| pubmed-article:9620988 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C0206679 | lld:lifeskim |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C0034805 | lld:lifeskim |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C0020852 | lld:lifeskim |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C1654934 | lld:lifeskim |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:9620988 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:9620988 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:9620988 | pubmed:dateCreated | 1998-7-1 | lld:pubmed |
| pubmed-article:9620988 | pubmed:abstractText | Herpes simplex virus (HSV) glycoproteins gE and gI form an immunoglobulin G (IgG) Fc receptor (FcgammaR) that binds the Fc domain of human anti-HSV IgG and inhibits Fc-mediated immune functions in vitro. gE or gI deletion mutant viruses are avirulent, probably because gE and gI are also involved in cell-to-cell spread. In an effort to modify FcgammaR activity without affecting other gE functions, we constructed a mutant virus, NS-gE339, that has four amino acids inserted into gE within the domain homologous to mammalian IgG FcgammaRs. NS-gE339 expresses gE and gI, is FcgammaR-, and does not participate in antibody bipolar bridging since it does not block activities mediated by the Fc domain of anti-HSV IgG. In vivo studies were performed with mice because the HSV-1 FcgammaR does not bind murine IgG; therefore, the absence of an FcgammaR should not affect virulence in mice. NS-gE339 causes disease at the skin inoculation site comparably to wild-type and rescued viruses, indicating that the FcgammaR- mutant virus is pathogenic in animals. Mice were passively immunized with human anti-HSV IgG and then infected with mutant or wild-type virus. We postulated that the HSV-1 FcgammaR should protect wild-type virus from antibody attack. Human anti-HSV IgG greatly reduced viral titers and disease severity in NS-gE339-infected animals while having little effect on wild-type or rescued virus. We conclude that the HSV-1 FcgammaR enables the virus to evade antibody attack in vivo, which likely explains why antibodies are relatively ineffective against HSV infection. | lld:pubmed |
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| pubmed-article:9620988 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9620988 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9620988 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9620988 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9620988 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9620988 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9620988 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:WangLL | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:FriedmanH MHM | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:GoldsteinL... | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:SundaresanPP | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:DubinGG | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:Nagashunmugam... | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:WeeksB SBS | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:LubinskiJJ | lld:pubmed |
| pubmed-article:9620988 | pubmed:author | pubmed-author:KangE HEH | lld:pubmed |
| pubmed-article:9620988 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9620988 | pubmed:volume | 72 | lld:pubmed |
| pubmed-article:9620988 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9620988 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9620988 | pubmed:pagination | 5351-9 | lld:pubmed |
| pubmed-article:9620988 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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