Innate immune recognition and modulation in hepatitis D virus infection
Autor: | Sebastian Maximilian Altstetter, Stephanie Jung, Ulrike Protzer |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Liver Cirrhosis
Hepatitis B virus Carcinoma Hepatocellular Interferon-Induced Helicase IFIH1 Hepatitis D Chronic viruses Organic Anion Transporters Sodium-Dependent Biology medicine.disease_cause Virus Replication Virus Hepatitis D virus 03 medical and health sciences 0302 clinical medicine Immune system Hepatitis B Chronic medicine Humans Immune Evasion Innate immunity Hepatitis delta Antigens Innate immune system Symporters Coinfection Pathogen-associated molecular pattern molecules Liver Neoplasms Gastroenterology virus diseases Minireviews General Medicine biochemical phenomena metabolism and nutrition medicine.disease Virology Immunity Innate Satellite virus ddc Liver 030220 oncology & carcinogenesis Helper virus Receptors Pattern Recognition Satellite Viruses RNA Viral 030211 gastroenterology & hepatology Hepatitis Delta Virus Immunosuppression |
Zdroj: | World Journal of Gastroenterology |
ISSN: | 2219-2840 1007-9327 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |