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Human cytomegalovirus suppresses Fas expression and function

Seirafian, Sepher, Prod'homme, Virginie, Sugrue, Daniel M., Davies, James, Fielding, Ceri Alan, Tomasec, Peter and Wilkinson, Gavin William Grahame 2014. Human cytomegalovirus suppresses Fas expression and function. Journal of General Virology 95 (4) , pp. 933-939. 10.1099/vir.0.058313-0

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Abstract

Human cytomegalovirus (HCMV) is known to evade extrinsic pro-apoptotic pathways not only by downregulating cell surface expression of the death receptors TNFR1, TRAIL receptor 1 (TNFRSF10A) and TRAIL receptor 2 (TNFRSF10B), but also by impeding downstream signalling events. Fas (CD95/APO-1/TNFRSF6) also plays a prominent role in apoptotic clearance of virus-infected cells, so its fate in HCMV-infected cells needs to be addressed. Here, we show that cell surface expression of Fas was suppressed in HCMV-infected fibroblasts from 24 h onwards through the late phase of productive infection, and was dependent on de novo virus-encoded gene expression but not virus DNA replication. Significant levels of the fully glycosylated (endoglycosidase-H-resistant) Fas were retained within HCMV-infected cells throughout the infection within intracellular membranous structures. HCMV infection provided cells with a high level of protection against Fas-mediated apoptosis. Downregulation of Fas was observed with HCMV strains AD169, FIX, Merlin and TB40.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: R Medicine > R Medicine (General)
Publisher: Society for General Microbiology
ISSN: 0022-1317
Funders: Wellcome Trust
Date of First Compliant Deposit: 30 March 2016
Last Modified: 28 Jun 2019 02:42
URI: http://orca.cf.ac.uk/id/eprint/59480

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