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Review
. 2015 Jul 1;5(8):a021428.
doi: 10.1101/cshperspect.a021428.

Immune Response in Hepatitis B Virus Infection

Anthony Tan  1 , Sarene Koh  2 , Antonio Bertoletti  3
Affiliations
Review

Immune Response in Hepatitis B Virus Infection

Anthony Tan et al. Cold Spring Harb Perspect Med. .

Abstract

Hepatitis B virus (HBV) can replicate within hepatocytes without causing direct cell damage. The host immune response is, therefore, not only essential to control the spread of virus infection, but it is also responsible for the inflammatory events causing liver pathologies. In this review, we discuss how HBV deals with host immunity and how we can harness it to achieve virus control and suppress liver damage.

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Figures

Figure 1.
Figure 1.
Proposed mechanisms for the suppression of the host innate immune response by different hepatitis B virus (HBV) proteins. Induction of interferon (IFN)-α/β (type I IFN) production might be suppressed by HBV polymerase through binding to DDX-3 (Wang and Ryu 2010; Yu et al. 2010) or by HBx through down-regulation of the mitochondrial antiviral-signaling protein MAV-5 (Wang et al. 2010; Wei et al. 2010; Kumar et al. 2011). IFN-α-induced response can also be blocked by the HBV polymerase as a result of a block of signal transducer and activator of transcription (STAT)-1 nuclear translocation (Foster et al. 1991; Christen et al. 2007; Wu et al. 2007). PRR, Pathogen-recognition receptor.
Figure 2.
Figure 2.
Antiviral adaptive immune response during hepatitis B virus (HBV infection). CTL, Cytotoxic T lymphocyte; INF, interferon; TNF, tumor necrosis factor.
Figure 3.
Figure 3.
Different immune-based therapeutic strategies that aim to increase hepatitis B virus (HBV) control: (1) T-cell receptor-like antibodies conjugated with interferon (IFN)-α, which specifically target HBV-infected hepatocytes, can increase intrahepatic IFN-α delivery. (2) Toll-like receptors (TLRs) or anti-CD40 agonists mature HBV-loaded monocytes into monocyte-derived dendritic cells (moDCs) that might stimulate intrahepatic HBV-specific T cells. (3) Activation of monocytes/macrophages producing interleukin (IL)-12 and IL-18 through cytokines and/or TLR agonists can stimulate intrahepatic HBV-specific T cells, mucosal-associated invariant T (MAIT) cells, or CD56bright natural killer (NK) cells to produce large quantities of IFN-γ, which can suppress HBV replication. (4) New HBV-specific T cells can be engineered through transfer of HBV-specific T-cell receptors to reconstitute functional HBV-specific immunity. (5) Vaccine therapy performed in combination with antiviral treatment and/or combining with immunomodulation methods, such as PD-1/PD-L1 blockade, might induce antiviral T-cell responses. APC, antigen-presenting cell; LSECs, liver sinusoidal endothelial cells; TCR, T-cell receptor.
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