Evidence map›Paper›PMID 16775334›Full record

ArticleJournal of virology2006

Genetic changes in hepatitis delta virus from acutely and chronically infected woodchucks.

John L Casey, Bud C Tennant, John L Gerin

Abstract readComparative Study
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Hepatitis D virus coinfection and superinfection.Cold Spring Harbor perspectives in medicine · 2014
    Review
  5. Host RNA circles and the origin of hepatitis delta virus.World journal of gastroenterology · 2014
    Review
  6. Review
  7. Review
  8. Article
  9. Control of ADAR1 editing of hepatitis delta virus RNAs.Current topics in microbiology and immunology · 2012
    Review
  10. Article
  11. Article
  12. 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.

John L CaseyDepartment of Microbiology and Immunology, Georgetown University Medical Center, 3900 Reservoir Road NW, Washington, DC 20007, USA. caseyj@georgetown.edu
Bud C Tennant
John L Gerin

Funding

HEPATITIS DELTA VIRUS RNA EDITINGR01AI042324 · NIAID · GEORGETOWN UNIVERSITY · PI CASEY, JOHN L · 1999 to 2007
$1.9M
BREEDING &EXPERIMENTAL FACILITYN01AI035164 · NIAID · CORNELL UNIVERSITY ITHACA · PI TENNANT, BUD C · 1993 to 1999
–
OPERATION OF A MOLECULAR VIROLOGY/IMMUNOLOGY LABORATORYN01AI045179 · NIAID · GEORGETOWN UNIVERSITY · PI GERIN, JOHN L. · 1994 to 1999
–
NIAID NIH HHS N01 AI 35164NIAID NIH HHS N01 AI 45179NIAID NIH HHS R01 AI042324NIAID NIH HHS R01 AI 42324
6 · The paper itself

Abstract

A woodchuck-derived hepatitis delta virus (HDV) inoculum was created by transfection of a genotype I HDV cDNA clone directly into the liver of a woodchuck that was chronically infected with woodchuck hepatitis virus. All woodchucks receiving this inoculum became positive for HDV RNA in serum, and 67% became chronically infected, similar to the rate of chronic HDV infection in humans. Analysis of HDV sequences obtained at 73 weeks postinfection indicated that changes had occurred at a rate of 0.5% per year; many of these modifications were consistent with editing by host RNA adenosine deaminase. The appearance of sequence changes, which were not evenly distributed on the genome, was correlated with the course of HDV infection. A limited number of modifications occurred in the consensus sequence of the viral genome that altered the sequence of the hepatitis delta antigen (HDAg). All chronically infected animals examined exhibited these changes 73 weeks following infection, but at earlier times, only one of the HDV carriers exhibited consensus sequence substitutions. On the other hand, sequence modifications in animals that eventually recovered from HDV infection were apparent after 27 weeks. The data are consistent with a model in which HDV sequence changes are selected by host immune responses. Chronic HDV infection in woodchucks may result from a delayed and weak immune response that is limited to a small number of epitopes on HDAg.

Indexed as

Acute DiseaseAdenosine DeaminaseAnimalsEpitopesGenetic VariationGenome, ViralHepatitis B Virus, WoodchuckHepatitis D, ChronicHepatitis Delta VirusHumansMarmotaRNA-Binding ProteinsRNA EditingRNA, ViralSequence Analysis, RNATime FactorsADARB1 protein, humanAdenosine DeaminaseEpitopesRNA-Binding ProteinsRNA, Viral

Identifiers

PMID16775334
PMCPMC1488942

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.