Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Sep 28;3(3):220-9.
doi: 10.14218/JCTH.2015.00018. Epub 2015 Sep 15.

Hepatitis B and Delta Virus: Advances on Studies about Interactions between the Two Viruses and the Infected Hepatocyte

Affiliations
Review

Hepatitis B and Delta Virus: Advances on Studies about Interactions between the Two Viruses and the Infected Hepatocyte

Katja Giersch et al. J Clin Transl Hepatol. .

Abstract

The mechanisms determining persistence of hepatitis B virus (HBV) infection and long-term pathogenesis of HBV-associated liver disease appear to be multifactorial. Although viral replication can be efficiently suppressed by the antiviral treatments currently available, viral clearance is generally not achieved since HBV has developed unique replication strategies, enabling persistence of its genome within the infected hepatocytes. Moreover, no direct antiviral therapy exists for the more than 15 million people worldwide that are also coinfected with the hepatitis delta virus (HDV), a defective virus that needs the HBV envelope proteins for propagation. The limited availability of robust HBV and HDV infection systems has hindered the understanding of the complex network of virus-virus and virus-host interactions that are established in the course of infection and slowed down progress in drug development. Since chronic HBV/HDV coinfection leads to the most severe form of chronic viral hepatitis, elucidation of the molecular mechanisms regulating virus-host interplay and pathogenesis are urgently needed. This article summarizes the current knowledge regarding the interactions among HBV, HDV, and the infected target cell and discusses the dependence of HDV on HBV activity and possible future therapeutic approaches.

Keywords: HBV; HBsAg; HDAg; HDV; Hepatocytes; Immune system; Virus interactions.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest: None

Figures

Fig. 1.
Fig. 1.. HBV as a helper virus for HDV.
Hepatitis B virus (HBV) shares its small, medium, and large hepatitis B surface antigens (HBsAg) with hepatitis D virus (HDV).

Similar articles

Cited by

References

    1. Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380:2095–2128. doi: 10.1016/S0140-6736(12)61728-0. - DOI - PMC - PubMed
    1. Dandri M, Locarnini S. New insight in the pathobiology of hepatitis B virus infection. Gut. 2012;61:i6–i17. doi: 10.1136/gutjnl-2012-302056. - DOI - PubMed
    1. Kao JH. Hepatitis B viral genotypes: clinical relevance and molecular characteristics. J Gastroenterol Hepatol. 2002;17:643–650. doi: 10.1046/j.1440-1746.2002.02737.x. - DOI - PubMed
    1. Tran TT, Trinh TN, Abe K. New complex recombinant genotype of hepatitis B virus identified in Vietnam. J Virol. 2008;82:5657–5663. doi: 10.1128/JVI.02556-07. - DOI - PMC - PubMed
    1. Olinger CM, Jutavijittum P, Hubschen JM, Yousukh A, Samountry B, Thammavong T, et al. Possible new hepatitis B virus genotype, southeast Asia. Emerg Infect Dis. 2008;14:1777–1780. doi: 10.3201/eid1411.080437. - DOI - PMC - PubMed