PMC:7781431 / 33193-34443 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7781431","sourcedb":"PMC","sourceid":"7781431","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7781431","text":"Hepatitis C virus (HCV) is a positive-sense single-stranded RNA virus of the family Flaviviridae with a small (55–65 nm size) envelope (Lee et al. 2017). The HCV is the cause of hepatitis C and some cancers such as liver cancer (hepatocellular carcinoma, abbreviated HCC) and lymphoma in humans (Ferri et al. 2015; Rusyn and Lemon 2014). To date, there appears to be no report on the effectiveness of SPMs against HCV. However, HCV peptide (C5A), an amphiphilic α-helix peptide of HCV, is an activator of the N-formyl peptide receptor in human phagocytes (Lin et al. 2011). This suggests the possibility of interaction between RvD1 and LXA4, FPR families, and HCV. Vitamin D metabolites inhibit HCV and upregulate GPR37 gene expression, which induces cellular autophagy (Gutierrez et al. 2014). PD1 was recently proposed as a new ligand for GPR37, and some studies suggest a possible relationship between PD1 and HCV (Fig. 4). SAA also has antiviral effects against HCV, however, it induces chronic inflammation through FPR2/ALX, causing liver damage (Abouelasrar Salama et al. 2019). Although research has not been conducted yet, RvD1 and LXA4, which inhibit the action of SAA, are likely to suppress liver damage caused by SAA during HCV 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