Evidence map›Paper›PMID 23300447›Full record

ArticlePLoS pathogens2012

An Epstein-Barr virus encoded inhibitor of Colony Stimulating Factor-1 signaling is an important determinant for acute and persistent EBV infection.

Makoto Ohashi, Mark H Fogg, Nina Orlova, Carol Quink, Fred Wang

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  5. Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Review
  11. Immune control of oncogenic γ-herpesviruses.Current opinion in virology · 2015
    Review
  12. Infectious Mononucleosis.Current topics in microbiology and immunology · 2015
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. 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

5 authors at 2 institutions in 1 country.

Makoto OhashiDepartment of Medicine, Brigham & Women's Hospital and Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America.
Mark H Fogg
Nina Orlova
Carol Quink
Fred Wang
Brigham and Women's Hospital · USHarvard University · 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
PATHOGENESIS OF EPSTEIN BARR VIRUS INFECTIONR01CA068051 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI WANG, FREDERICK C. · 1995 to 2014
$5.8M
Pathogenesis of oral rhesus lymphocryptovirus infectionR01DE018926 · NIDCR · BRIGHAM AND WOMEN'S HOSPITAL · PI WANG, FREDERICK C. · 2007 to 2011
$1.9M
NCI NIH HHS CA68051NCI NIH HHS R01 CA068051NCRR NIH HHS P51 RR000168NCRR NIH HHS P51RR00168NIDCR NIH HHS DE18926NIDCR NIH HHS R01 DE018926
6 · The paper itself

Abstract

Acute Epstein-Barr virus (EBV) infection is the most common cause of Infectious Mononucleosis. Nearly all adult humans harbor life-long, persistent EBV infection which can lead to development of cancers including Hodgkin Lymphoma, Burkitt Lymphoma, nasopharyngeal carcinoma, gastric carcinoma, and lymphomas in immunosuppressed patients. BARF1 is an EBV replication-associated, secreted protein that blocks Colony Stimulating Factor 1 (CSF-1) signaling, an innate immunity pathway not targeted by any other virus species. To evaluate effects of BARF1 in acute and persistent infection, we mutated the BARF1 homologue in the EBV-related herpesvirus, or lymphocryptovirus (LCV), naturally infecting rhesus macaques to create a recombinant rhLCV incapable of blocking CSF-1 (ΔrhBARF1). Rhesus macaques orally challenged with ΔrhBARF1 had decreased viral load indicating that CSF-1 is important for acute virus infection. Surprisingly, ΔrhBARF1 was also associated with dramatically lower virus setpoints during persistent infection. Normal acute viral load and normal viral setpoints during persistent rhLCV infection could be restored by Simian/Human Immunodeficiency Virus-induced immunosuppression prior to oral inoculation with ΔrhBARF1 or infection of immunocompetent animals with a recombinant rhLCV where the rhBARF1 was repaired. These results indicate that BARF1 blockade of CSF-1 signaling is an important immune evasion strategy for efficient acute EBV infection and a significant determinant for virus setpoint during persistent EBV infection.

Indexed as

AnimalsDefective VirusesDisease Models, AnimalEpstein-Barr Virus InfectionsGene Knockout TechniquesHerpesviridae InfectionsHerpesvirus 4, HumanImmunity, InnateLymphocryptovirusMacaca mulattaMacrophage Colony-Stimulating FactorTumor Virus InfectionsViral LoadViral ProteinsVirus ReplicationBARF1 protein, Human herpesvirus 4Macrophage Colony-Stimulating FactorViral Proteins

Identifiers

PMID23300447
PMCPMC3531511
OpenAlexW2140689184

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.