Hepatitis B virus infection

Yuen, Man‐Fung; Chen, Ding‐Shinn; Dusheiko, Geoffrey; Janssen, Harry L.A.; Lau, Daryl; Locarnini, Stephen; Peters, Marion G.; Lai, Ching–Lung

doi:10.1038/nrdp.2018.35

Cited by 593 publications

(543 citation statements)

References 194 publications

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“…In HCV infection in particular, hepatocellular carcinoma generally arises after a stage of fibrosis and cirrhosis of the liver, which supports a key role of inflammation for the oncogenesis process [58,59]. Several different aspects of inflammation may contribute to the development of these tumors.…”

Section: Modalities Of Viral Oncogenesismentioning

confidence: 99%

More than just oncogenes: mechanisms of tumorigenesis by human viruses

Gaglia

Münger

2018

Current Opinion in Virology

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Most humans are infected with at least one of the known human cancer viruses during their lifetimes. While the initial infection with these viruses does not cause major disease, infected cells can acquire cancer hallmarks, particularly upon immunosuppression or exposure to co-carcinogenic stimuli. Even though cancer formation represents a rare outcome of a viral infection, approximately one out of eight human cancers has a viral etiology. Viral cancers present unique opportunities for prophylaxis, diagnosis, and therapy, as demonstrated by the success of HBV and HPV vaccines and HCV antivirals in decreasing the incidence of tumors that are caused by these viruses. Here we review common characteristics and mechanisms of action of the human oncogenic viruses.

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Section: Modalities Of Viral Oncogenesismentioning

confidence: 99%

More than just oncogenes: mechanisms of tumorigenesis by human viruses

Gaglia

Münger

2018

Current Opinion in Virology

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“…Chronic HBV infection is most endemic in the Western Pacific and Africa where 6.2% and 6.1% of the adult population is infected . In contrast, the prevalence is low in Europe and the United States of America (US) (<2%) . In 2009, around 2.2 million people were living with HBV in the US and 15 million people in Europe .…”

Section: Introductionmentioning

confidence: 99%

“…The most important complication of a chronic HBV infection is liver damage. Cirrhosis or hepatocellular carcinoma (HCC) occurs in 20%‐30% of the patients that fail to clear the virus . These complications take years to develop.…”

Section: Introductionmentioning

confidence: 99%

“…Next, entry is facilitated by the hepatic bile acid transporter, sodium taurocholate co‐transporting polypeptide (NTCP). NTCP has high affinity for the preS1 domain of the large HBsAg (L) protein . After entry, the virion is uncoated and relaxed circular partially double stranded DNA (rcDNA) is released in the cytoplasm, which is then transported to the nucleus.…”

Section: Introductionmentioning

confidence: 99%

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Review article: clinical pharmacology of current and investigational hepatitis B virus therapies

Smolders

Burger

Feld

et al. 2019

Aliment Pharmacol Ther

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Summary Background Treatment of hepatitis B virus (HBV) infection with current therapy suppresses HBV DNA, but loss of hepatitis B surface antigen (HBsAg; functional cure), is rare. Multiple compounds are under investigation. Aims To describe the pharmacology, including drug interactions, efficacy, safety and mechanisms of action of investigational compounds for HBV infection. Methods Descriptive review using PubMed and Google to identify literature/conference papers on investigational compounds (≥Phase 2) with data on efficacy and safety in HBV‐infected patients. Results Bulevirtide, JNJ‐56136379, ABI‐H0731, REP‐2139, and inarigivir decrease HBV DNA/RNA, with greater potency than current nucleos(t)ide analogues. REP‐2139 (25%‐75% of patients, 20‐48 weeks treatment) and inarigivir (26% of patients, 12‐24 weeks treatment) induce HBsAg loss. ARO‐HBV reduced (>1.5 log10 UI/mL) HBsAg in 85% of patients (12 weeks treatment). There are some safety concerns with investigational agents (e.g., increased bile acids with bulevirtide, and liver enzyme flares with REP‐2139) which will require a risk benefit assessment compared with current therapies. Single and multidose pharmacokinetic data are available for bulevirtide, JNJ‐56136379, ABI‐H0731; no such data are available for REP‐2139, ARO‐HBV, inarigivir. Initial drug interaction assessments have been performed with bulevirtide and inarigivir (only in vitro). Conclusions There are promising investigational therapies for HBV infection. Increasing the potential for HBsAg loss may result in more patients achieving functional cure. However, many knowledge gaps remain such as pharmacokinetics in those with HBV, cirrhosis and renal impairment but also the interaction potential between investigational therapies, risk‐benefit profiles, and potential for drug interactions with medications used to treat comorbidities associated with aging.

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“…There are approximately 350 million people infected with hepatitis B virus (HBV) worldwide, and approximately 1.3‐1.5 million of those are estimated to be in Japan. Persistent HBV infection leads to chronic hepatitis, liver cirrhosis and ultimately hepatocellular carcinoma (HCC) . HBV is currently classified into 10 genotypes (A–J) with different clinical pathologies and response to therapy .…”

Section: Introductionmentioning

confidence: 99%

Incidence of development of hepatocellular carcinoma in Japanese patients infected with hepatitis B virus is equivalent between genotype B and C in long term

Haga

Saito

Okumoto

et al. 2019

Journal of Viral Hepatitis

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Hepatitis B virus (HBV) genotypes B (HBV/B) and C (HBV/C) are the most prevalent genotypes among Japanese patients with hepatitis. Reportedly, HBV/C infection has been associated with more severe disease progression, manifesting as developing cirrhosis and hepatocellular carcinoma (HCC), than HBV/B infection. However, no long‐term studies have examined the development of HCC in HBV/B‐infected patients in Japan. The aims of our study were to compare the incidence of HCC in HBV/B‐ or HBV/C‐infected patients. A total of 241 patients were followed up among 295 hepatitis B surface antigen (HBsAg)‐positive carriers. Genotypes of HBV were A in 1% (4/295), B in 61% (179/295), C in 37% (110/295) and D in 1% (2/295) patients, and 96% of HBV/B were infected with subgenotype Bj. The mean age at HCC diagnosis was significantly higher in HBV/B than in HBV/C (67.0 ± 10.0 vs 57.7 ± 8.0 years, P < 0.001). The value of FIB‐4 index was significantly higher in HBV/B than in HBV/C (P < 0.01). The rate of HCC was higher in HBV/C than in HBV/B, and a significant difference was observed until the 20‐year observation period (P = 0.048). However, thereafter, HCC associated with HBV/B increased, and no significant difference was observed between HBV/B and HBV/C. HCC development was consistently observed even in HBV/B infection, especially among elderly patients with advanced fibrosis compared with HBV/C. HBV/B‐infected patients developed HCC later in life, and in the long term, we found no differences in incidence of HCC development rates between these two genotypes.

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Hepatitis B virus infection

Cited by 593 publications

References 194 publications

More than just oncogenes: mechanisms of tumorigenesis by human viruses

More than just oncogenes: mechanisms of tumorigenesis by human viruses

Review article: clinical pharmacology of current and investigational hepatitis B virus therapies

Incidence of development of hepatocellular carcinoma in Japanese patients infected with hepatitis B virus is equivalent between genotype B and C in long term

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