Seirafian, Sepher, Prod'homme, Virginie ![]() ![]() ![]() ![]() |
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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 |
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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: | 11 Oct 2023 17:43 |
URI: | https://orca.cardiff.ac.uk/id/eprint/59480 |
Citation Data
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