Abstract
Hepatitis E virus (HEV) infection represents an emerging global health issue, whereas the clinical outcomes vary dramatically among different populations. The host innate immune system provides a first-line defense against the infection, but dysregulation may partially contribute to severe pathogenesis. A growing body of evidence has indicated the active response of the host innate immunity to HEV infection both in experimental models and in patients. In turn, HEV has developed sophisticated strategies to counteract the host immune system. In this review, we aim to comprehensively decipher the processes of pathogen recognition, interferon, and inflammatory responses, and the involvement of innate immune cells in HEV infection. We further discuss their implications in understanding the pathogenic mechanisms and developing antiviral therapies.
Highlights
Hepatitis E virus (HEV) represents an emerging zoonotic pathogen imposing a growing health burden [1]
IFN-β expression induced by poly (I:C) transfection in cell culture [89]. This is mainly attributed to the Papain-like cysteine protease domain (PCP) and macro domain (X) that are responsible for inhibiting the activation of retinoic-acid-inducible gene I (RIG-I) and TBK-1 as well as the phosphorylation of IRF3 (Figure 1) [89]
ORF3 of genotype 1 has been reported to downregulate the expression of tumor necrosis factor receptor 1-associated death domain protein (TRADD) and receptor-interacting protein kinase 1 (RIP1), inhibiting TLR3 mediated activation of NF-κB upon poly (I:C) treatment [103]
Summary
Hepatitis E virus (HEV) represents an emerging zoonotic pathogen imposing a growing health burden [1]. Acute infection in pregnant women bears high risk of triggering acute liver failure (ALF), leading to a high mortality rate, and most of these patients are from resource-limited regions infected with the non-zoonotic genotype 1 HEV [3,4]. The host immune system, including innate and adaptive immunity, essentially protects against pathogen invasions, but over-activation or dysregulation may cause pathogenesis [9]. The host produces a large spectrum of cytokines and chemokines, in particular, the antiviral interferons (IFNs). The quantity and quality of host immune responses essentially determine the infection course of HEV and the clinical outcome in patients. The response of host innate immunity to HEV infection has been widely observed in experimental models and in patients. We aim to in depth decipher the dynamic interplay between HEV and the host innate immunity
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