Evidence map›Paper›PMID 18094171›Full record

ArticleJournal of virology2008

CD4 T cells contribute to virus control and pathology following central nervous system infection with neurotropic mouse hepatitis virus.

Stephen A Stohlman, David R Hinton, Beatriz Parra, Roscoe Atkinson, Cornelia C Bergmann

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. T helper 1 effector memory CD4Cell reports · 2023
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Stephen A StohlmanDepartment of Neurosciences NC30, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA. stohlms2@ccf.org
David R Hinton
Beatriz Parra
Roscoe Atkinson
Cornelia C Bergmann
University of Southern California · US

Funding

VIRUS ENTRY AS A DETERMINANT OF MOUSE HEPATITIS VIRUS NEUROTROPISMP01NS018146 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BERGMANN, CORNELIA · 1985 to 2007
$10.4M
PERSISTENT VIRUS ON CENTRAL NERVOUS SYSTEM IMMUNITYR01NS040667 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STOHLMAN, STEPHEN A. · 2000 to 2004
$1.5M
NINDS NIH HHS NS18146NINDS NIH HHS NS40667NINDS NIH HHS P01 NS018146NINDS NIH HHS R01 NS040667
6 · The paper itself

Abstract

Replication of the neurotropic mouse hepatitis virus strain JHM (JHMV) is controlled primarily by CD8(+) T-cell effectors utilizing gamma interferon (IFN-gamma) and perforin-mediated cytotoxicity. CD4(+) T cells provide an auxiliary function(s) for CD8(+) T-cell survival; however, their direct contribution to control of virus replication and pathology is unclear. To examine a direct role of CD4(+) T cells in viral clearance and pathology, pathogenesis was compared in mice deficient in both perforin and IFN-gamma that were selectively reconstituted for these functions via transfer of virus-specific memory CD4(+) T cells. CD4(+) T cells from immunized wild-type, perforin-deficient, and IFN-gamma-deficient donors all initially reduced virus replication. However, prolonged viral control by IFN-gamma-competent donors suggested that IFN-gamma is important for sustained virus control. Local release of IFN-gamma was evident by up-regulation of class II molecules on microglia in recipients of IFN-gamma producing CD4(+) T cells. CD4(+) T-cell-mediated antiviral activity correlated with diminished clinical symptoms, pathology, and demyelination. Both wild-type donor CD90.1 and recipient CD90.2 CD4(+) T cells trafficked into the central nervous system (CNS) parenchyma and localized to infected white matter, correlating with decreased numbers of virus-infected oligodendrocytes in the CNS. These data support a direct, if limited, antiviral role for CD4(+) T cells early during acute JHMV encephalomyelitis. Although the antiviral effector mechanism is initially independent of IFN-gamma secretion, sustained control of CNS virus replication by CD4(+) T cells requires IFN-gamma.

Indexed as

AnimalsCD4-Positive T-LymphocytesCentral Nervous System InfectionsFlow CytometryHepatitis, Viral, AnimalInterferon-gammaMiceMice, Inbred BALB CMurine hepatitis virusPerforinVirus ReplicationInterferon-gammaPerforin

Identifiers

PMID18094171
PMCPMC2258904
OpenAlexW2141173211

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.