Journal
JOURNAL OF VIROLOGY
Volume 89, Issue 14, Pages 6974-6977Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01918-14
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Funding
- NIH/NIAID [K22 AI100935]
- Duke University Center for AIDS Research (CFAR)
- NIH [5P30 AI064518]
- Duke School of Medicine Whitehead Scholarship
- Ford Foundation
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RNA virus infection is sensed in the cytoplasm by the retinoic acid-inducible gene I (RIG-I)-like receptors. These proteins signal through the host adaptor protein MAVS to trigger the antiviral innate immune response. Here, we describe how MAVS subcellular localization impacts its function and the regulation underlying MAVS signaling. We propose a model to describe how the coordination of MAVS functions at the interface between the mitochondria and the mitochondrion-associated endoplasmic reticulum (ER) membrane programs antiviral signaling.
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