Evidence map›Paper›PMID 7707512›Full record

ArticleJournal of virology1995

Replication in vitro and in vivo of an equine infectious anemia virus mutant deficient in dUTPase activity.

D L Lichtenstein, K E Rushlow, R F Cook, M L Raabe, C J Swardson, G J Kociba, C J Issel, R C Montelaro

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
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  6. Review
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  8. Uracil DNA glycosylase initiates degradation of HIV-1 cDNA containing misincorporated dUTP and prevents viral integration.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  9. Article
  10. HIV DNA is heavily uracilated, which protects it from autointegration.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  11. Article
  12. Article
  13. Article
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  16. Review
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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

8 authors at 1 institution in 1 country.

D L LichtensteinDepartment of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.
K E Rushlow
R F Cook
M L Raabe
C J Swardson
G J Kociba
C J Issel
R C Montelaro
University of Pittsburgh · US

Funding

IMMUNOLOGIC MANAGEMENT OF LENTIVIRUS INFECTIONS--EIAVR01AI025850 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MONTELARO, RONALD C · 1987 to 2013
$7.1M
NCI NIH HHS CA 49296NIAID NIH HHS AI 25850
6 · The paper itself

Abstract

As an important enzyme in DNA synthesis, dUTPase is present in a wide variety of organisms and viruses and has been identified as a component of the equine infectious anemia virus (EIAV) pol gene. The role of EIAV dUTPase, designated DU, in virus replication in vitro and in vivo was investigated with a recently described infectious molecular clone of EIAV. A deletion mutant that was deficient in dUTPase activity was constructed, and its replication kinetics was examined in fetal equine kidney (FEK) cells and primary equine bone marrow macrophage (EBMM) cells. In FEK cells, which are permissive for EIAV replication, the mutant virus replicated as well as the parental virus. In primary cultures of EBMM cells, which are primary targets of EIAV infection in vivo, the DU mutant showed delayed replication kinetics and replicated to a lower extent than did the parental virus. As the multiplicity of infection decreased, the difference between the parental and mutant viruses increased, such that at the lowest multiplicity of infection tested, there was over a 100-fold difference in virus production. The mutant virus was also much less cytopathic. The role of DU in replication in vivo was examined using a Shetland pony model of EIAV infection. Shetland ponies that were infected with the parental and mutant viruses showed transient virus RNA levels in plasma approximately 5 to 10 days postinfection. The peak virus levels in plasma (as measured by a quantitative reverse transcriptase PCR assay) were 10- to 100-fold lower in the mutant virus-infected animals than in the animals infected with the parental virus. However, ponies infected with the mutant virus mounted similar antibody responses despite the marked differences in virus replication. These studies demonstrate that EIAV DU is important for the efficient replication of the virus in macrophages in vitro and in vivo and suggests that variations in the DU sequence could markedly affect the biological and pathogenic properties of EIAV.

Indexed as

Gene DeletionAmino Acid SequenceAnimalsAntibodies, ViralBase SequenceCell LineCytopathogenic Effect, ViralDNA PrimersDNA, ViralEquine Infectious AnemiaGenes, polHorsesInfectious Anemia Virus, EquineMolecular Sequence DataPolymerase Chain ReactionPyrophosphatasesAntibodies, ViralDNA PrimersDNA, ViraldUTP pyrophosphatasePyrophosphatasesRNA, Viral

Identifiers

PMID7707512
PMCPMC188985
OpenAlexW1826522072

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.