Hepatitis E Virus: How It Escapes Host Innate Immunity.
Sebastien LhommeMarion MigueresFlorence AbravanelOlivier MarionNassim KamarJacques IzopetPublished in: Vaccines (2020)
Hepatitis E virus (HEV) is a leading cause of viral hepatitis in the world. It is usually responsible for acute hepatitis, but can lead to a chronic infection in immunocompromised patients. The host's innate immune response is the first line of defense against a virus infection; there is growing evidence that HEV RNA is recognized by toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), leading to interferon (IFN) production. The IFNs activate interferon-stimulated genes (ISGs) to limit HEV replication and spread. HEV has developed strategies to counteract this antiviral response, by limiting IFN induction and signaling. This review summarizes the advances in our knowledge of intracellular pathogen recognition, interferon and inflammatory response, and the role of virus protein in immune evasion.
Keyphrases
- immune response
- dendritic cells
- inflammatory response
- end stage renal disease
- ejection fraction
- genome wide
- newly diagnosed
- healthcare
- respiratory failure
- liver failure
- toll like receptor
- chronic kidney disease
- lipopolysaccharide induced
- prognostic factors
- copy number
- peritoneal dialysis
- dna methylation
- gene expression
- candida albicans
- aortic dissection
- amino acid
- lps induced
- small molecule
- mechanical ventilation
- disease virus