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Review
. 2014 Sep;34(5):895-917.
doi: 10.1002/med.21292. Epub 2013 May 30.

Molecular biology and inhibitors of hepatitis A virus

Yannick Debing  1 , Johan Neyts, Hendrik Jan Thibaut
Affiliations
Review

Molecular biology and inhibitors of hepatitis A virus

Yannick Debing et al. Med Res Rev. 2014 Sep.

Abstract

Hepatitis A virus (HAV) is a faeco-orally transmitted picornavirus and is one of the main causes of acute hepatitis worldwide. An overview of the molecular biology of HAV is presented with an emphasis on recent findings. Immune evasion strategies and a possible correlation between HAV and atopy are discussed as well. Despite the availability of efficient vaccines, antiviral drugs targeting HAV are required to treat severe cases of fulminant hepatitis, contain outbreaks, and halt the potential spread of vaccine-escape variants. Additionally, such drugs could be used to shorten the period of illness and decrease associated economical costs. Several known inhibitors of HAV with various mechanisms of action will be discussed. Since none of these molecules is readily useable in the clinic and since the availability of an anti-HAV drug would be of clinical importance, increased efforts should be targeted toward discovery and development of such antivirals.

Keywords: antiviral drugs; atopy; hepatitis A virus; immune evasion; virus replication.

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Figures

Figure 1
Figure 1
HAV genome organization and proteolytic processing of the structural proteins (IRES, internal ribosome entry site; UTR, untranslated region).
Figure 2
Figure 2
Inhibition of IFNβ transcription by HAV through proteolytic cleavage of MAVS (by 3ABC) and TRIF (by 3CD) and through direct inhibition of MAVS, IKKε, and TBK1 (by 2B). (dsRNA, double‐stranded RNA; IKK, inhibitor of NF‐κB kinase; IRF‐3, interferon regulatory factor 3; MAVS, mitochondrial antiviral signaling protein; MDA‐5, melanoma differentiation‐associated gene 5; RIG‐I, retinoic acid‐inducible gene I; TBK1, TANK‐binding kinase 1; TLR3, Toll‐like receptor 3; TRIF, Toll/IL‐1 receptor domain‐containing adaptor inducing IFNβ).
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