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dc.contributor.authorRichards, Kathryn H.
dc.contributor.authorClapham, Paul R.
dc.date2022-08-11T08:08:57.000
dc.date.accessioned2022-08-23T16:13:48Z
dc.date.available2022-08-23T16:13:48Z
dc.date.issued2007-09-18
dc.date.submitted2008-09-11
dc.identifier.citationJ Gen Virol. 2007 Oct;88(Pt 10):2780-92. <a href="http://dx.doi.org/10.1099/vir.0.83120-0">Link to article on publisher's site</a>
dc.identifier.issn0022-1317 (Print)
dc.identifier.doi10.1099/vir.0.83120-0
dc.identifier.pmid17872532
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33710
dc.description.abstractThe human immunodeficiency virus type 1 (HIV-1) vpu protein increases the release of virus particles from infected cells. Mutations that abrogate vpu function have a profound effect on HIV-1 replication in primary macrophage cultures. About 1.24 % of primary isolates in the HIV databases have vpu start-codon mutations. In addition, the envelope of the AD8 isolate was reported to compensate for the lack of vpu, whilst the YU-2 virus (cloned directly from the brain tissue of an infected individual) is macrophage-tropic, despite having a vpu start-codon mutation. These observations raise the possibility that envelopes evolve to compensate for the loss of vpu function in vivo. Chimeric vpu+ and vpu- replication-competent clones were constructed that contained the envelopes of SF162, AD8 or YU-2. Macrophages were infected with these chimeras and virus release was measured over time by a reverse transcriptase ELISA. It was found that vpu-deficient chimeras carrying AD8 and YU-2 envelopes were consistently released at lower levels than their wild-type (wt) vpu counterparts, indicating that these envelopes did not compensate for the lack of vpu. Non-chimeric vpu+ and vpu- AD8 and YU-2 followed similar patterns, although replication by vpu-deficient AD8 was variable, with virion release reaching 60 % of that recorded for AD8 with a wt vpu. In summary, no evidence was found that the AD8 or YU-2 envelopes can compensate for the lack of vpu for replication in macrophages.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17872532&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1099/vir.0.83120-0
dc.subjectCell Line; Cells, Cultured; Cloning, Molecular; Codon; Genome, Viral; HIV Core Protein p24; HIV-1; Human Immunodeficiency Virus Proteins; Humans; Kidney; Macrophages; *Polymorphism, Single Nucleotide; RNA-Directed DNA Polymerase; Restriction Mapping; Viral Envelope Proteins; Viral Regulatory and Accessory Proteins; Virus Replication
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of vpu start-codon mutations on human immunodeficiency virus type 1 replication in macrophages
dc.typeJournal Article
dc.source.journaltitleThe Journal of general virology
dc.source.volume88
dc.source.issuePt 10
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/373
dc.identifier.contextkey626924
html.description.abstract<p>The human immunodeficiency virus type 1 (HIV-1) vpu protein increases the release of virus particles from infected cells. Mutations that abrogate vpu function have a profound effect on HIV-1 replication in primary macrophage cultures. About 1.24 % of primary isolates in the HIV databases have vpu start-codon mutations. In addition, the envelope of the AD8 isolate was reported to compensate for the lack of vpu, whilst the YU-2 virus (cloned directly from the brain tissue of an infected individual) is macrophage-tropic, despite having a vpu start-codon mutation. These observations raise the possibility that envelopes evolve to compensate for the loss of vpu function in vivo. Chimeric vpu+ and vpu- replication-competent clones were constructed that contained the envelopes of SF162, AD8 or YU-2. Macrophages were infected with these chimeras and virus release was measured over time by a reverse transcriptase ELISA. It was found that vpu-deficient chimeras carrying AD8 and YU-2 envelopes were consistently released at lower levels than their wild-type (wt) vpu counterparts, indicating that these envelopes did not compensate for the lack of vpu. Non-chimeric vpu+ and vpu- AD8 and YU-2 followed similar patterns, although replication by vpu-deficient AD8 was variable, with virion release reaching 60 % of that recorded for AD8 with a wt vpu. In summary, no evidence was found that the AD8 or YU-2 envelopes can compensate for the lack of vpu for replication in macrophages.</p>
dc.identifier.submissionpathgsbs_sp/373
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages2780-92


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