1998
DOI: 10.1002/(sici)1099-1654(199801/03)8:1<13::aid-rmv208>3.0.co;2-l
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Hepatitis D virus

Abstract: The hepatitis D virus (HDV) relies on the helper hepatitis B virus (HBV) for the provision of its envelope, which consists of hepatitis B surface antigen (HBsAg). The RNA genome of HDV is a circular rod‐like structure due to its extensive intramolecular base‐pairing. HDV‐RNA has ribozyme activity which includes autocatalytic cleavage and self‐ligation properties, essential in virus replication via the rolling circle mechanism. Replication of the RNA is thought to be effected by cellular RNA polymerase II. Hepa… Show more

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Cited by 26 publications
(10 citation statements)
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References 123 publications
(167 reference statements)
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“…In a study from Mongolia, the prevalence of positive HBsAg cases among 249 apparently healthy individuals was 10% which 83% of whom were positive for HDV RNA (18). Our results are similar to those of Nakasone study in Myiako Islands from Japan, where they reported HDV prevalence rate to be 10.6% in 196 chronic HBV carriers (19). Chakraborty et al also determined the HDV prevalence as high as 10.6% in 123 patients with HBV-related liver diseases in a hospital based study in India in 2005.…”
Section: Discussionsupporting
confidence: 87%
“…In a study from Mongolia, the prevalence of positive HBsAg cases among 249 apparently healthy individuals was 10% which 83% of whom were positive for HDV RNA (18). Our results are similar to those of Nakasone study in Myiako Islands from Japan, where they reported HDV prevalence rate to be 10.6% in 196 chronic HBV carriers (19). Chakraborty et al also determined the HDV prevalence as high as 10.6% in 123 patients with HBV-related liver diseases in a hospital based study in India in 2005.…”
Section: Discussionsupporting
confidence: 87%
“…In the individual host, coinfection may lead to aggravated disease, often resulting from extracellular cooperativity of independently replicating viruses, by which one virus modulates the host response to infection to the benefit of the other [49,50]. In addition, direct interactions of different viruses in co-infected cells may result in complementation of highly pathogenic defective genotypes, in increased virus replication or in modified cell and tissue tropisms [e.g., [51][52][53][54][55][56][57]]. Alternatively, there is also evidence that mixed infections of pathogens result in reduced pathogenicity and less severe disease [17].…”
Section: Discussionmentioning
confidence: 99%
“…387 Setrobuvir 389 (194) is another HCV non-nucleoside inhibitor that inhibits NS5b RNA polymerase. 387 BI 201335 390 (195) is an oral HCV NS3/4A protease inhibitor that was stopped at Phase III clinical trials managed by Boehringer-Ingelheim. Similarly BI 207127 or deleobuvir (196), 390,391 an oral HCV NS5B RNA-dependent polymerase inhibitor, was undergoing Phase II clinical trials.…”
Section: Hcvmentioning
confidence: 99%