scholarly journals Delta hepatitis: molecular biology and clinical and epidemiological features.

1993 ◽  
Vol 6 (3) ◽  
pp. 211-229 ◽  
Author(s):  
L B Polish ◽  
M Gallagher ◽  
H A Fields ◽  
S C Hadler

Hepatitis delta virus, discovered in 1977, requires the help of hepatitis B virus to replicate in hepatocytes and is an important cause of acute, fulminant, and chronic liver disease in many regions of the world. Because of the helper function of hepatitis delta virus, infection with it occurs either as a coinfection with hepatitis B or as a superinfection of a carrier of hepatitis B surface antigen. Although the mechanisms of transmission are similar to those of hepatitis B virus, the patterns of transmission of delta virus vary widely around the world. In regions of the world in which hepatitis delta virus infection is not endemic, the disease is confined to groups at high risk of acquiring hepatitis B infection and high-risk hepatitis B carriers. Because of the propensity of this viral infection to cause fulminant as well as chronic liver disease, continued incursion of hepatitis delta virus into areas of the world where persistent hepatitis B infection is endemic will have serious implications. Prevention depends on the widespread use of hepatitis B vaccine. This review focuses on the molecular biology and the clinical and epidemiologic features of this important viral infection.

Digestion ◽  
1993 ◽  
Vol 54 (1) ◽  
pp. 9-14
Author(s):  
Nicola Napoli ◽  
Giorgio Fiore ◽  
Giacomo Fera ◽  
Angela Modugno ◽  
Gianluigi Giannelli ◽  
...  

2019 ◽  
Vol 93 (8) ◽  
Author(s):  
Kaneemozhe Harichandran ◽  
Yiran Shen ◽  
Susannah Stephenson Tsoris ◽  
See-Chi Lee ◽  
John L. Casey

ABSTRACTHepatitis delta virus (HDV) is a satellite of hepatitis B virus that increases the severity of acute and chronic liver disease. HDV produces three processed RNAs that accumulate in infected cells: the circular genome; the circular antigenome, which serves as a replication intermediate; and lesser amounts of the mRNA, which encodes the sole viral protein, hepatitis delta antigen (HDAg). The HDV genome and antigenome RNAs form ribonucleoprotein complexes with HDAg. Although HDAg is required for HDV replication, it is not known how the relative amounts of HDAg and HDV RNA affect replication, or whether HDAg synthesis is regulated by the virus. Using a novel transfection system in which HDV replication is initiated usingin vitro-synthesized circular HDV RNAs, HDV replication was found to depend strongly on the relative amounts of HDV RNA and HDAg. HDV controls these relative amounts via differential effects of HDAg on the production of HDV mRNA and antigenome RNA, both of which are synthesized from the genome RNA template. mRNA synthesis is favored at low HDAg levels but becomes saturated at high HDAg concentrations. Antigenome RNA accumulation increases linearly with HDAg and dominates at high HDAg levels. These results provide a conceptual model for how HDV antigenome RNA production and mRNA transcription are controlled from the earliest stage of infection onward and also demonstrate that, in this control, HDV behaves similarly to other negative-strand RNA viruses, even though there is no genetic similarity between them.IMPORTANCEHepatitis delta virus (HDV) is a satellite of hepatitis B virus that increases the severity of liver disease; approximately 15 million people are chronically infected worldwide. There are no licensed therapies available. HDV is not related to any known virus, and few details regarding its replication cycle are known. One key question is whether and how HDV regulates the relative amounts of viral RNA and protein in infected cells. Such regulation might be important because the HDV RNA and protein form complexes that are essential for HDV replication, and the proper stoichiometry of these complexes could be critical for their function. Our results show that the relative amounts of HDV RNA and protein in cells are indeed important for HDV replication and that the virus does control them. These observations indicate that further study of these regulatory mechanisms is required to better understand replication of this serious human pathogen.


2018 ◽  
Vol 41 (3) ◽  
pp. 171-174 ◽  
Author(s):  
Alessandra Maria Mont`Alverne Pierre ◽  
Ana Cristina de Castro Amaral Feldner ◽  
Roberto José de Carvalho Filho ◽  
Edmundo Pessoa de Almeida Lopes ◽  
Michele Soares Gomes Gouvea ◽  
...  

Introduction: Hepatitis B virus infection is an important cause of liver disease in hemodialysis patients and renal transplant recipients. Hepatitis Delta virus is a defective virus transmitted by the same route of hepatitis B virus, which requires the helper function of hepatitis B virus. Data about hepatitis B virus/hepatitis delta virus coinfection are scarce and there are no studies regarding the coinfection among hemodialysis patients and renal transplant in our country. Objective: This study aimed to investigate the prevalence of hepatitis delta virus infection among hemodialysis patients and renal transplant recipients. Methods: Cross-sectional study analyzing virological markers of hepatitis B virus and hepatitis delta virus infection and biochemical and clinical features of liver disease of patients infected with hepatitis B virus in hemodialysis and renal transplant. Results: A total of 117 HBsAg-positive patients (46 hemodialysis and 71 renal transplant) were included. The mean age was 48.5 ± 11.8 years and 67% were males. Antiviral therapy was given to 74% of patients. Liver function tests were within the normal range. HBeAg-positive was found in 35% of patients and median hepatitis B virus DNA was 2.98 log (IU/mL). Cirrhosis was detected in 26.5% of patients. The prevalence of anti–hepatitis delta virus total antibody (+) was 1.7% (2/117). None of the 2 patients had active hepatitis delta virus infection, since all samples tested negative for hepatitis delta virus–RNA. Conclusion: The results suggest a low prevalence rate of coinfection B and D in hemodialysis and renal transplant recipients in this population.


2020 ◽  
Vol 12 (4) ◽  
pp. 197
Author(s):  
Ekta Gupta ◽  
Krithiga Ramachandran ◽  
Reshu Agarwal ◽  
ManojKumar Sharma ◽  
Vikram Bhatia

2001 ◽  
Vol 65 (3) ◽  
pp. 478-484 ◽  
Author(s):  
Hiroshi Sakugawa ◽  
Hiroki Nakasone ◽  
Tomofumi Nakayoshi ◽  
Yuko Kawakami ◽  
Tsuyoshi Yamashiro ◽  
...  

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