Evidence map›Paper›PMID 9658125›Full record

ArticleJournal of virology1998

A role for herpesvirus saimiri orf14 in transformation and persistent infection.

M Duboise, J Guo, S Czajak, H Lee, R Veazey, R C Desrosiers, J U Jung

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Herpesvirus saimiri.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001
    Review
  10. Article
  11. Article
  12. Evolutionary aspects of oncogenic herpesviruses.Molecular pathology : MP · 2000
    Review
  13. Article
  14. Article
  15. 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

7 authors at 3 institutions in 2 countries.

M DuboiseDepartment of Microbiology and Molecular Genetics, New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772-9102, USA.
J Guo
S Czajak
H Lee
R Veazey
R C Desrosiers
J U Jung
Laboratory of Molecular Genetics · PLNew England Biolabs (United States) · USUniversity of Southern Maine · US

Funding

ZETA CHAIN OF T CELL RECEPTOR INTERACTS W/ NEF OF SIV &HIV2P51RR000168 · NCRR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WESTMORELAND, SUSAN V. · 1985 to 2011
$139.3M
MOLECULAR BASIS FOR HERPESVIRUS SAIMIRI ONCOGENICITYR01CA031363 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 1985 to 2014
$4.9M
MOUSE MODELS OF CANCER, BONE DISEASE, AND LACTATIONK26RR000168 · NCRR · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2000 to 2004
$547k
HERPESVIRUS VECTORS AS VACCINES FOR SIMIAN IMMUNODEFICIENCY VIRUSU19AI038131 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI DESROSIERS, RONALD C · 1995 to 1998
–
NCI NIH HHS CA31363NCI NIH HHS R01 CA031363NCRR NIH HHS K26 RR000168NCRR NIH HHS P51 RR000168NCRR NIH HHS RR00168NIAID NIH HHS AI38131
6 · The paper itself

Abstract

The product of open reading frame 14 (orf14) of herpesvirus saimiri (HVS) exhibits significant homology with mouse mammary tumor virus superantigen. orf14 encodes a 50-kDa secreted glycoprotein, as shown previously (Z. Yao, E. Maraskovsky, M. K. Spriggs, J. I. Cohen, R. J. Armitage, and M. R. Alderson, J. Immunol. 156:3260-3266, 1996). orf14 expressed from recombinant baculovirus powerfully induces proliferation of CD4-positive cells originating from several different species. To study the role of orf14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in the orf14 gene. The transforming potential of HVS Deltaorf14 was tested in cell culture and in common marmosets. Parental HVS subgroup C strain 488 immortalized common marmoset T lymphocytes in vitro to interleukin-2-independent growth, while the HVS Deltaorf14 mutant did not produce such a growth transformation. In addition, HVS Deltaorf14 was nononcogenic in common marmosets. In contrast to other nononcogenic HVS mutant viruses which were repeatedly isolated from peripheral blood mononuclear cells of infected marmosets for more than 5 months, HVS Deltaorf14 did not persist at a high level in vivo. These results demonstrate that orf14 of HVS is not required for replication but is required for transformation and for high-level persistence in vivo.

Indexed as

Cell Transformation, ViralVirus LatencyAnimalsAotidaeCallithrixCell DivisionCell LineDisease Models, AnimalHerpesviridae InfectionsHerpesvirus 2, SaimiriineHumansLymphomaMacaca mulattaMutagenesisOncogene Proteins, ViralOpen Reading FramesOncogene Proteins, ViralRecombinant Fusion ProteinsSTP protein, Herpesvirus saimiri

Identifiers

PMID9658125
PMCPMC109885
OpenAlexW1622616824

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.