Hepatitis D virus RNA editing: specific modification of adenosine in the antigenomic RNA

Casey, John; Gerin, John L.

doi:10.1128/jvi.69.12.7593-7600.1995

Cited by 171 publications

(65 citation statements)

References 36 publications

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“…The P proteins from members of the genera Morbillivirus, Respirovirus, Henipavirus, and Avulavirus are ex-pressed from unedited transcripts, whereas the V and W/D (W protein in Nipah virus and D protein in bovine parainfluenza virus 3) proteins require the insertion of one or two guanosine residues into the editing site, respectively (7,22,24,32,50). Transcriptional editing has also been observed in both the genomic and antigenomic RNA of hepatitis delta virus (HDV) (5,6,60). For paramyxoviruses it has been postulated that RNA editing occurs through a mechanism of RNA-dependent RNA polymerase stuttering during template elongation, similar to the polyadenylation of RNA transcripts, indicating that editing sites may have evolved from polyadenylation sites (16).…”

Section: Discussionmentioning

confidence: 99%

“…For HDV, RNA editing of the hepatitis delta antigen (HDAg) p24 gene results in HDAg p27. Both of these proteins are essential: p24 is required for HDV replication, whereas p27 is required for viral RNA packaging (5,6,23,37). For EBOV, the transmembrane glycoprotein GP 1,2 plays a major role in viral pathogenesis by mediating receptor binding and fusion (12,14,21,39).…”

Section: Vol 85 2011mentioning

confidence: 99%

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A New Ebola Virus Nonstructural Glycoprotein Expressed through RNA Editing

Mehedi

Falzarano

Seebach

et al. 2011

J Virol

169

134

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Ebola virus (EBOV), an enveloped, single-stranded, negative-sense RNA virus, causes severe hemorrhagic fever in humans and nonhuman primates. The EBOV glycoprotein (GP) gene encodes the nonstructural soluble glycoprotein (sGP) but also produces the transmembrane glycoprotein (GP 1,2 ) through transcriptional editing. A third GP gene product, a small soluble glycoprotein (ssGP), has long been postulated to be produced also as a result of transcriptional editing. To identify and characterize the expression of this new EBOV protein, we first analyzed the relative ratio of GP gene-derived transcripts produced during infection in vitro (in Vero E6 cells or Huh7 cells) and in vivo (in mice). The average percentages of transcripts encoding sGP, GP 1,2 , and ssGP were approximately 70, 25, and 5%, respectively, indicating that ssGP transcripts are indeed produced via transcriptional editing. N-terminal sequence similarity with sGP, the absence of distinguishing antibodies, and the abundance of sGP made it difficult to identify ssGP through conventional methodology. Optimized 2-dimensional (2D) gel electrophoresis analyses finally verified the expression and secretion of ssGP in tissue culture during EBOV infection. Biochemical analysis of recombinant ssGP characterized this protein as a disulfide-linked homodimer that was exclusively N glycosylated. In conclusion, we have identified and characterized a new EBOV nonstructural glycoprotein, which is expressed as a result of transcriptional editing of the GP gene. While ssGP appears to share similar structural properties with sGP, it does not appear to have the same anti-inflammatory function on endothelial cells as sGP.

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Section: Discussionmentioning

confidence: 99%

Section: Vol 85 2011mentioning

confidence: 99%

A New Ebola Virus Nonstructural Glycoprotein Expressed through RNA Editing

Mehedi

Falzarano

Seebach

et al. 2011

J Virol

169

134

View full text Add to dashboard Cite

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“…97,98 Subsequent work concluded that the genomic strand of HDV is the actual editing substrate, and that for this to occur, sequences from the apposing side of the rod-structure need to be present. 99,100 More recent findings however suggest that in fact, the antigenomic RNA of HDV is the target for HDV-RNA editing, which is therefore a conversion from A to G 101,102 and the enzyme involved is possibly the host double-stranded RNA adenosine deaminase. 101 It is now clear that the editing of the RNA, and production of the two HDAgs, are essential steps in the life cycle of HDV, the latter with distinct biological activities as explained later.…”

Section: Hepatitis Delta Antigenmentioning

confidence: 99%

Hepatitis D virus

Karayiannis

1998

Rev. Med. Virol.

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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. Hepatitis D antigen (HDAg) is the only protein encoded by HDV‐RNA and its long and short forms have a regulatory role in the replication and morphogenesis of the virus. Superinfected HBV carriers who become chronically infected with HDV are at increased risk of developing cirrhosis. Attempts to treat such carriers with interferon have not been particularly successful. In recent years the epidemiology of HDV has changed primarily due to the impact of HBV vaccination in preventing an increase in the pool of susceptible individuals. © 1998 John Wiley & Sons, Ltd.

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“…6. In addition to the changes close to the original insertion site, we detected a number of single-nucleotide substitutions, often quite close to the original insertion site (as underlined in Table 2), but also at sites more distant (data not shown) that were predominantly of A to G or U to C. We interpreted these, based on previous experience with changes occurring during RNA replication, as having arisen as consequences of post-transcriptional RNA editing by ADAR (Casey and Gerin 1995;Netter et al 1995b;Gudima et al 2002;Chang et al 2005b).…”

Section: Nucleotide Sequence Analysis Of Replicating Rna Genomesmentioning

confidence: 68%

Restoration in vivo of defective hepatitis delta virus RNA genomes

Gudima

Chang²,

Taylor³

2006

RNA

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The 1679-nt single-stranded RNA genome of hepatitis delta virus (HDV) is circular in conformation. It is able to fold into an unbranched rodlike structure via intramolecular base-pairing. This RNA is replicated by host RNA polymerase II (Pol II). Such transcription is unique, because Pol II is known only for its ability to act on DNA templates. The present study addressed the ability of the HDV RNA replication to tolerate insertions of up to 1000 nt of non-HDV sequence either at an end of the rodlike RNA structure or at a site embedded within the rod. The insertions did not interfere with the ability of primary transcripts to be processed in vivo by ribozyme cleavage and ligation. The insertions greatly reduced the ability of genomes to replicate. However, when total RNA from such transfected cells was used to transfect new recipient cells, replicating HDV RNAs could be detected by Northern analyses. The size of the emerged RNAs was consistent with loss of the inserted sequences. RT-PCR, cloning, and sequencing showed that recovery involved removal of inserted sequences with or without small deletions of adjacent RNA sequences. Such restoration of the RNA genome is consistent with a model requiring intramolecular templateswitching (RNA recombination) during RNA-directed transcription, in combination with biological selection for maintenance of the rodlike structure of the template.

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Hepatitis D virus RNA editing: specific modification of adenosine in the antigenomic RNA

Abstract: RNA editing plays a central role in the life cycle of hepatitis D virus (HDV), a subviral human pathogen.

Cited by 171 publications

References 36 publications

A New Ebola Virus Nonstructural Glycoprotein Expressed through RNA Editing

A New Ebola Virus Nonstructural Glycoprotein Expressed through RNA Editing

Hepatitis D virus

Restoration in vivo of defective hepatitis delta virus RNA genomes

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