Evidence map›Paper›PMID 12639986›Full record

ArticleThe Journal of clinical investigation2003

Measles virus infection results in suppression of both innate and adaptive immune responses to secondary bacterial infection.

Mark K Slifka, Dirk Homann, Antoinette Tishon, Robb Pagarigan, Michael B A Oldstone

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  14. Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  15. Article
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  18. Tropism illuminated: lymphocyte-based pathways blazed by lethal morbillivirus through the host immune system.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  19. Developing animal models for polymicrobial diseases.Nature reviews. Microbiology · 2004
    Review
  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 2 institutions in 1 country.

Mark K SlifkaOregon Health and Science University Vaccine and Gene Therapy Institute, Beaverton, Oregon, USA.
Dirk Homann
Antoinette Tishon
Robb Pagarigan
Michael B A Oldstone
Scripps Research Institute · USOregon Health & Science University · US

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
MEASLES VIRUS STUDIES IN A TRANSGENIC MODELR01AI036222 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1994 to 2007
$2.6M
NEUROBIOLOGIC AND IMMUNOLOGIC ASPECTS OF AGINGT32AG000080 · NIA · SCRIPPS RESEARCH INSTITUTE · PI BUXBAUM, JOEL N · 1985 to 2003
$743k
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163NCRR NIH HHS RR00163NIAID NIH HHS AI36222NIAID NIH HHS R01 AI036222NIA NIH HHS AG00080NIA NIH HHS T32 AG000080
6 · The paper itself

Abstract

Among infectious agents, measles virus (MV) remains a scourge responsible for 1 million deaths per year and is a leading cause of childhood deaths in developing countries. Although MV infection itself is not commonly lethal, MV-induced suppression of the immune system results in a greatly increased susceptibility to opportunistic bacterial infections that are largely responsible for the morbidity and mortality associated with this disease. Despite its clinical importance, the underlying mechanisms of MV-induced immunosuppression remain unresolved. To begin to understand the basis of increased susceptibility to bacterial infections during MV infection, we inoculated transgenic mice expressing the MV receptor, CD46, with MV and Listeria monocytogenes. We found that MV-infected mice were more susceptible to infection with Listeria and that this corresponded with significantly decreased numbers of macrophages and neutrophils in the spleen and substantial defects in IFN-gamma production by CD4(+) T cells. The reduction in CD11b(+) macrophages and IFN-gamma-producing T cells was due to reduced proliferative expansion and not to enhanced apoptosis or to altered distribution of these cells between spleen, blood, and the lymphatic system. These results document that MV infection can suppress both innate and adaptive immune responses and lead to increased susceptibility to bacterial infection.

Indexed as

Immune ToleranceAnimalsAntigens, CDBacterial InfectionsCD11b AntigenCD4-Positive T-LymphocytesImmunity, InnateInterferon-gammaListeriosisMeaslesMembrane Cofactor ProteinMembrane GlycoproteinsMiceAntigens, CDCD11b AntigenInterferon-gammaMcp protein, mouseMembrane Cofactor ProteinMembrane Glycoproteins

Identifiers

PMID12639986
PMCPMC153759
OpenAlexW2058221032

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.