Control and Eradication Strategies of Hepatitis B Virus

Shih, Chiaho; Chou, Shu-Fan; Yang, Ching-Chun; Huang, Jyun-Yuan; Choijilsuren, Gansukh; Jhou, Ren-Shiang

doi:10.1016/j.tim.2016.05.006

Cited by 44 publications

(48 citation statements)

References 107 publications

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“…Viral hepatitis is an important public health concern that is mainly caused by the hepatitis B (HBV) and C (HCV) viruses. Chronic infection leads to persistent liver inflammation and damage, which may ultimately end up in hepatocellular carcinoma (HCC) due to the development of oncogenic changes (Shih et al, 2016). To date, there is mounting evidence attesting to the importance of aberrant miRNA expression in the pathogenesis of viral hepatitis.…”

Section: Microrna Signaling In Hbv and Hcv Infectionmentioning

confidence: 99%

MicroRNA Involvement in Signaling Pathways During Viral Infection

Barbu

Condrat

Thompson

et al. 2020

Front. Cell Dev. Biol.

117

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Section: Microrna Signaling In Hbv and Hcv Infectionmentioning

confidence: 99%

MicroRNA Involvement in Signaling Pathways During Viral Infection

Barbu

Condrat

Thompson

et al. 2020

Front. Cell Dev. Biol.

117

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“…Two billion people have been infected with HBV worldwide, and to date, there is still no effective treatment to eradicate the virus in chronic carriers3. HBV replicates by reverse transcription via a pregenomic RNA (pgRNA) intermediate45.…”

mentioning

confidence: 99%

HBV maintains electrostatic homeostasis by modulating negative charges from phosphoserine and encapsidated nucleic acids

Yang

Chu

et al. 2016

Sci Rep

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Capsid assembly and stability of hepatitis B virus (HBV) core protein (HBc) particles depend on balanced electrostatic interactions between encapsidated nucleic acids and an arginine-rich domain (ARD) of HBc in the capsid interior. Arginine-deficient ARD mutants preferentially encapsidated spliced viral RNA and shorter DNA, which can be fully or partially rescued by reducing the negative charges from acidic residues or serine phosphorylation of HBc, dose-dependently. Similarly, empty capsids without RNA encapsidation can be generated by ARD hyper-phosphorylation in insect, bacteria, and human hepatocytes. De-phosphorylation of empty capsids by phosphatase induced capsid disassembly. Empty capsids can convert into RNA-containing capsids by increasing HBc serine de-phosphorylation. In an HBV replicon system, we observed a reciprocal relationship between viral and non-viral RNA encapsidation, suggesting both non-viral RNA and serine-phosphorylation could serve as a charge balance buffer in maintaining electrostatic homeostasis. In addition, by comparing the biochemistry assay results between a replicon and a non-replicon system, we observed a correlation between HBc de-phosphorylation and viral replication. Balanced electrostatic interactions may be important to other icosahedral particles in nature.

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“…Therapeutic vaccines are currently of considerable interest because it is thought that they could help counter HBV-specific T cell exhaustion, restoring the level of the HBV-specific T cell population, boosting CD4+ T cell responses, and activating humoral and cytolytic immune responses against HBV antigens [154, 155]. There is considerable genetic diversity in HBV, with eight distinct genotypes and multiple subtypes, giving complexity to the development of effective vaccines.…”

Section: Host-targeting Agentsmentioning

confidence: 99%

Drugs in Development for Hepatitis B

Dawood

Basit

Jayaraj

et al. 2017

Drugs

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With high morbidity and mortality worldwide, there is great interest in effective therapies for chronic hepatitis B (CHB) virus. There are currently several dozen investigational agents being developed for treatment of CHB. They can be broadly divided into two categories: (1) direct-acting antivirals (DAAs) that interfere with a specific step in viral replication; and (2) host-targeting agents that inhibit viral replication by modifying host cell function, with the latter group further divided into the subcategories of immune modulators and agents that target other host functions. Included among the DAAs being developed are RNA interference therapies, covalently closed circular DNA (cccDNA) formation and transcription inhibitors, core/capsid inhibitors, reverse transcriptase inhibitors, hepatitis B surface antigen (HBsAg) release inhibitors, antisense oligonucleotides, and helioxanthin analogues. Included among the host-targeting agents are entry inhibitors, cyclophilin inhibitors, and multiple immunomodulatory agents, including Toll-like receptor agonists, immune checkpoint inhibitors, therapeutic vaccines, engineered T cells, and several cytokine agents, including recombinant human interleukin-7 (CYT107) and SB 9200, a novel therapy that is believed to both have direct antiviral properties and to induce endogenous interferon. In this review we discuss agents that are currently in the clinical stage of development for CHB treatment as well as strategies and agents currently at the evaluation and discovery phase and potential future targets. Effective approaches to CHB may require suppression of viral replication combined with one or more host-targeting agents. Some of the recent research advances have led to the hope that with such a combined approach we may have a functional cure for CHB in the not distant future.

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Control and Eradication Strategies of Hepatitis B Virus

Cited by 44 publications

References 107 publications

MicroRNA Involvement in Signaling Pathways During Viral Infection

MicroRNA Involvement in Signaling Pathways During Viral Infection

HBV maintains electrostatic homeostasis by modulating negative charges from phosphoserine and encapsidated nucleic acids

Drugs in Development for Hepatitis B

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