Production of hepatitis B defective particles is dependent on liver status

Redelsperger, François; Lekbaby, Bouchra; Mandouri, Yassmina; Giang, Eric; Duriez, Marion; Désiré, Nathalie; Afonso, Anne-Marie Roque; Brichler, Ségolène; Dubreuil, Pascal; Dobrin, A.S.; Perlemuter, Gabriel; Prévôt, Sophie; Bacon, Nathalie; Grangé, Jean Didier; Zatla, Fadila; Pendeven, Catherine Le; Pol, Stanislas; Strick‐Marchand, Hélène; Santo, James P. Di; Kremsdorf, Dina; Soussan, Patrick Ben

doi:10.1016/j.virol.2012.05.008

Cited by 23 publications

(19 citation statements)

References 32 publications

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“…defective viral particles (4). Recent reports have shown in vivo that the proportion of defective particles is associated with viral multiplication and, interestingly, increases according to the severity of the liver disease as it progresses toward HCC in HBV chronic carriers (5)(6)(7). Thus, these observations suggest a modulation of alternate splicing event along liver disease, as previously described for multiple cellular transcripts (8).…”

supporting

confidence: 60%

“…We and others have observed an increase of viral RNA splicing during the course of HBV infection, suggesting an increase of HBSP expression with the severity of liver disease (5)(6)(7). In regards to the results obtained in HBSP Tg mice, HBSP expression may favor immune escape of HBVinfected liver cells by limiting the recruitment of leukocytes.…”

Section: Discussionmentioning

confidence: 64%

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Alternative splicing‐regulated protein of hepatitis B virus hacks the TNF‐α‐stimulated signaling pathways and limits the extent of liver inflammation

et al. 2015

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supporting

confidence: 60%

Section: Discussionmentioning

confidence: 64%

Alternative splicing‐regulated protein of hepatitis B virus hacks the TNF‐α‐stimulated signaling pathways and limits the extent of liver inflammation

et al. 2015

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“…Although different techniques for the development of the humanized mouse model exist, a number of groups have adapted their use for the study of HBV. These studies cover a broad range of aspects of HBV biology, including studies of the HBV-mediated immune response, [175, 176] investigation of potential HBV therapeutics, [177, 178] and aspects of the HBV life cycle such as particle formation, [179] receptor binding, [180] and cccDNA regulation. [181] …”

Section: Model Systems Used In the Study Of Hbvmentioning

confidence: 99%

Hepatitis B virus molecular biology and pathogenesis

Lamontagne¹,

Bagga²,

Bouchard³

2016

145

109

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As obligate intracellular parasites, viruses need a host cell to provide a milieu favorable to viral replication. Consequently, viruses often adopt mechanisms to subvert host cellular signaling processes. While beneficial for the viral replication cycle, virus-induced deregulation of host cellular signaling processes can be detrimental to host cell physiology and can lead to virus-associated pathogenesis, including, for oncogenic viruses, cell transformation and cancer progression. Included among these oncogenic viruses is the hepatitis B virus (HBV). Despite the availability of an HBV vaccine, 350–500 million people worldwide are chronically infected with HBV, and a significant number of these chronically infected individuals will develop hepatocellular carcinoma (HCC). Epidemiological studies indicate that chronic infection with HBV is the leading risk factor for the development of HCC. Globally, HCC is the second highest cause of cancer-associated deaths, underscoring the need for understanding mechanisms that regulate HBV replication and the development of HBV-associated HCC. HBV is the prototype member of the Hepadnaviridae family; members of this family of viruses have a narrow host range and predominately infect hepatocytes in their respective hosts. The extremely small and compact hepadnaviral genome, the unique arrangement of open reading frames, and a replication strategy utilizing reverse transcription of an RNA intermediate to generate the DNA genome are distinguishing features of the Hepadnaviridae. In this review, we provide a comprehensive description of HBV biology, summarize the model systems used for studying HBV infections, and highlight potential mechanisms that link a chronic HBV-infection to the development of HCC. For example, the HBV X protein (HBx), a key regulatory HBV protein that is important for HBV replication, is thought to play a cofactor role in the development of HBV-induced HCC, and we highlight the functions of HBx that may contribute to the development of HBV-associated HCC.

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“…spHBV RNAs can be incorporated into the nucleocapsids and then reverse transcribed into HBV DNA to generate defective HBV (dHBV) particles 9 10 11 12 . The level of dHBV particles in the sera of patients with chronic hepatitis B (CHB) was shown to be related with liver disease 13 14 and was enhanced prior to development of HCC 15 . spHBV RNAs also serve as the translation templates for a number of non-canonical HBV proteins.…”

mentioning

confidence: 99%

Hepatitis B virus spliced variants are associated with an impaired response to interferon therapy

Chen

Wang

et al. 2015

Sci Rep

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During hepatitis B virus (HBV) replication, spliced HBV genomes and splice-generated proteins have been widely described, however, their biological and clinical significance remains to be defined. Here, an elevation of the proportion of HBV spliced variants in the sera of patients with chronic hepatitis B (CHB) is shown to correlate with an impaired respond to interferon-α (IFN-α) therapy. Transfection of the constructs encoding the three most dominant species of spliced variants into cells or ectopic expression of the two major spliced protein including HBSP and N-terminal-truncated viral polymerase protein result in strong suppression of IFN-α signaling transduction, while mutation of the major splicing-related sites of HBV attenuates the viral anti-IFN activities in both cell and mouse models. These results have associated the productions of HBV spliced variants with the failure response to IFN therapy and illuminate a novel mechanism where spliced viral products are employed to resist IFN-mediated host defense.

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Production of hepatitis B defective particles is dependent on liver status

Cited by 23 publications

References 32 publications

Alternative splicing‐regulated protein of hepatitis B virus hacks the TNF‐α‐stimulated signaling pathways and limits the extent of liver inflammation

Alternative splicing‐regulated protein of hepatitis B virus hacks the TNF‐α‐stimulated signaling pathways and limits the extent of liver inflammation

Hepatitis B virus molecular biology and pathogenesis

Hepatitis B virus spliced variants are associated with an impaired response to interferon therapy

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