Life Cycle of Hepatitis D Virus (HDV) and HDV-Like Agents

Dear Colleagues,

As the smallest human virus, hepatitis D virus (HDV) represents the prototype of a large family of pathogenic agents with a unique life cycle. HDV depends on the self-assembly competent envelope proteins of its helper virus, the human hepatitis B virus (HBV), in order to exit and specifically enter hepatocytes. However, the replication of its single-stranded highly backfolded circular RNA genome is not restricted to liver cells. Recently, a number of HDV-like agents in different species were discovered without an apparent association with HBV-like helper viruses, which implies other strategies of HDV propagation. Similar to plant viroids, the circular single-stranded RNA genome of HDV explores host RNA polymerase to replicate via the amplification of the rolling circle. HDV causes the most severe form of viral hepatitis, affecting at least 12 million individuals. This burden is probably underestimated due to large gaps in reliable epidemiological data. Since the discovery the viral receptor NTCP in 2012 and the development of convenient infection models thereafter, important progress has been made regarding the virus life cycle, virus–host interaction, innate immune responses, and drug development, with the first medication (bulevirtide/Hepcludex) obtaining approval in Europe in 2020.

This Special Issue aims to collate new findings in terms of the biology of HDV and HDV-like agents. The topics to be addressed in this Issue shall cover all of the steps of the replication cycle, virus–host interaction, innate and adaptive immune responses, virus evolution, the pathogenesis of infection, epidemiology, diagnostics, and translational research with clinical implications. Both original research articles and reviews are welcome.

We look forward to receiving your contributions.

Dr. Zhenfeng Zhang
Prof. Dr. Stephan Urban
Guest Editors

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