Innate immune recognition and modulation in hepatitis D virus Infection

Stephanie Jung, Sebastian Maximilian Altstetter, Ulrike Protzer

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

Hepatitis D virus (HDV) is a global health threat with more than 15 million humans affected. Current treatment options are largely unsatisfactory leaving chronically infected humans at high risk to develop liver cirrhosis and hepatocellular carcinoma. HDV is the only human satellite virus known. It encodes only two proteins, and requires Hepatitis B virus (HBV) envelope protein expression for productive virion release and spread of the infection. How HDV could evolve and why HBV was selected as a helper virus remains unknown. Since the discovery of Na+-taurocholate co-transporting polypeptide as the essential uptake receptor for HBV and HDV, we are beginning to understand the interactions of HDV and the immune system. While HBV is mostly regarded a stealth virus, that escapes innate immune recognition, HBV-HDV coinfection is characterized by a strong innate immune response. Cytoplasmic RNA sensor melanoma differentiation antigen 5 has been reported to recognize HDV RNA replication and activate innate immunity. Innate immunity, however, seems not to impair HDV replication while it inhibits HBV. In this review, we describe what is known up-to-date about the interplay between HBV as a helper and HDV's immune evasion strategy and identify where additional research is required.

Original languageEnglish
Pages (from-to)2781-2791
Number of pages11
JournalWorld Journal of Gastroenterology
Volume26
Issue number21
DOIs
StatePublished - 7 Jun 2020

Keywords

  • Hepatitis b virus
  • Hepatitis d virus
  • Immune evasion
  • Immunosuppression
  • Innate immunity
  • Pathogen-associated molecular pattern molecules

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