Evidence map›Paper›PMID 16710479›Full record

ArticleThe Journal of clinical investigation2006

Reprogramming of antiviral T cells prevents inactivation and restores T cell activity during persistent viral infection.

David G Brooks, Dorian B McGavern, Michael B A Oldstone

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

86 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Review
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  6. The PD-1/PD-L1 pathway and Epstein-Barr virus.European journal of medical research · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Regulation of CD8Cellular & molecular immunology · 2023
    Review
  14. Article
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  16. Review
  17. Article
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26 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

David G BrooksViral Immunobiology Laboratory, Molecular and Integrative Neuroscience Department, The Scripps Research Institute, La Jolla, California, USA. dbrooks@scripps.edu
Dorian B McGavern
Michael B A Oldstone
Scripps Research Institute · US

Funding

PATHOGENESIS AND IMMUNOLOGY OF DISEASET32AI007244 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 1985 to 2022
$8.8M
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR01AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1985 to 2016
$7.2M
T cell Interactions in the CNS During Viral PersistenceR21NS048866 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI MCGAVERN, DORIAN B · 2004 to 2005
$477k
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR37AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 1988 to 1997
–
NIAID NIH HHS AI07244-22NIAID NIH HHS AI09484NIAID NIH HHS R01 AI009484NIAID NIH HHS T32 AI007244NINDS NIH HHS NS048866-01NINDS NIH HHS R21 NS048866
6 · The paper itself

Abstract

Failure to clear persistent viral infections results from the early loss of T cell activity. A pertinent question is whether the immune response is programmed to fail or if nonresponsive T cells can specifically be fixed to eliminate infection. Although evidence indicates that T cell expansion is permanently programmed during the initial priming events, the mechanisms that determine the acquisition of T cell function are less clear. Herein we show that in contrast to expansion, the functional programming of T cell effector and memory responses in vivo in mice is not hardwired during priming but is alterable and responsive to continuous instruction from the antigenic environment. As a direct consequence, dysfunctional T cells can be functionally reactivated during persistent infection even after an initial program of inactivation has been instituted. We also show that early therapeutic reductions in viral replication facilitate the preservation of antiviral CD4+ T cell activity, enabling the long-term control of viral replication. Thus, dysfunctional antiviral T cells can regain activity, providing a basis for future therapeutic strategies to treat persistent viral infections.

Indexed as

Immunologic MemoryAdoptive TransferAnimalsAntiviral AgentsCD4 AntigensHumansInterferon-gammaInterleukin-2Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicRibavirinSpleenT-LymphocytesAntiviral AgentsCD4 AntigensInterferon-gammaInterleukin-2RibavirinTumor Necrosis Factor-alpha

Identifiers

PMID16710479
PMCPMC1462941
OpenAlexW2052690812

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.