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
. 2010 Jul;2(7):1394-1410.
doi: 10.3390/v2071394. Epub 2010 Jul 5.

Innate antiviral immune responses to hepatitis B virus

Malika Ait-Goughoulte  1   2 , Julie Lucifora  1   2 , Fabien Zoulim  1   2   3 , David Durantel  1   2   3
Affiliations

Innate antiviral immune responses to hepatitis B virus

Malika Ait-Goughoulte et al. Viruses. 2010 Jul.

Abstract

Hepatitis B virus (HBV) is a major cause of acute and chronic hepatitis in humans. As HBV itself is currently viewed as a non-cytopathic virus, the liver pathology associated with hepatitis B is mainly thought to be due to immune responses directed against HBV antigens. The outcome of HBV infection is the result of complex interactions between replicating HBV and the immune system. While the role of the adaptive immune response in the resolution of HBV infection is well understood, the contribution of innate immune mechanisms remains to be clearly defined. The innate immune system represents the first line of defense against viral infection, but its role has been difficult to analyze in humans due to late diagnosis of HBV infection. In this review, we discuss recent advances in the field of innate immunity to HBV infection.

Keywords: Hepatitis B virus; cytokines; innate immunity; pathogenesis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Natural history of HBV infections. HCC, hepatocellular carcinoma; NK, natural killer cells; NKT, natural killer T cells.
Figure 2
Figure 2
HBV life cycle and putative ‘pathogen associated molecular patterns’ (PAMPs).
Figure 3
Figure 3
Overview of early events after HBV infection. 1. Infection step (direct or via liver sinusoidal endothelial (LSEC) or Kupffer (KC) cells taking up and presentation). 2. Recognition step by toll like (TLRs), RIG-like (RLRs) or Nod-like (NLRs) receptors. 3. Direct antiviral action of produced cytokines. 3bis. Cell protection against infection. 4. Cross talk with specialized cells. BC, Bile caniculus; SD, Space of Dissé.
Figure 4
Figure 4
Inhibition of host sensors and IFN pathway by HBV.
See this image and copyright information in PMC

References

    1. Dienstag JL. Hepatitis B virus infection. N Engl J Med. 2008;359:1486–1500. - PubMed
    1. Lavanchy D. Worldwide epidemiology of HBV infection, disease burden, and vaccine prevention. J Clin Virol. 2005;34(Suppl. 1):S1–3. - PubMed
    1. Bertoletti A, Gehring AJ. The immune response during hepatitis B virus infection. J Gen Virol. 2006;87:1439–1449. - PubMed
    1. Rehermann B, Nascimbeni M. Immunology of hepatitis B virus and hepatitis C virus infection. Nat Rev Immunol. 2005;5:215–229. - PubMed
    1. Biron CA, Sen GN. Innate responses to viral infections. In: Knipe DM, Howley PM, editors. Fields Virology. 5th ed. Vol. 1. Lippincott Williams & Wilkins; Philadelphia, PA, USA: 2007. pp. 249–278.