Hepatitis C virus: Enslavement of host factors

IUBMB Life. 2018 Jan;70(1):41-49. doi: 10.1002/iub.1702.

Abstract

Hepatitis C virus (HCV) has infected over 170 million people world-wide. This infection causes severe liver damage that can progress to hepatocellular carcinoma leading to death of the infected patients. Development of a cell culture model system for the study of HCV infection in the recent past has helped the researchers world-wide to understand the biology of this virus. Studies over the past decade have revealed the tricks played by the virus to sustain itself, for as long as 40 years, in the host setup without being eliminated by the immune system. Today we understand that the host organelles and different cellular proteins are affected during HCV infection. This cytoplasmic virus has all the cellular organelles at its disposal to successfully replicate, from ribosomes and intracellular membranous structures to the nucleus. It modulates these organelles at both the structural and the functional levels. The vast knowledge about the viral genome and viral proteins has also helped in the development of drugs against the virus. Despite the achieved success rate to cure the infected patients, we struggle to eliminate the cases of recurrence and the non-responders. Such cases might emerge owing to the property of the viral genome to accumulate mutations during its succeeding replication cycles which favours its survival. The current situation calls an urgent need for alternate therapeutic strategies to counter this major problem of human health. © 2017 IUBMB Life, 70(1):41-49, 2018.

Keywords: HCV replication; HCV translation; hepatitis C virus; host factors; host-virus interaction.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antiviral Agents / therapeutic use
  • Carcinoma, Hepatocellular / etiology
  • Carcinoma, Hepatocellular / immunology
  • Carcinoma, Hepatocellular / prevention & control
  • Carcinoma, Hepatocellular / virology*
  • Cell Nucleus / immunology
  • Cell Nucleus / virology
  • Endoplasmic Reticulum / immunology
  • Endoplasmic Reticulum / virology
  • Gene Expression Regulation
  • Hepacivirus / drug effects
  • Hepacivirus / genetics
  • Hepacivirus / pathogenicity*
  • Hepatitis C, Chronic / complications
  • Hepatitis C, Chronic / drug therapy
  • Hepatitis C, Chronic / immunology
  • Hepatitis C, Chronic / virology*
  • Hepatocytes / immunology
  • Hepatocytes / virology*
  • Humans
  • Immune Evasion*
  • Lipid Droplets / immunology
  • Lipid Droplets / virology
  • Lipoproteins, VLDL / genetics
  • Lipoproteins, VLDL / immunology
  • Liver Neoplasms / etiology
  • Liver Neoplasms / immunology
  • Liver Neoplasms / prevention & control
  • Liver Neoplasms / virology*
  • RNA, Viral / biosynthesis
  • RNA, Viral / genetics
  • Ribosomes / immunology
  • Ribosomes / virology
  • Signal Transduction
  • Viral Proteins / genetics
  • Viral Proteins / immunology
  • Virus Replication / drug effects

Substances

  • Antiviral Agents
  • Lipoproteins, VLDL
  • RNA, Viral
  • Viral Proteins