Abstract
Chronic viral hepatitis is a main cause of liver disease and hepatocellular carcinoma. There are striking similarities in the pathological impact of hepatitis B, C, and D, although these diseases are caused by very different viruses. Paired with the conventional study of protein–host interactions, the rapid technological development of -omics and bioinformatics has allowed highlighting the important role of signaling networks in viral pathogenesis. In this review, we provide an integrated look on the three major viruses associated with chronic viral hepatitis in patients, summarizing similarities and differences in virus-induced cellular signaling relevant to the viral life cycles and liver disease progression.
Highlights
Baumert, T.F.; Verrier, E.R.; Viral hepatitis predominantly affects and damages the liver by commonly causing the progression from chronic inflammation to fibrosis, cirrhosis, and cancer
We summarize similarities and differences in virusinduced cellular signaling associated with the three major viruses that cause chronic viral hepatitis in patients
A particular feature of Hepatitis C virus (HCV) infection is its association with insulin resistance (IR) in patients, which is less frequently observed in Hepatitis B virus (HBV)- or HBV/Hepatitis Delta virus (HDV)-infected patients [132], a recent genetic screen highlighted the importance of metabolic pathways in HDV lifecycle, including insulin resistance-related genes [133]
Summary
T.F.; Verrier, E.R.; Viral hepatitis predominantly affects and damages the liver by commonly causing the progression from chronic inflammation to fibrosis, cirrhosis, and cancer. During a chronic infection of the liver, hepatic viruses persistently tweak and attenuate the host antiviral defenses and modulate cellular pathways that impact liver homeostasis and disease progression. The three hepatotropic viruses causing chronic liver infection are Hepatitis B virus (HBV), Hepatitis C virus (HCV), and Hepatitis Delta virus (HDV). HBV/HDV coinfection causes the most severe form of chronic viral hepatitis, with accelerated liver disease progression to cirrhosis and HCC and increased liver-related and overall mortality [9]. Evidence points towards an epigenetic imprinting by hepatic viruses (HCV, HBV) and underlying liver fibrosis in the host genome which maintains a persistent transcriptomic environment in cured livers that acts in a pro-oncogenic manner [17,19,20]
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