Evidence map›Paper›PMID 21368232›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Simian immunodeficiency virus infection in the brain and lung leads to differential type I IFN signaling during acute infection.

Luna Alammar, Lucio Gama, Janice E Clements

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Limited in vivo production of type I or type III interferon after infection of macaques with vaccine or wild-type strains of measles virus.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Article
  17. Article
  18. Article
  19. Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Luna AlammarDepartment of Molecular and Comparative Pathobiology, The Johns Hopkins School of Medicine, Baltimore, MD 21201, USA.
Lucio Gama
Janice E Clements
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Project 4: Intracellular mechanism of virus persistence in astrocytes/macrophagesP01MH070306 · NIMH · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2004 to 2015
$16.0M
Minocycline Inhibits Immune Reactivation of CNS SIVR01NS055648 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2007 to 2011
$3.2M
Glial Cell Inflammatory Mechanisms &CNS RegulationR01NS047984 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2004 to 2008
$1.8M
NIMH NIH HHS MH070306NIMH NIH HHS P01 MH070306NINDS NIH HHS NS047984NINDS NIH HHS NS055648NINDS NIH HHS R01 NS047984NINDS NIH HHS R01 NS055648
6 · The paper itself

Abstract

Using an accelerated and consistent SIV pigtailed macaque model of HIV-associated neurologic disorders, we have demonstrated that virus enters the brain during acute infection. However, neurologic symptoms do not manifest until late stages of infection, suggesting that immunological mechanisms exist within the CNS that control viral replication and associated inflammation. We have shown that IFN-β, a type I IFN central to viral innate immunity, is a major cytokine present in the brain during acute infection and is responsible for limiting virus infection and inflammatory cytokine expression. However, the induction and role of IFN-α in the CNS during acute SIV infection has never been examined in this model. In the classical model of IFN signaling, IFN-β signals through the IFN-α/β receptor, leading to expression of IFN-α. Surprisingly, although IFN-β is upregulated during acute SIV infection, we found that IFN-α is downregulated. We demonstrate that this downregulation is coupled with a suppression of signaling molecules downstream of the IFN receptor, namely tyrosine kinase 2, STAT1, and IFN regulatory factor 7, as indicated by either lack of protein phosphorylation, lack of nuclear accumulation, or transcriptional and/or translational repression. In contrast to brain, IFN-α is upregulated in lung and accompanied by activation of tyrosine kinase 2 and STAT1. These data provide a novel observation that during acute SIV infection in the brain, there is differential signaling through the IFN-α/β receptor that fails to activate expression of IFN-α in the brain.

Indexed as

Acute DiseaseAnimalsDisease Models, AnimalDown-RegulationEncephalitis, ViralInterferon-alphaLung DiseasesMacaca nemestrinaParietal LobeRNA, MessengerSignal TransductionSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusInterferon-alphaRNA, Messenger

Identifiers

PMID21368232
PMCPMC3076806
OpenAlexW1891164717

What OpenQuestion holds

Textmetadata
LicenceTDM
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.