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dc.rights.licenseCC-BY-NC-ND
dc.contributor.advisorBosch, B.J.
dc.contributor.authorBakkers, M.J.G.
dc.date.accessioned2011-11-29T18:01:26Z
dc.date.available2011-11-29
dc.date.available2011-11-29T18:01:26Z
dc.date.issued2011
dc.identifier.urihttps://studenttheses.uu.nl/handle/20.500.12932/9665
dc.description.abstractThe development of effective therapies to combat the threat of emerging viruses requires a thorough understanding of the mechanisms governing virus tropism. Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin (DC-SIGN) was identified as a C-type lectin that mediates the initial interaction between dendritic cell and T cell, as well as serving additional roles in immunology. DC-SIGN and the related L-SIGN were also found to play a role in the cis and trans infection of cells by a wide array of viruses. Their role in cis infection can be explained either by functioning as attachment factor or, in some cases, as true entry receptors. Though differentiating the two experimentally is very difficult, the best approach seems to be overexpression of either lectin in permissive, completely non-susceptible cells and determine whether their expression can make these cells susceptible. Furthermore, it might be prudent to change the current nomenclature and instead address attachment factors and entry receptors as first and second line receptors, respectively.
dc.description.sponsorshipUtrecht University
dc.language.isoen
dc.titleHow viruses hijack the SIGN’s
dc.type.contentMaster Thesis
dc.rights.accessrightsOpen Access
dc.subject.keywordsDC-SIGN, L-SIGN, virus, attachment factor, entry receptor, arbovirus
dc.subject.courseuuInfection and Immunity


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