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Hepatitis B and Delta Virus: Advances on Studies about Interactions between the Two Viruses and the Infected Hepatocyte.

Giersch K, Dandri M - J Clin Transl Hepatol (2015)

Bottom Line: The mechanisms determining persistence of hepatitis B virus (HBV) infection and long-term pathogenesis of HBV-associated liver disease appear to be multifactorial.Since chronic HBV/HDV coinfection leads to the most severe form of chronic viral hepatitis, elucidation of the molecular mechanisms regulating virus-host interplay and pathogenesis are urgently needed.This article summarizes the current knowledge regarding the interactions among HBV, HDV, and the infected target cell and discusses the dependence of HDV on HBV activity and possible future therapeutic approaches.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

ABSTRACT
The mechanisms determining persistence of hepatitis B virus (HBV) infection and long-term pathogenesis of HBV-associated liver disease appear to be multifactorial. Although viral replication can be efficiently suppressed by the antiviral treatments currently available, viral clearance is generally not achieved since HBV has developed unique replication strategies, enabling persistence of its genome within the infected hepatocytes. Moreover, no direct antiviral therapy exists for the more than 15 million people worldwide that are also coinfected with the hepatitis delta virus (HDV), a defective virus that needs the HBV envelope proteins for propagation. The limited availability of robust HBV and HDV infection systems has hindered the understanding of the complex network of virus-virus and virus-host interactions that are established in the course of infection and slowed down progress in drug development. Since chronic HBV/HDV coinfection leads to the most severe form of chronic viral hepatitis, elucidation of the molecular mechanisms regulating virus-host interplay and pathogenesis are urgently needed. This article summarizes the current knowledge regarding the interactions among HBV, HDV, and the infected target cell and discusses the dependence of HDV on HBV activity and possible future therapeutic approaches.

No MeSH data available.


Related in: MedlinePlus

HBV as a helper virus for HDV.Hepatitis B virus (HBV) shares its small, medium, and large hepatitis B surface antigens (HBsAg) with hepatitis D virus (HDV).
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f01: HBV as a helper virus for HDV.Hepatitis B virus (HBV) shares its small, medium, and large hepatitis B surface antigens (HBsAg) with hepatitis D virus (HDV).

Mentions: The hepatitis delta virion is the smallest RNA pathogen known to interact with a human host and to cause substantial global morbidity and mortality. The inner nucleocapsid of the virus contains a 1,679 nucleotide long, single-stranded, circular RNA (genomic HDV RNA) and around 200 molecules of hepatitis delta antigen (HDAg), which is the only known protein encoded by the HDV RNA. Within the hepatocyte, replication leads to the accumulation of three HDV RNAs: the circular genomic RNA, the antigenomic RNA, and a smaller linear mRNA, which is the template for the translation of HDAg. HDV uses a so-called rolling cycle amplification mechanism and the host RNA polymerase II to transform the genomic HDV RNA into its exact complementary form, the antigenomic HDV RNA and then into new viral genomes.39,40 A unique open reading frame on the antigenomic HDV RNA leads to the synthesis of the HDAg, which occurs in two different forms: small HDAg and large HDAg.41 The small HDAg (24 kDa) is important for virus replication, whereas the large form (27 kDa) inhibits replication and leads to virion assembly.42,43 HDV is a defective virus, whose genome is surrounded by three HBV envelope proteins and host lipids (Fig. 1).44 HBV plays an essential role as a helper virus for HDV, since its envelope proteins are stringently necessary for HDV propagation.45 Therefore, the release of hepatitis delta virions from the infected hepatocytes can only occur if the cells are coinfected with HBV or when HDV super-infection occurs in individuals already infected with HBV.


Hepatitis B and Delta Virus: Advances on Studies about Interactions between the Two Viruses and the Infected Hepatocyte.

Giersch K, Dandri M - J Clin Transl Hepatol (2015)

HBV as a helper virus for HDV.Hepatitis B virus (HBV) shares its small, medium, and large hepatitis B surface antigens (HBsAg) with hepatitis D virus (HDV).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663204&req=5

f01: HBV as a helper virus for HDV.Hepatitis B virus (HBV) shares its small, medium, and large hepatitis B surface antigens (HBsAg) with hepatitis D virus (HDV).
Mentions: The hepatitis delta virion is the smallest RNA pathogen known to interact with a human host and to cause substantial global morbidity and mortality. The inner nucleocapsid of the virus contains a 1,679 nucleotide long, single-stranded, circular RNA (genomic HDV RNA) and around 200 molecules of hepatitis delta antigen (HDAg), which is the only known protein encoded by the HDV RNA. Within the hepatocyte, replication leads to the accumulation of three HDV RNAs: the circular genomic RNA, the antigenomic RNA, and a smaller linear mRNA, which is the template for the translation of HDAg. HDV uses a so-called rolling cycle amplification mechanism and the host RNA polymerase II to transform the genomic HDV RNA into its exact complementary form, the antigenomic HDV RNA and then into new viral genomes.39,40 A unique open reading frame on the antigenomic HDV RNA leads to the synthesis of the HDAg, which occurs in two different forms: small HDAg and large HDAg.41 The small HDAg (24 kDa) is important for virus replication, whereas the large form (27 kDa) inhibits replication and leads to virion assembly.42,43 HDV is a defective virus, whose genome is surrounded by three HBV envelope proteins and host lipids (Fig. 1).44 HBV plays an essential role as a helper virus for HDV, since its envelope proteins are stringently necessary for HDV propagation.45 Therefore, the release of hepatitis delta virions from the infected hepatocytes can only occur if the cells are coinfected with HBV or when HDV super-infection occurs in individuals already infected with HBV.

Bottom Line: The mechanisms determining persistence of hepatitis B virus (HBV) infection and long-term pathogenesis of HBV-associated liver disease appear to be multifactorial.Since chronic HBV/HDV coinfection leads to the most severe form of chronic viral hepatitis, elucidation of the molecular mechanisms regulating virus-host interplay and pathogenesis are urgently needed.This article summarizes the current knowledge regarding the interactions among HBV, HDV, and the infected target cell and discusses the dependence of HDV on HBV activity and possible future therapeutic approaches.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

ABSTRACT
The mechanisms determining persistence of hepatitis B virus (HBV) infection and long-term pathogenesis of HBV-associated liver disease appear to be multifactorial. Although viral replication can be efficiently suppressed by the antiviral treatments currently available, viral clearance is generally not achieved since HBV has developed unique replication strategies, enabling persistence of its genome within the infected hepatocytes. Moreover, no direct antiviral therapy exists for the more than 15 million people worldwide that are also coinfected with the hepatitis delta virus (HDV), a defective virus that needs the HBV envelope proteins for propagation. The limited availability of robust HBV and HDV infection systems has hindered the understanding of the complex network of virus-virus and virus-host interactions that are established in the course of infection and slowed down progress in drug development. Since chronic HBV/HDV coinfection leads to the most severe form of chronic viral hepatitis, elucidation of the molecular mechanisms regulating virus-host interplay and pathogenesis are urgently needed. This article summarizes the current knowledge regarding the interactions among HBV, HDV, and the infected target cell and discusses the dependence of HDV on HBV activity and possible future therapeutic approaches.

No MeSH data available.


Related in: MedlinePlus