Journal article
Inhibition of the TRAIL death receptor by CMV reveals its importance in NK Cell-Mediated antiviral defense
PLoS Pathogens, Vol.10(8), e1004268
2014
Abstract
TNF-related apoptosis inducing ligand (TRAIL) death receptors (DR) regulate apoptosis and inflammation, but their role in antiviral defense is poorly understood. Cytomegaloviruses (CMV) encode many immune-modulatory genes that shape host immunity, and they utilize multiple strategies to target the TNF-family cytokines. Here we show that the m166 open reading frame (orf) of mouse CMV (MCMV) is strictly required to inhibit expression of TRAIL-DR in infected cells. An MCMV mutant lacking m166 expression (m166stop) is severely compromised for replication in vivo, most notably in the liver, and depleting natural killer (NK) cells, or infecting TRAIL-DR−/− mice, restored MCMV-m166stop replication completely. These results highlight the critical importance for CMV to have evolved a strategy to inhibit TRAIL-DR signaling to thwart NK-mediated defenses.
Details
- Title
- Inhibition of the TRAIL death receptor by CMV reveals its importance in NK Cell-Mediated antiviral defense
- Authors/Creators
- S. Verma (Author/Creator)A. Loewendorf (Author/Creator)Q. Wang (Author/Creator)B. McDonald (Author/Creator)A. Redwood (Author/Creator)C.A. Benedict (Author/Creator)
- Publication Details
- PLoS Pathogens, Vol.10(8), e1004268
- Publisher
- Public Library of Science
- Identifiers
- 991005545456507891
- Copyright
- © 2014 Verma et al.
- Murdoch Affiliation
- Murdoch University
- Language
- English
- Resource Type
- Journal article
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- Collaboration types
- Domestic collaboration
- International collaboration
- Citation topics
- 1 Clinical & Life Sciences
- 1.6 Immunology
- 1.6.1021 Natural Killer Cells
- Web Of Science research areas
- Microbiology
- Parasitology
- Virology
- ESI research areas
- Microbiology