Hepatitis B Virus Biology

Abstract

SUMMARY Hepadnaviruses (hepatitis B viruses) cause transient and chronic infections of the liver. Transient infections run a course of several months, and chronic infections are often lifelong. Chronic infections can lead to liver failure with cirrhosis and hepatocellular carcinoma. The replication strategy of these viruses has been described in great detail, but virus-host interactions leading to acute and chronic disease are still poorly understood. Studies on how the virus evades the immune response to cause prolonged transient infections with high-titer viremia and lifelong infections with an ongoing inflammation of the liver are still at an early stage, and the role of the virus in liver cancer is still elusive. The state of knowledge in this very active field is therefore reviewed with an emphasis on past accomplishments as well as goals for the future.

Long-term hepatitis B surface antigen (HBsAg) kinetics during nucleoside/nucleotide analogue therapy: Finite treatment duration unlikely

“…Stéphane Chevaliez, 1,2 Christophe Hézode, 2,3 Stéphane Bahrami, 4 Marion Grare, 1 and Jean-Michel Pawlotsky 1, 2 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3…”

Hepatitis B virus X protein suppresses virus-triggered IRF3 activation and IFN-β induction by disrupting the VISA-associated complex

“…HBV causes transient and chronic infection of the liver. 25 Unlike most viruses, HBV infection does not induce the expression of antiviral genes in chimpanzees; thus, the virus spreads throughout the liver. 26 Recently, several groups demonstrated that forced induction of type I IFNs by the overexpression of TLR or RLR signaling components inhibits HBV replication in the following experimental systems: in vivo, 27 in mice non-parenchymal cells 28 and in HepG2 and Huh7 cells.…”

“…A wide variety of cis-elements, designated as xenobiotic responsive elements, have been documented to be responsive to HBx, including binding sites for AP-1, AP-2, NF-kB, SRF, c/EBP, Ets, ATF1 and CREB. 25,31,32 Replication of the HBx-deficient HBV replicon in HepG2 cells was reduced by threefold compared with wild-type HBV, suggesting that HBx plays a stimulatory role in HBV replication. 33 The information on HBx protein continues to grow, although many of the roles and functions of HBx remain controversial.…”

Blockade of Tim-3 Pathway Ameliorates Interferon-γ Production from Hepatic CD8+ T Cells in a Mouse Model of Hepatitis B Virus Infection

“…Hepatitis B virus (HBV) is a noncytopathic, enveloped virus, which causes acute and chronic necroinflammatory liver diseases and affects more than 350 million people worldwide (1)(2)(3). Liver damage during HBV infection is thought to be mediated by the host cellular immune response to viral antigens (4,5).…”