{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T07:00:21Z","timestamp":1782457221454,"version":"3.54.5"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"14","license":[{"start":{"date-parts":[[2008,7,15]],"date-time":"2008-07-15T00:00:00Z","timestamp":1216080000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2008,7,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Herpes simplex virus type 1 (HSV-1) glycoprotein C (gC) blocks complement activation, and glycoprotein E (gE) interferes with IgG Fc-mediated activities. While evaluating gC- and gE-mediated immune evasion in human immunodeficiency virus (HIV)-HSV-1-coinfected subjects, we noted that antibody alone was more effective at neutralizing a strain with mutations in gC and gE (gC\/gE) than a wild-type (WT) virus. This result was unexpected since gC and gE are postulated to interfere with complement-mediated neutralization. We used pooled human immunoglobulin G (IgG) from HIV-negative donors to confirm the results and evaluated mechanisms of the enhanced antibody neutralization. We demonstrated that differences in antibody neutralization cannot be attributed to the concentrations of HSV-1 glycoproteins on the two viruses or to the absence of an IgG Fc receptor on the gC\/gE mutant virus or to enhanced neutralization of the mutant virus by antibodies that target only gB, gD, or gH\/gL, which are the glycoproteins involved in virus entry. Since sera from HIV-infected subjects and pooled human IgG contain antibodies against multiple glycoproteins, we determined whether differences in neutralization become apparent when antibodies to gB, gD, or gH\/gL are used in combination. Neutralization of the gC\/gE mutant was greatly increased compared that of WT virus when any two of the antibodies against gB, gD, or gH\/gL were used in combination. These results suggest that gC and gE on WT virus provide a shield against neutralizing antibodies that interfere with gB-gD, gB-gH\/gL, or gD-gH\/gL interactions and that one function of virus neutralization is to prevent interactions between these glycoproteins.<\/jats:p>","DOI":"10.1128\/jvi.02599-07","type":"journal-article","created":{"date-parts":[[2008,5,15]],"date-time":"2008-05-15T01:39:34Z","timestamp":1210815574000},"page":"6935-6941","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":36,"title":["Blocking Antibody Access to Neutralizing Domains on Glycoproteins Involved in Entry as a Novel Mechanism of Immune Evasion by Herpes Simplex Virus Type 1 Glycoproteins C and E"],"prefix":"10.1128","volume":"82","author":[{"given":"Lauren M.","family":"Hook","sequence":"first","affiliation":[{"name":"Infectious Disease Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jialing","family":"Huang","sequence":"additional","affiliation":[{"name":"Infectious Disease Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Jiang","sequence":"additional","affiliation":[{"name":"Infectious Disease Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Hodinka","sequence":"additional","affiliation":[{"name":"Clinical Virology Laboratory, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harvey M.","family":"Friedman","sequence":"additional","affiliation":[{"name":"Infectious Disease Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0707452104"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.77.17.9542-9552.2003"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-131-1-199907060-00004"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni0304-233"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/jmv.10350"},{"key":"e_1_3_2_7_2","first-page":"90","volume":"21","year":"1999","unstructured":"Calistri, A., C. 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