A Novel Target of Hepatitis B Virus Mutations: Splicing of Surface RNA * #

Baumert, Thomas F.; Köck, Josef; Blum, Hubert E.

doi:10.1002/hep.20791

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…In addition to 'vaccine escape mutants' and 'immune escape mutants', 'diagnosis escape mutants' have been described, since most of the HBsAg detection assays are based on anti-HBs antibodies [57,67] . Diagnostic escape may also be the result of a posttranscriptional effect of viral mutations on HBsAg expression as described by Hass et al in an elegant study isolating a naturally occurring mutation targeting splicing of subgenomic RNA [68,69] . The emergence of these variants may potentially contribute to occult HBsAg-negative HBV infection [70] .…”

Section: Variants Of Hbsag and Immune Escapementioning

confidence: 99%

Pathogenesis of hepatitis B virus infection

Baumert

Thimme²,

Weizsäcker³

2007

WJG

123

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Infection with hepatitis B virus (HBV) leads to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma. Infection with HBV is one of the most common viral diseases affecting man. Both viral factors as well as the host immune response have been implicated in the pathogenesis and clinical outcome of HBV infection. In this review, we will discuss the impact of virus-host interactions for the pathogenesis of HBV infection and liver disease. These interactions include the relevance of naturally occurring viral variants for clinical disease, the role of virus-induced apoptosis for HBV-induced liver cell injury and the impact of antiviral immune responses for outcome of infection.

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Section: Variants Of Hbsag and Immune Escapementioning

confidence: 99%

Pathogenesis of hepatitis B virus infection

Baumert

Thimme²,

Weizsäcker³

2007

WJG

123

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“…Diagnostic escape mutants might be a result of posttranscriptional effect of the mutation on hepatitis B surface antigen expression (2,3). This would reduce the effectiveness of diagnostics and vaccine-induced immunity, leading to escape of neutralization by the current vaccine and occult infection (4).…”

Section: Summary Of Resultsmentioning

confidence: 99%

P32: Investigation of factors affecting time to initiation of hepatitis B virus treatment

2014

Journal of Viral Hepatitis

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“…Su et al confirmed that this 2.2 kb transcript corresponds to a splice variant (SV), most likely derived from the pgRNA, by in vitro experiments in Huh-7 hepatoma cells [ 83 ]. Moreover, in vitro experiments performed in COS-7 and in Huh-7 cells identified a spliced variant derived from PreS2/S mRNA [ 84 , 85 ]. To date, 22 HBV SVs have been identified in the serum of patients and in cellular models, and can be generated from all HBV genotypes.…”

Section: Co-transcriptional Regulation Of Hbv Rnasmentioning

confidence: 99%

Co-Transcriptional Regulation of HBV Replication: RNA Quality Also Matters

Giraud,

El Achi,

Zoulim

et al. 2024

Viruses

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Chronic hepatitis B (CHB) virus infection is a major public health burden and the leading cause of hepatocellular carcinoma. Despite the efficacy of current treatments, hepatitis B virus (HBV) cannot be fully eradicated due to the persistence of its minichromosome, or covalently closed circular DNA (cccDNA). The HBV community is investing large human and financial resources to develop new therapeutic strategies that either silence or ideally degrade cccDNA, to cure HBV completely or functionally. cccDNA transcription is considered to be the key step for HBV replication. Transcription not only influences the levels of viral RNA produced, but also directly impacts their quality, generating multiple variants. Growing evidence advocates for the role of the co-transcriptional regulation of HBV RNAs during CHB and viral replication, paving the way for the development of novel therapies targeting these processes. This review focuses on the mechanisms controlling the different co-transcriptional processes that HBV RNAs undergo, and their contribution to both viral replication and HBV-induced liver pathogenesis.

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A Novel Target of Hepatitis B Virus Mutations: Splicing of Surface RNA * #

Cited by 7 publications

References 23 publications

Pathogenesis of hepatitis B virus infection

Pathogenesis of hepatitis B virus infection

P32: Investigation of factors affecting time to initiation of hepatitis B virus treatment

Co-Transcriptional Regulation of HBV Replication: RNA Quality Also Matters

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