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Innate immunity in hepatitis B and D virus infection: consequences for viral persistence, inflammation, and T cell recognition
Semin Immunopathol. 2021 May 21. doi: 10.1007/s00281-021-00864-x.Online ahead of print.
Maura Dandri12, Antonio Bertoletti34, Marc Lütgehetmann56
1I. Department of Internal Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Martinistr. 52, D-20246, Hamburg, Germany. firstname.lastname@example.org.
2Hamburg-Lübeck-Borstel-Riems partner site, German Center for Infection Research (DZIF), Hamburg, Germany. email@example.com.
3Singapore Immunology Network (SIgN), Agency of Science Technology and Research (ASTAR), Singapore, Singapore.
4Program Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
5Hamburg-Lübeck-Borstel-Riems partner site, German Center for Infection Research (DZIF), Hamburg, Germany.
6Institute of Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Chronic infections with human hepatitis viruses continue to be a major health burden worldwide. Despite the availability of an effective prophylactic vaccine against the hepatitis B virus (HBV) and of antiviral agents efficiently suppressing HBV replication, more than 250 million people are currently chronically infected with this hepatotropic DNA virus, and resolution of chronic hepatitis B (CHB) is rarely achieved. Moreover, coinfection with the hepatitis D virus (HDV), a human RNA satellite virus requiring the envelope proteins of HBV for productive viral spreading, substantially aggravates the disease course of CHB. The molecular mechanisms by which these viruses interact with each other and with the intrinsic innate responses of the hepatocytes are not fully understood. While HBV appears to avoid innate immune recognition, HDV elicits a strong enhancement of innate responses. Notwithstanding, such induction does not hamper HDV replication but contributes to liver inflammation and pathogenesis. Intriguingly, HDV appears to influence the ability of T cells to recognize infected hepatocytes by boosting antigen presentation. This review focuses on current knowledge regarding how these viruses can shape and counteract the intrinsic innate responses of the hepatocytes, thus affecting the immune system and pathogenesis. Understanding the distinct strategies of persistence that HBV and HDV have evolved is central for advancing the development of curative therapies.