Sequence conservation and divergence of hepatitis δ virus RNA

Chao, You‐Chen; Chang, Shan‐Chwen; Gust, Ian D.; Lai, Michael M. C.

doi:10.1016/0042-6822(90)90335-o

Cited by 91 publications

(71 citation statements)

References 30 publications

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“…The lower degree of editing observed for the double mutants 578G-1012C and 583G-1009C, which restore base pairing, suggests that some positions contribute sequence specificity, which may modulate editing levels. This observation could be important for the naturally occurring variation found in the Nauru isolate (25).…”

Section: Resultsmentioning

confidence: 74%

“…4 B and C) and HDAg levels (data not shown), these mutant constructs replicated as well as the wild type. The substitution of 578A-1014U with 578G-1014C is a naturally occurring variation found in an isolate of HDV from the South Pacific island of Nauru (25) 1012U, while restoration of the structure with the naturally occurring G-C pair (578G-1014C) restored editing to -75% of wild-type levels. Similar to the observations for the 578-1014 pair, the 583A-1009U base pair was found to be important for maximal editing activity.…”

Section: Resultsmentioning

confidence: 98%

“…Cloning and sequencing of HDV genomes has revealed microheterogeneity within isolates; while position 1012 (or its equivalent) is heterogeneous in several isolates (5,24,25), other positions of microheterogeneity vary from one isolate to another. Furthermore, in transfection studies in which 1012U was modified to 1012C in 3-5% of the genomes, possible modification of other sites was estimated to occur at rates 500-fold lower (19).…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Structural requirements for RNA editing in hepatitis delta virus: evidence for a uridine-to-cytidine editing mechanism.

Casey

Bergmann

Brown

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

129

132

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Hepatitis 6 virus (HDV) nucleotide 1012 is edited from uridine to cytidine in 10-40% of the RNA gonomes during replication. This editing event is an important control point in the HDV life cycle because it results in both the packaging of viral RNA and the inhibition of HDV replication. We find that the editing event is highly specific for both the sequences neighboring nucleotide 1012 and the base-paired context of position 1012 within the unbranched rod structure of HDV RNA. Prior studies identified the base transition at nucleotide 1012 but were unable to distinguish between editing of the genomic versus the antigenomic strands [Luo, G. X., Chao, M., Hsieh, S. Y., Sureau, C., Nishikura, K. & Taylor, J. (1990) J. Virol. 64, 1021-1027. In this study, comparisons of mutations that differentiate between base pairing in genomic and antigenomic RNAs indicate that the genomic strand of HDV is the actual editing substrate. We conclude that the virus uses a uridine to cytidine editing mechanism, which is provided by the host cell.Hepatitis 6 virus (HDV) is a subviral pathogen of humans. It requires concurrent infection with hepatitis B, which provides the viral coat protein (1, 2). Compared to infection with hepatitis B virus alone, coinfection or superinfection with HDV significantly increases the risk of more severe liver disease, including fulminant hepatitis (3). The HDV genome is an -1.7-kilobase, single-stranded, circular RNA molecule, which shares some unusual features with plant viroid RNAs (reviewed in ref. 4). The circular RNA molecule possesses significant intramolecular complementarity such that 70%o of the nucleotides can form base pairs in an unbranched rod structure (5, 6). Consistent with a rolling circle replication mechanism similar to that of the plant viroid agents, monomers and multimers of both genomic and antigenomic RNAs are found in infected and transfected cells (7-9). Unlike the viroids, HDV produces a single protein, the hepatitis 8 antigen (HDAg), which is translated from an antigenomic sense mRNA (9, 10). HDAg is an RNA binding protein (11-13) and is found as a mixture of 24-and 27-kDa species in both infected cells and virions (14, 15). The two forms of HDAg play central roles in the HDV replication cycle. p24 is necessary for HDV RNA replication in transfected cells in culture (8), while p27 both inhibits replication (16, 17) and enables packaging of the HDV RNA genome (18). As shown by others (19), the heterogeneity of HDAg likely arises via an RNA editing mechanism wherein the antigenomically encoded stop codon for p24 is changed from UAG to UGG; the resultant translation product, p27, contains an additional 19 amino acids at the C terminus. Because of the circular replication cycle of HDV RNA, the base change was found in both the genomic and antigenomic RNAs (19); it was therefore unclear whether the genomic or the antigenomic RNA is the actual substrate for editing. An A-to-G transition in the antigenomic strand, possibly involving a host doublestranded RNA modifying activi...

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Section: Resultsmentioning

confidence: 74%

Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Structural requirements for RNA editing in hepatitis delta virus: evidence for a uridine-to-cytidine editing mechanism.

Casey

Bergmann

Brown

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

129

132

View full text Add to dashboard Cite

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“…HDV genotype I is widespread in Italy, the United States, Taiwan, Nauru, France, Lebanon and China (Niro et al, 1997 ;Chao et al, 1990Chao et al, , 1991Wang et al, 1986 ;Makino et al, 1987 ;Kuo et al, 1988 ;Saldanha et al, 1990 ;Lee et al, 1992 ;Zhou et al, 1994). Genotype II has been isolated only in Japan and Taiwan Imazeki et al, 1990 ;Lee et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Characterization and phylogenetic analysis of a novel hepatitis D virus strain discovered by restriction fragment length polymorphism analysis.

Chiang²,

Sheen³

1998

Journal of General Virology

125

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“…New genotyping identifications have been added in the 2000's to the three major genotypes (I, II, III) identified in the 1990's with subtypes (A, B) [3,4]. The Deltavirus genre is nowadays classified into eight genotypes (HDV-1 to HDV-8) with a genomic variability of 15% and specific geographic distributions [5][6][7].…”

Section: Genomic Structurementioning

confidence: 99%

Hepatitis Delta Virus: Epidemiology, Natural Course and Treatment

Sultanik¹,

Pol²

2016

J Infect Dis Ther

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The hepatitis delta virus (HDV) is a defective hepatotropic virus that affects only patients with hepatitis B virus (HBV) infection. These 2 viruses share the same routes of transmission (parenteral, sexual, and mother to child). The hepatitis delta virus infection may result in acute hepatitis, including fulminant presentation or spontaneously resolving infection, and chronic infection. The prognosis depends on the chronology of the 2 infections, co-infection (higher risk of fulminant hepatitis) or super-infection (frequent evolution to chronicity). The harmfull impact of HIVassociated infection is today debated even if HDV antibodies are present in 12% and 4% of HIV/HBV co-infected and HBV-mono-infected patients respectively. HDV may be treated by interferon, the unique treatment, but relapse is observed in 50% of cases after discontinuation of therapy: only 25% of treated patients achieved a sustained virologic response. Entry HBV/HDV inhibitors (Myrcludex) and prenylation inhibitors are awaited encouraging progress in treating HDV infection. The treatment is recommended in patients with significant fibrosis; viral suppression may result in fibrosis stabilization or reversal which may be also observed in the absence of complete viral eradication. The prevention of hepatitis delta virus infection is based on hepatitis B virus vaccination

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Sequence conservation and divergence of hepatitis δ virus RNA

Cited by 91 publications

References 30 publications

Structural requirements for RNA editing in hepatitis delta virus: evidence for a uridine-to-cytidine editing mechanism.

Structural requirements for RNA editing in hepatitis delta virus: evidence for a uridine-to-cytidine editing mechanism.

Characterization and phylogenetic analysis of a novel hepatitis D virus strain discovered by restriction fragment length polymorphism analysis.

Hepatitis Delta Virus: Epidemiology, Natural Course and Treatment

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