Evidence map›Paper›PMID 28856681›Full record

ArticleJournal of medical virology2018

Reduced activation and proliferation of human lymphocytes exposed to respiratory syncytial virus compared to cells exposed to influenza virus.

Elisa H Fleming, Eliana E Ochoa, Joan E Nichols, M Kerry O'Banion, Alan R Salkind, Norbert J Roberts

Abstract read
In one paragraph

Article in Journal of medical virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Elisa H FlemingDivision of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.
Eliana E OchoaDivision of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.
Joan E NicholsDivision of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.
M Kerry O'BanionDepartment of Neuroscience and Department of Neurology, University of Rochester School of Medicine, Rochester, New York.
Alan R SalkindDepartment of Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
Norbert J RobertsDivision of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.
The University of Texas Medical Branch at Galveston · USUniversity of Missouri–Kansas City · USUniversity of Rochester · US

Funding

EMERGING AND TROPICAL INFECTIOUS DISEASEST32AI007526 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SOONG, LYNN · 1997 to 2025
$3.1M
NIAID NIH HHS T32 AI007526
6 · The paper itself

Abstract

Both respiratory syncytial virus (RSV) and influenza A virus (IAV) may infect human peripheral blood mononuclear leukocytes (PBMC) during the immune response to viral challenge as the cells are recruited to the respiratory tract. The current studies demonstrated differences in PBMC responses to the two viruses very early after exposure, including reduced fos protein and CD69 expression and IL-2 production by RSV-exposed T lymphocytes. Exposure to RSV resulted in reduced lymphocyte proliferation despite evidence of a virus-specific T lymphocyte frequency equivalent to that for influenza virus. Reduced RSV-induced proliferation was not due to apoptosis, which was itself reduced relative to that of influenza virus-exposed T lymphocytes. The data indicate that differential immune responses to RSV and influenza virus are determined early after exposure of human PBMC and support the concept that the anamnestic immune response that might prevent clinically evident reinfection is attenuated very soon after exposure to RSV. Thus, candidate RSV vaccines should be expected to reduce but not prevent clinical illness upon subsequent infection by RSV. Furthermore, effective therapeutic agents for RSV are likely to be needed, especially for high-risk populations, even after vaccine development.

Indexed as

Cell ProliferationLymphocyte ActivationAntigens, CDAntigens, Differentiation, T-LymphocyteApoptosisCD69 AntigensHumansInfluenza A virusInterleukin-2Lectins, C-TypeLeukocytes, MononuclearRespiratory Syncytial Virus, HumanT-LymphocytesAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensInterleukin-2Lectins, C-Typehuman lymphocytesinfluenza viruslymphocyte activationlymphocyte proliferationrespiratory syncytial virus

Identifiers

PMID28856681
PMCPMC5690850
OpenAlexW2751665499

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.