Characterization of the guinea pig CMV gH/gL/GP129/GP131/GP133 complex in infection and spread

被引：38

作者：

Auerbach, Marcy ^{[1
]}

Yan, Donghong ^{[2
]}

Fouts, Ashley ^{[1
]}

Xu, Min ^{[2
]}

Estevez, Alberto ^{[3
]}

Austin, Cary D. ^{[4
]}

Bazan, Fernando ^{[5
]}

Feierbach, Becket ^{[1
]}

机构：

[1] Hoffmann LaRoche Ltd, Genentech Inc, Dept Infect Dis, 1 DNA Way,Bldg 11,MS 33, San Francisco, CA 94080 USA

[2] Hoffmann LaRoche Ltd, Genentech Inc, Dept Translat Immunol, San Francisco, CA 94080 USA

[3] Hoffmann LaRoche Ltd, Genentech Inc, Baculovirus Express Grp, San Francisco, CA 94080 USA

[4] Hoffmann LaRoche Ltd, Genentech Inc, Dept Pathol, San Francisco, CA 94080 USA

[5] 4th & Aspen Life Sci Consulting LLC, Stillwater, MN 55082 USA

来源：

VIROLOGY | 2013年 / 441卷 / 01期

关键词：

Cytomegalovirus; Congenital infection; Viral entry; Animal model; CONGENITAL CYTOMEGALOVIRUS-INFECTION; ENDOTHELIAL-CELLS; ANTIBODY-RESPONSE; IDENTIFICATION; VIRUS; PATHOGENESIS; MODELS; IMPACT; GROWTH; HCMV;

D O I：

10.1016/j.virol.2013.03.008

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

In human cytomegalovirus (HCMV), the UL128-131A locus plays an essential role in cellular tropism and spread. Here, we report the complete annotation of the GP129-133 locus from guinea pig cytomegalovirus (GPCMV) and the discovery of the UL131A homolog, named GP133. We have found that similar to HCMV the GP129-133 proteins form a pentamer complex with the GPCMV glycoproteins gH and gL. In addition, we find that the GP129-133 proteins play a critical role in entry as the GP129-133 deletion mutant shows a defect in both endothelial and fibroblast cell entry. Although the GP129-133 deletion strain can propagate in vitro, we find that the deletion fails to spread in vivo. Interestingly, the wildtype strain can spontaneously give rise to the GP129-133 deletion strain during in vivo spread, suggesting genetic instability at this locus. (C) 2013 Elsevier Inc. All rights reserved.

引用

页码：75 / 84

页数：10

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