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dc.contributor.authorHovden, Arnt-Oveeng
dc.date.accessioned2006-03-02T09:27:08Z
dc.date.available2006-03-02T09:27:08Z
dc.date.issued2001eng
dc.identifier.isbn82-8088-003-8 (electronic version)eng
dc.identifier.otherhttp://www.ub.uib.no/elpub/2001/h/402001/eng
dc.identifier.urihttp://hdl.handle.net/1956/1117
dc.description.abstractMaedi visna virus (MVV) is a retrovirus that is member of the Lentivirus genus. MVV infects sheep and goats and causes progressive pneumonia or paralysis, leading to death. Since the discovery of the receptor for Human immunodeficiency virus (HIV), Simian immunodeficiency virus (SIV) and Feline immunodeficiency virus (FIV) all include the chemokine receptor CXCR4, it has been postulated that all members of the Lentivirus share a common mechanism of entry that involves the use of CXCR4. With the use of syncytia assays, infection-, inhibition- and enhancement studies, it was shown that CXCR4 is not a common lentivirus receptor. U87 and HOS cells, both celllines lacking CXCR4, were susceptible to infection. However, cells transfected with CD4 and CXCR4 showed an increased syncytia formation and the presence of CD¤ and CXCR4 augments virus-induced cell fusion. The nature of MVV receptor is still not known, but our data suggest the use of CD4 and/or CXCR4 as accessory molecules or as part of a receptor complex.en
dc.format.extent716235 byteseng
dc.format.mimetypeapplication/pdfeng
dc.language.isoengeng
dc.publisherThe University of Bergeneng
dc.titleThe influence of CXCR4 on Maedi visna virus-induced syncytium formationeng
dc.typeMaster thesiseng
dc.subject.nsiVDP::Matematikk og Naturvitenskap: 400::Basale biofag: 470::Molekylærbiologi: 473nob
dc.subject.archivecodeMastergradeng
dc.rights.holderCopyright the author. All rights reserved
dc.rights.holderThe authoreng


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