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dc.contributor.authorQuitadamo, Briana
dc.contributor.authorPeters, Paul J.
dc.contributor.authorKoch, Matthew
dc.contributor.authorLuzuriaga, Katherine
dc.contributor.authorCheng-Mayer, Cecilia
dc.contributor.authorClapham, Paul R.
dc.contributor.authorGonzalez-Perez, Maria Paz
dc.date2022-08-11T08:09:52.000
dc.date.accessioned2022-08-23T16:46:53Z
dc.date.available2022-08-23T16:46:53Z
dc.date.issued2019-02-01
dc.date.submitted2019-05-06
dc.identifier.citation<p>Arch Virol. 2019 Feb;164(2):473-482. doi: 10.1007/s00705-018-4094-1. Epub 2018 Nov 10. <a href="https://doi.org/10.1007/s00705-018-4094-1">Link to article on publisher's site</a></p>
dc.identifier.issn0304-8608 (Linking)
dc.identifier.doi10.1007/s00705-018-4094-1
dc.identifier.pmid30415390
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40968
dc.description.abstractMacrophage (mac)-tropic human immnunodeficiency virus type 1 (HIV-1) and simian immnunodeficiency virus (SIV) in brain are associated with neurological disease. Mac-tropic HIV-1 evolves enhanced CD4 interactions that enable macrophage infection via CD4, which is in low abundance. In contrast, mac-tropic SIV is associated with CD4-independent infection via direct CCR5 binding. Recently, mac-tropic simian-human immunodeficiency virus (SHIV) from macaque brain was also reported to infect cells via CCR5 without CD4. Since SHIV envelope proteins (Envs) are derived from HIV-1, we tested more than 100 HIV-1 clade B Envs for infection of CD4-negative, CCR5(+) Cf2Th/CCR5 cells. However, no infection was detected. Our data suggest that there are differences in the evolution of mac-tropism in SIV and SHIV compared to HIV-1 clade B due to enhanced interactions with CCR5 and CD4, respectively.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30415390&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rights© The Author(s) 2018. Open Access: This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectAnimal Experimentation and Research
dc.subjectHemic and Immune Systems
dc.subjectImmunology of Infectious Disease
dc.subjectNervous System
dc.subjectVirology
dc.subjectViruses
dc.titleNo detection of CD4-independent human immunodeficiency virus 1 envelope glycoproteins in brain tissue of patients with or without neurological complications
dc.typeJournal Article
dc.source.journaltitleArchives of virology
dc.source.volume164
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4781&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3767
dc.identifier.contextkey14438105
refterms.dateFOA2022-08-23T16:46:53Z
html.description.abstract<p>Macrophage (mac)-tropic human immnunodeficiency virus type 1 (HIV-1) and simian immnunodeficiency virus (SIV) in brain are associated with neurological disease. Mac-tropic HIV-1 evolves enhanced CD4 interactions that enable macrophage infection via CD4, which is in low abundance. In contrast, mac-tropic SIV is associated with CD4-independent infection via direct CCR5 binding. Recently, mac-tropic simian-human immunodeficiency virus (SHIV) from macaque brain was also reported to infect cells via CCR5 without CD4. Since SHIV envelope proteins (Envs) are derived from HIV-1, we tested more than 100 HIV-1 clade B Envs for infection of CD4-negative, CCR5(+) Cf2Th/CCR5 cells. However, no infection was detected. Our data suggest that there are differences in the evolution of mac-tropism in SIV and SHIV compared to HIV-1 clade B due to enhanced interactions with CCR5 and CD4, respectively.</p>
dc.identifier.submissionpathoapubs/3767
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages473-482


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© The Author(s) 2018.  Open Access: This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Except where otherwise noted, this item's license is described as © The Author(s) 2018. Open Access: This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.