OPEN Journal of microbiology and biotechnology | 12 Oct 2017
S Kang and J Myoung
Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences such as chronic hepatitis and liver damages, mortality of the latter of which reaches up to 20~30%. Type I Interferon (IFN)-induced antiviral immunity is known to be the first line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors (PRRs), leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of interferon-stimulated genes (ISGs), helping the cells cope with viral infection. Interestingly, some of HEV-encoded genes seem to be involved in disrupting signaling cascades for anti-viral immune responses, and thus crippling cytokine/chemokine productions. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge and in this review we summarize known HEV evasion strategies and compare them to those of other hepatitis viruses.
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