Evidence map›Paper›PMID 15254184›Full record

ArticleJournal of virology2004

By inhibiting replication, the large hepatitis delta antigen can indirectly regulate amber/W editing and its own expression.

Shuji Sato, Cromwell Cornillez-Ty, David W Lazinski

Abstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Hepatitis Delta Infection: A Clinical Review.Seminars in liver disease · 2023
    Review
  10. Diagnosis of HDV: From virology to non-invasive markers of fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2023
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Shuji SatoDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02111-1817, USA.
Cromwell Cornillez-Ty
David W Lazinski

Funding

HEPATITIS DELTA VIRUS REPLICATION AND PATHOGENESISR01AI040472 · NIAID · TUFTS UNIVERSITY BOSTON · PI LAZINSKI, DAVID W · 1997 to 2001
$412k
NIAID NIH HHS R01-AI40472
6 · The paper itself

Abstract

Hepatitis delta virus (HDV) expresses two essential proteins with distinct functions. The small hepatitis delta antigen (HDAg-S) is expressed throughout replication and is needed to promote that process. The large form (HDAg-L) is farnesylated, is expressed only at later times via RNA editing of the amber/W site, and is required for virion assembly. When HDAg-L is artificially expressed at the onset of replication, it strongly inhibits replication. However, there is controversy concerning whether HDAg-L expressed naturally at later times as a consequence of editing and replication can similarly inhibit replication. Here, by stabilizing the predicted secondary structure downstream from the amber/W site, a replication-competent HDV mutant that exhibited levels of editing higher than those of the wild type was created. This mutant expressed elevated levels of HDAg-L early during replication, and at later times, its replication aborted prematurely. No further increase in amber/W editing was observed following the cessation of replication, indicating that editing was coupled to replication. A mutation in HDAg-L and a farnesyl transferase inhibitor were both used to abolish the ability of HDAg-L to inhibit replication. Such treatments rescued the replication defect of the overediting mutant, and even higher levels of amber/W editing resulted. It was concluded that when expressed naturally during replication, HDAg-L is able to inhibit replication and thereby inhibit amber/W editing and its own synthesis. In addition, the structure adjacent to the amber/W site is suboptimal for editing, and this creates a window of time in which replication can occur in the absence of HDAg-L.

Indexed as

Gene Expression Regulation, ViralRNA EditingVirus ReplicationCells, CulturedCodonHepatitis delta AntigensHepatitis Delta VirusHumansOpen Reading FramesRNA, ViralCodonHepatitis delta Antigenshepatitis delta virus large antigenRNA, Viral

Identifiers

PMID15254184
PMCPMC446097

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.