Evidence map›Paper›PMID 20980520›Full record

ArticleJournal of virology2011

Persistent Friend virus replication and disease in Apobec3-deficient mice expressing functional B-cell-activating factor receptor.

Mario L Santiago, Diana S Smith, Bradley S Barrett, Mauricio Montano, Robert L Benitez, Roberta Pelanda, Kim J Hasenkrug, Warner C Greene

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Immunoglobulin somatic hypermutation by APOBEC3/Rfv3 during retroviral infection.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
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  11. Review
  12. Article
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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 4 institutions in 1 country.

Mario L SantiagoDivision of Infectious Diseases, University of Colorado Denver, Mail Stop B-168, 12700 E. 19th Avenue, Aurora, CO 80045, USA. mario.santiago@ucdenver.edu
Diana S Smith
Bradley S Barrett
Mauricio Montano
Robert L Benitez
Roberta Pelanda
Kim J Hasenkrug
Warner C Greene
University of Colorado Denver · USUniversity of California, San Francisco · USGladstone Institutes · USNational Institute of Allergy and Infectious Diseases · US

Funding

Immunology And Pathology Of Acute Murine Leukemia Virus InfectionsZIAAI000753 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2009 to 2022
$8.1M
Innate Restriction Factor Modulation of Retrovirus-specific Humoral ImmunityR01AI090795 · NIAID · UNIVERSITY OF COLORADO DENVER · PI SANTIAGO, MARIO LUIS · 2010 to 2013
$2.8M
Apobec3 and the Neutralizing Antibody Response Against Pathogenic RetrovirusesR56AI084123 · NIAID · UNIVERSITY OF COLORADO DENVER · PI SANTIAGO, MARIO LUIS · 2009 to 2009
$658k
NIAID NIH HHS R01 AI090795NIAID NIH HHS R56 AI084123NIAID NIH HHS R56 AI-0841230PHS HHS R01 A065329
6 · The paper itself

Abstract

Rfv3 is an autosomal dominant gene that influences the recovery of resistant mice from Friend retrovirus (FV) infection by limiting viremia and promoting a more potent neutralizing antibody response. We previously reported that Rfv3 is encoded by Apobec3, an innate retrovirus restriction factor. However, it was recently suggested that the Rfv3 susceptible phenotype of high viremia at 28 days postinfection (dpi) was more dominantly controlled by the B-cell-activating factor receptor (BAFF-R), a gene that is linked to but located outside the genetically mapped region containing Rfv3. Although one prototypical Rfv3 susceptible mouse strain, A/WySn, indeed contains a dysfunctional BAFF-R, two other Rfv3 susceptible strains, BALB/c and A.BY, express functional BAFF-R genes, determined on the basis of genotyping and B-cell immunophenotyping. Furthermore, transcomplementation studies in (C57BL/6 [B6] × BALB/c)F(1) and (B6 × A.BY)F(1) mice revealed that the B6 Apobec3 gene significantly influences recovery from FV viremia, cellular infection, and disease at 28 dpi. Finally, the Rfv3 phenotypes of prototypic B6, A.BY, A/WySn, and BALB/c mouse strains correlate with reported Apobec3 mRNA expression levels. Overall, these findings argue against the generality of BAFF-R polymorphisms as a dominant mechanism to explain the Rfv3 recovery phenotype and further strengthen the evidence that Apobec3 encodes Rfv3.

Indexed as

Virus ReplicationAnimalsB-Cell Activation Factor ReceptorCytidine DeaminaseFriend murine leukemia virusGenotypeMiceMice, Inbred BALB CMice, Inbred C57BLRetroviridae InfectionsTumor Virus InfectionsApobec3 protein, mouseB-Cell Activation Factor ReceptorCytidine DeaminaseTnfrsf13c protein, mouse

Identifiers

PMID20980520
PMCPMC3014173
OpenAlexW2030903604

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.