Hepatitis B virus: a small selection of research interest in the current literature

Hepatitis B, a potentially life-threatening liver infection caused by the hepatitis B virus, is a major global health problem. It can cause chronic infection and puts people at high risk of death from cirrhosis and liver cancer. The following is a small selection of research published in the literature in 2020.

HBV genome and life cycle Wang J, Huang H, Liu Y et al. Adv Exp Med Biol 2020; 1179: 17–37. doi: 10.1007/978-981-13-9151-4_2.

Chronic hepatitis B virus (HBV) infection remains a serious threat to public health and is associated with many liver diseases including chronic hepatitis B (CHB), liver cirrhosis, and hepatocellular carcinoma. Although nucleos(t)ide analogues (NA) and pegylated interferon-α (Peg-IFNα) have been confirmed to be efficient in inhibiting HBV replication, it is difficult to eradicate HBV and achieve the clinical cure of CHB. Therefore, long-term therapy has been recommended for CHB treatment under the current antiviral therapy.

In this context, the new antiviral therapy targeting multiple critical steps of viral life cycle may be an alternative approach. In the past decade, the functional receptor (sodium-taurocholate cotransporting polypeptide [NTCP]) of HBV entry into hepatocytes has been discovered, and the immature nucleocapsids containing the non- or partially reverse-transcribed pregenomic

RNA, the nucleocapsids containing double-stranded linear DNA (dslDNA), and the empty particles devoid of any HBV nucleic acid have been found to be released into the circulation, which have supplemented the life cycle of HBV. Understanding of HBV life cycle may

offer a new instruction for searching the potential antiviral targets and the new viral markers used to monitor the efficacy of future antiviral therapy for CHB patients.

The interactions between HBV and the innate immunity of hepatocytes Megahed FAK, Zhou X, Sun P. Viruses 2020; 12 (3): 285. doi: 10.3390/v12030285.

Hepatitis B virus (HBV) infection affects around 350 million people and poses a major public health problem worldwide. HBV is a major cause of cirrhosis and hepatocellular carcinoma. Fewer than 5% of HBV-infected adults (but up to 90% of HBV-infected infants and children) develop chronic HBV infection as indicated by continued, detectable expression of hepatitis B surface antigen (HBsAg) for at least six months after the initial infection.

Increasing evidence indicates that HBV interacts with innate immunity signalling pathways of hepatocytes to suppress innate immunity. However, it is still not clear how HBV avoids monitoring by the innate immunity of hepatocytes, and whether or not the innate immunity of hepatocytes can be effective against HBV if re-triggered. Moreover, a deep understanding of virus-host interactions is important in developing new therapeutic strategies for the treatment of HBV infection. In this review, the authors summarise

the current knowledge regarding how HBV represses innate immune recognition, as well as recent progress with respect to in vitro models for studying HBV infection and innate immunity.

An HBV-encoded miRNA activates innate immunity to restrict HBV replication

Zhao X, Sun L, Mu T et al. J Mol Cell Biol 2020; 12 (4): 263–76. doi: 10.1093/jmcb/mjz104.

Hepatitis B virus (HBV) virions (orange; transmission electron microscope [TEM) image). WWW.PATHOLOGYINPRACTICE.COM DECEMBER 2020

The authors previously identified that hepatitis B virus (HBV) encodes a microRNA (HBV-miR-3) that restrains HBV replication by targeting the HBV transcript. However, whether or not HBV-miR-3 affects host innate immunity to modulate HBV replication remains unclear. In the study, the authors examined the vital functions of HBV-miR-3 in the innate immune response after HBV infection. They found that HBV-miR-3 expression gradually increased in a dose- and time- dependent manner in HBV-infected HepG2-NTCP cells. HBV-miR-3 activated the JAK/STAT signalling pathway by downregulating SOCS5 in hepatocytes, thereby enhancing the interferon (IFN)- induced anti-HBV effect. In addition, HBV-miR-3 in exosomes facilitated the M1 polarisation of macrophages. Furthermore, exosomes containing HBV-miR-3 enhanced the secretion of interleukin (IL)-6 via inhibiting


CDC/Dr Erskine Palmer

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