Evidence map›Paper›PMID 2726753›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1989

Role of early region 3 (E3) in pathogenesis of adenovirus disease.

H S Ginsberg, U Lundholm-Beauchamp, R L Horswood, B Pernis, W S Wold, R M Chanock, G A Prince

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
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

107 citing papers in PubMed, 289 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Adenoviral E3/49K: CD45-targeted immune evasion and therapeutic potential.Frontiers in cellular and infection microbiology · 2026
    Review
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  7. Article
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  9. Article
  10. Article
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  13. Role of EGF Receptor Regulatory Networks in the Host Response to Viral Infections.Frontiers in cellular and infection microbiology · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

47 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

H S GinsbergDepartment of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032.
U Lundholm-Beauchamp
R L Horswood
B Pernis
W S Wold
R M Chanock
G A Prince
Columbia University · USNational Institute of Allergy and Infectious Diseases · US

Funding

MOLECULAR PATHOGENESIS OF ADENO DISEASES-ANIMAL MODELSR01AI012052 · NIAID · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SIMONELLI, PAUL F · 1985 to 1995
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ADENOVIRUS TWO CODED EARLY GLYCOPROTEINR01CA024710 · NCI · SAINT LOUIS UNIVERSITY · PI WOLD, WILLIAM SM · 1985 to 1997
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NCI NIH HHS CA24710NIAID NIH HHS AI12052
6 · The paper itself

Abstract

The cotton rat Sigmodon hispidus has provided an animal model of adenovirus pneumonia that permits investigation of the viral gene products required to produce the disease and the molecular mechanisms effecting the damage. This study was carried out to test the hypothesis that early region 3 (E3) of the adenovirus genome plays a critical role in pathogenesis of the virus's disease process even though none of its gene products are essential for its replication. Mutants whose E3 region is largely deleted (i.e., H2dl801 and H5dl327) replicated like wild-type virus in the cotton rats' lungs, but the lymphocyte and macrophage/monocyte inflammatory response was markedly increased. Viruses containing mutations that ablated production of the 19-kDa glycoprotein had the same effect as H2dl801 and H5dl327. However, mutants with deletions in the other E3 open reading frames, some of which encode known proteins, did not differ from wild-type virus in their pathogenic properties. The 19-kDa glycoprotein markedly reduces expression of the class I major histocompatibility complex antigens on the surface of infected cells. A complete correlation was found between those mutants that had increased pathogenic effects and those that lost the ability to reduce transport of the class I major histocompatibility complex antigens to surface of infected cells (i.e., all mutants unable to express the 19-kDa glycoprotein). H5sub304, which has a deletion between 83.2 and 85.1 map units in the E3B region and expresses the 19-kDa glycoprotein, did not increase the extent of pneumonia but qualitatively changed the inflammatory response in that increased numbers of polymorphonuclear leukocytes accumulated, often in small foci.

Indexed as

Genes, ViralAdenoviruses, HumanAnimalsChromosome DeletionDNA Mutational AnalysisGlycoproteinsHistocompatibility Antigens Class ILungMuridaePneumonia, ViralViral ProteinsGlycoproteinsHistocompatibility Antigens Class IViral Proteins

Identifiers

PMID2726753
PMCPMC287233
OpenAlexW2006733381

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.