Evidence map›Paper›PMID 21921207›Full record

ArticleThe Journal of infectious diseases2011

Virus infection stages and distinct Th1 or Th17/Th22 T-cell responses in malaria/SHIV coinfection correlate with different outcomes of disease.

Bridgett Ryan-Payseur, Zahida Ali, Dan Huang, Crystal Y Chen, Lin Yan, Richard C Wang, William E Collins, Yunqi Wang, Zheng W Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Interleukin-22 Polymorphisms inMediators of inflammation · 2020
    Article
  5. Article
  6. Immunization of Vγ2Vδ2 T cells programs sustained effector memory responses that control tuberculosis in nonhuman primates.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
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  13. Article
  14. Review
  15. Article
  16. T helper cytokines in dry eye disease.Experimental eye research · 2013
    Review
  17. Review
  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

9 authors at 4 institutions in 1 country.

Bridgett Ryan-PayseurDepartment of Microbiology and Immunology, Center for Primate Biomedical Research, University of Illinois College of Medicine, Chicago 60612, USA.
Zahida Ali
Dan Huang
Crystal Y Chen
Lin Yan
Richard C Wang
William E Collins
Yunqi Wang
Zheng W Chen
University of Illinois Chicago · USIllinois College · USUniversity of Illinois Urbana-Champaign · USCenters for Disease Control and Prevention · US

Funding

MODEL OF AIDS VIRUS-RELATED PULMONARY TUBERCULOSISR01HL064560 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHEN, ZHENG W · 1999 to 2014
$9.5M
SIV/MYCOBACTERIUM COINFECTIONR01RR013601 · NCRR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHEN, ZHENG W · 1998 to 2008
$4.4M
NCRR NIH HHS R01 RR013601NCRR NIH HHS R01 RR13601NHLBI NIH HHS R01 HL064560NHLBI NIH HHS R01 HL64560
6 · The paper itself

Abstract

backgroundMalaria and AIDS represent 2 leading causes of death from infectious diseases worldwide, and their high geographic overlap means coinfection is prevalent. It remains unknown whether distinct immune responses during coinfection with malaria and human immunodeficiency virus (HIV) affect clinical outcomes.

methodsWe tested this hypothesis by employing macaque models of coinfection with malaria and simian-human immunodeficiency virus (SHIV).

resultsPlasmodium fragile malaria coinfection of acutely SHIV-infected macaques induced hyperimmune activation and remarkable expansion of CD4+ and CD8+ T effector cells de novo producing interferon γ or tumor necrosis factor α. Malaria-driven cellular hyperactivation/expansion and high-level Th1-cytokines enhanced SHIV disease characterized by increasing CD4+ T-cell depletion, profound lymphoid depletion or destruction, and even necrosis in lymph nodes and spleens. Importantly, malaria/SHIV-mediated depletion, destruction, and necrosis in lymphoid tissues led to bursting parasite replication and fatal virus-associated malaria. Surprisingly, chronically SHIV-infected macaques without AIDS employed different defense mechanisms during malaria coinfection, and mounted unique ∼200-fold expansion of interleukin 17+/interleukin 22+ T effectors with profound Th1 suppression. Such remarkable expansion of Th17/Th22 cells and inhibition of Th1 response coincided with development of immunity against fatal virus-associated malaria without accelerating SHIV disease.

conclusionsThese novel findings suggest that virus infection status and selected Th1 or Th17/Th22 responses after malaria/AIDS-virus coinfection correlate with distinct outcomes of virus infection and malaria.

Indexed as

AnimalsDisease Models, AnimalMacaca mulattaMalariaPlasmodiumPrimate DiseasesSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusTh17 CellsTh1 CellsTreatment Outcome

Identifiers

PMID21921207
PMCPMC3218650
OpenAlexW2129622590

What OpenQuestion holds

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Registered trials

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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.