Host functions used by hepatitis B virus to complete its life cycle: Implications for developing host-targeting agents to treat chronic hepatitis B

Antiviral Res. 2018 Oct:158:185-198. doi: 10.1016/j.antiviral.2018.08.014. Epub 2018 Aug 24.

Abstract

Similar to other mammalian viruses, the life cycle of hepatitis B virus (HBV) is heavily dependent upon and regulated by cellular (host) functions. These cellular functions can be generally placed in to two categories: (a) intrinsic host restriction factors and innate defenses, which must be evaded or repressed by the virus; and (b) gene products that provide functions necessary for the virus to complete its life cycle. Some of these functions may apply to all viruses, but some may be specific to HBV. In certain cases, the virus may depend upon the host function much more than does the host itself. Knowing which host functions regulate the different steps of a virus' life cycle, can lead to new antiviral targets and help in developing novel treatment strategies, in addition to improving a fundamental understanding of viral pathogenesis. Therefore, in this review we will discuss known host factors which influence key steps of HBV life cycle, and further elucidate therapeutic interventions targeting host-HBV interactions.

Keywords: Antiviral agents; Direct acting antiviral agents; Hepatitis; Hepatitis B virus (HBV); Host targeting agents; Liver; Virus-host interaction.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antiviral Agents / pharmacology*
  • Capsid / metabolism
  • DNA, Viral
  • Hepatitis B / drug therapy*
  • Hepatitis B virus / drug effects*
  • Hepatitis B virus / genetics
  • Hepatitis B virus / pathogenicity
  • Hepatitis B virus / physiology*
  • Hepatocytes / drug effects
  • Hepatocytes / virology
  • Host-Pathogen Interactions / drug effects*
  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / physiology*
  • Humans
  • Life Cycle Stages
  • Liver / virology
  • Nucleocapsid
  • Reverse Transcription / drug effects
  • Viral Envelope Proteins / metabolism
  • Virus Assembly / physiology
  • Virus Attachment
  • Virus Internalization / drug effects
  • Virus Replication

Substances

  • Antiviral Agents
  • DNA, Viral
  • Viral Envelope Proteins