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Incorporation of this determinant onto retroviral membranes by passage of viruses in cells encoding \u03b1-1-3-galactosyltransferase (GT) renders retroviruses sensitive to lysis by natural Ab and complement in normal human serum (NHS). Plasma membrane-budding viruses representing four additional virus groups were examined for their sensitivities to serum inactivation after passage through human cell lines that lack a functional GT or human cells expressing recombinant porcine GT. The inactivation of lymphocytic choriomeningitis virus (LCMV) by NHS directly correlated with host modification of the virus via expression of Gal\u03b11-3Gal and was blocked by incorporation of soluble Gal\u03b11-3Gal disaccharide into the inactivation assay. GT-deficient mice immunized to make high levels of Ab to Gal\u03b11-3Gal (anti-Gal Ab) were tested for resistance to LCMV passaged in GT-expressing cells. Resistance was not observed, but in vitro analyses of the mouse immune sera revealed that the antiviral activity of the sera was insufficient to eliminate LCMV infectivity on its natural targets of infection, macrophages, which express receptors for Ab and complement. Newcastle disease virus and vesicular stomatitis virus (VSV) were inactivated by NHS regardless of cell passage history, whereas Sindbis virus (SV) passaged in human cells resisted inactivation. Both VSV and SV passaged in Gal\u03b11-3Gal-expressing human cells incorporated this sugar moiety onto their major envelope glycoproteins. SV passaged in mouse cells expressing Gal\u03b11-3Gal was moderately sensitive to inactivation by NHS. These results indicate that enveloped viruses expressing Gal\u03b11-3Gal differ in their sensitivities to NHS and that a potent complement source, such as that in NHS, is required for efficient inactivation of sensitive viruses in vitro and in vivo.<\/jats:p>","DOI":"10.1128\/jvi.72.6.4650-4656.1998","type":"journal-article","created":{"date-parts":[[2019,12,31]],"date-time":"2019-12-31T18:13:29Z","timestamp":1577816009000},"page":"4650-4656","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["Evaluation of the Gal\u03b11-3Gal Epitope as a Host Modification Factor Eliciting Natural Humoral Immunity to Enveloped Viruses"],"prefix":"10.1128","volume":"72","author":[{"given":"Raymond M.","family":"Welsh","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Pathology, University of Massachusetts Medical Center, Worcester, Massachusetts 01655,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carey L.","family":"O\u2019Donnell","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Pathology, University of Massachusetts Medical Center, Worcester, Massachusetts 01655,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah J.","family":"Reed","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Department of Molecular Development, Alexion Pharmaceuticals, Inc., New Haven, Connecticut 065112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell P.","family":"Rother","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Department of Molecular Development, Alexion Pharmaceuticals, Inc., New Haven, Connecticut 065112"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-3527(08)60878-7"},{"key":"e_1_3_2_3_2","unstructured":"Ausubel F. 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