3eFXSXLAyziSS7_4hHy9upBqI_7edcfHZequpTjMpqaQF22rNH6Hi0ri2dbSNsTE-Sfg4SYhMwLvQwOC9Wvz88f_s1fWUfX_ALhHasPSuHYJ1nZ-C2Q6se-d9j2bfY0rU1vUP3VBb16vR9THtzeF89kkPNud_AG5W-w8</recordid><startdate>20120103</startdate><enddate>20120103</enddate><creator>Gan, Xin</creator><creator>Gould, Stephen J</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120103</creationdate><title>HIV Pol inhibits HIV budding and mediates the severe budding defect of Gag-Pol</title><author>Gan, Xin ; Gould, Stephen J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-4e4fda8a8da2d1e672027bb768fd84fb7acc1f003aab93e51ff06e3f3d5d4a523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Amino acids</topic><topic>Base Sequence</topic><topic>Biology</topic><topic>Biosynthesis</topic><topic>Budding</topic><topic>Carbohydrates</topic><topic>Defects</topic><topic>DNA, Viral - genetics</topic><topic>DNA, Viral - metabolism</topic><topic>Drug resistance</topic><topic>Exosomes - virology</topic><topic>Fusion Proteins, gag-pol - metabolism</topic><topic>Gag protein</topic><topic>Genomes</topic><topic>HEK293 Cells</topic><topic>HIV</topic><topic>HIV - metabolism</topic><topic>HIV - physiology</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Localization</topic><topic>Medicine</topic><topic>Peptides</topic><topic>Proteases</topic><topic>Proteins</topic><topic>Virus Release</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gan, Xin</creatorcontrib><creatorcontrib>Gould, Stephen J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gan, Xin</au><au>Gould, Stephen J</au><au>Kim, Baek</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIV Pol inhibits HIV budding and mediates the severe budding defect of Gag-Pol</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-01-03</date><risdate>2012</risdate><volume>7</volume><issue>1</issue><spage>e29421</spage><epage>e29421</epage><pages>e29421-e29421</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The prevailing hypothesis of HIV budding posits that the viral Gag protein drives budding, and that the Gag p6 peptide plays an essential role by recruiting host-cell budding factors to sites of HIV assembly. HIV also expresses a second Gag protein, p160 Gag-Pol, which lacks p6 and fails to bud from cells, consistent with the prevailing hypothesis of HIV budding. However, we show here that the severe budding defect of Gag-Pol is not caused by the absence of p6, but rather, by the presence of Pol. Specifically, we show that (i) the budding defect of Gag-Pol is unaffected by loss of HIV protease activity and is therefore an intrinsic property of the Gag-Pol polyprotein, (ii) the N-terminal 433 amino acids of Gag and Gag-Pol are sufficient to drive virus budding even though they lack p6, (iii) the severe budding defect of Gag-Pol is caused by a dominant, cis-acting inhibitor of budding in the HIV Pol domain, and (iv) Gag-Pol inhibits Gag and virus budding in trans, even at normal levels of Gag and Gag-Pol expression. These and other data support an alternative hypothesis of HIV budding as a process that is mediated by the normal, non-viral pathway of exosome/microvesicle biogenesis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22235295</pmid><doi>10.1371/journal.pone.0029421</doi><tpages>e29421</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino acids Base Sequence Biology Biosynthesis Budding Carbohydrates Defects DNA, Viral - genetics DNA, Viral - metabolism Drug resistance Exosomes - virology Fusion Proteins, gag-pol - metabolism Gag protein Genomes HEK293 Cells HIV HIV - metabolism HIV - physiology Human immunodeficiency virus Humans Hypotheses Localization Medicine Peptides Proteases Proteins Virus Release Viruses |
| title | HIV Pol inhibits HIV budding and mediates the severe budding defect of Gag-Pol |
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