TY - JOUR
T1 - Interplay between hepatitis E virus and host cell pattern recognition receptors
AU - Devhare, Pradip
AU - Madiyal, Mridula
AU - Mukhopadhyay, Chiranjay
AU - Shetty, Shiran
AU - Shastry, Shamee
N1 - Funding Information:
Acknowledgments: The author acknowledges the institutional support from Manipal Academy of Higher Education (Institution of Eminence Deemed to be University) in the publication of this article.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/9/1
Y1 - 2021/9/1
N2 - Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can be-come chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.
AB - Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can be-come chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.
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U2 - 10.3390/ijms22179259
DO - 10.3390/ijms22179259
M3 - Review article
AN - SCOPUS:85113461095
SN - 1661-6596
VL - 22
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 17
M1 - 9259
ER -
