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pubmed-article:12655085pubmed:abstractTextTheiler's murine encephalomyelitis virus (TMEV) infects most mammalian cells, but a TMEV receptor has not been identified. Studies have demonstrated that the UDP-galactose transporter (UGT) is critical for TMEV attachment and entry into mammalian cells (Hertzler et al., Virology 286, 336-344, 2001). It was suggested that UGT might function as a TMEV receptor. We have demonstrated that polyclonal rabbit antibodies to human UGT that cross-react with hamster UGT do not block binding to or infection of mammalian cells by either high- or low-neurovirulence TMEV. In addition, incubation of virus with galactose, or blocking galactose on the cell surface with lectins, does not inhibit TMEV binding or infection. Thus, TMEV needs UGT for its transporter activity and galactose for assembly of its co-receptors (attachment factors) but does not bind directly to galactose. Excluding direct involvement of UGT and galactose in TMEV binding and entry provides further insight into how TMEV interacts with the host cell and should facilitate ongoing studies to identify a TMEV receptor.lld:pubmed
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pubmed-article:12655085pubmed:pagination845-9lld:pubmed
pubmed-article:12655085pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:12655085pubmed:articleTitleGalactose is needed only for expression of co-receptors used by Theiler's murine encephalomyelitis virus as the virus does not directly bind galactose or use the UDP-galactose transporter as a receptor.lld:pubmed
pubmed-article:12655085pubmed:affiliationDepartment of Neurology, Evanston Hospital, 2650 Ridge Avenue, Evanston, IL 60201, USA.lld:pubmed
pubmed-article:12655085pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12655085pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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