Human cytomegalovirus suppresses Fas expression and function

Seirafian, Sepher, Prod'homme, Virginie ORCID: https://orcid.org/0000-0002-9664-4710, Sugrue, Daniel, Davies, James ORCID: https://orcid.org/0000-0003-3569-4500, Fielding, Ceri ORCID: https://orcid.org/0000-0002-5817-3153, Tomasec, Peter and Wilkinson, Gavin W. G. ORCID: https://orcid.org/0000-0002-5623-0126 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:	Published Online
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI)
Subjects:	R Medicine > R Medicine (General)
Publisher:	Microbiology Society
ISSN:	0022-1317
Funders:	Wellcome Trust
Date of First Compliant Deposit:	30 March 2016
Date of Acceptance:	5 January 2014
Last Modified:	12 Jul 2024 14:48
URI:	https://orca.cardiff.ac.uk/id/eprint/59480

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