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. 2017 Aug 12;9(8):224. doi: 10.3390/v9080224

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hepatitis C virus (HCV) recognition by the host and HCV-induced autophagy. After infection, HCV genomic RNA and other HCV products such as double-stranded RNA (dsRNA) replication intermediates and viral proteins can activate retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated protein 5 (MDA5) and Toll-like receptors (TLRs) to activate signaling pathways to produce interferons (IFNs) and pro-inflammatory cytokines. HCV can also induce autophagy indirectly via the induction of endoplasmic reticulum (ER) stress or directly via its protein products to suppress host innate immune responses. IRAKs: Interleukin (IL)-1 receptor-associated kinases; MAVS: Mitochondrial antiviral signaling protein; MyD88: Myeloid differentiation primary-response protein 88; ssRNA: Single-stranded RNA; TRAF6: Tumor necrosis factor receptor-associated factor 6; TRIF: Toll/IL-1 receptor domain-containing adaptor protein inducing IFN-β.