Evidence map›Paper›PMID 26696552›Full record

ArticleArchives of medical research2015

Differential Immune Profiles in Two Pandemic Influenza A(H1N1)pdm09 Virus Waves at Pandemic Epicenter.

Lourdes Arriaga-Pizano, Eduardo Ferat-Osorio, Gabriela Rodríguez-Abrego, Ismael Mancilla-Herrera, Esteban Domínguez-Cerezo, Nuriban Valero-Pacheco, Marisol Pérez-Toledo, Fernando Lozano-Patiño, Fernando Laredo-Sánchez, José Malagón-Rangel and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Archives of medical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Genes · 2021
    Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 3 countries.

Lourdes Arriaga-PizanoMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
Eduardo Ferat-OsorioMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico; Gastrointestinal Surgery Service, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
Gabriela Rodríguez-AbregoClinical Epidemiology Service, Regional Hospital No, 1, IMSS, Mexico.
Ismael Mancilla-HerreraInfectology and Immunology department, National Institute of Perinatology, SSA, Mexico City, Mexico.
Esteban Domínguez-CerezoMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico; Graduate Program on Immunology, ENCB-IPN, Mexico City, Mexico.
Nuriban Valero-PachecoMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico; Graduate Program on Immunology, ENCB-IPN, Mexico City, Mexico.
Marisol Pérez-ToledoMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico; Graduate Program on Immunology, ENCB-IPN, Mexico City, Mexico.
Fernando Lozano-PatiñoInternal Medicine Service, Specialties Hospital of the National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
Fernando Laredo-SánchezInternal Medicine Service, Specialties Hospital of the National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
José Malagón-RangelInternal Medicine Service, Specialties Hospital of the National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
Haiko Nellen-HummelInternal Medicine Service, Specialties Hospital of the National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
César González-BonillaUnit for Epidemiological Surveillance, National Medical Center La Raza, IMSS, Mexico City, Mexico.
Gabriel Arteaga-TroncosoCellular Biology department, National Institute of Perinatology, SSA, Mexico City, Mexico.
Arturo Cérbulo-VázquezEducation and Research Division, Woman's Hospital, Health Ministry, Mexico City, Mexico.
Rodolfo Pastelin-PalaciosChemistry Faculty, National Autonomous University of Mexico (UNAM), Mexico City, Mexico.
Paul KlenermanOxford Biomedical Research Centre and Oxford Martin School, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Armando IsibasiMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico.
Constantino López-MacíasMedical Research Unit in Immunochemistry, Specialties Hospital, National Medical Center Siglo XXI, IMSS, Mexico City, Mexico; Visiting Professor of Immunology, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Electronic address: constantino@sminmunologia.org.
Mexican Social Security Institute · MXInstituto Nacional de Perinatología · MXUniversity of Oxford · GBCentro Médico Nacional La Raza · MXInstituto Politécnico Nacional · MXUniversidad Nacional Autónoma de México · MXWoman's Hospital · US

Funding

Wellcome Trust 091663
6 · The paper itself

Abstract

BACKGROUND AND

aimsSevere influenza A(H1N1)pdm2009 virus infection cases are characterized by sustained immune activation during influenza pandemics. Seasonal flu data suggest that immune mediators could be modified by wave-related changes. Our aim was to determine the behavior of soluble and cell-related mediators in two waves at the epicenter of the 2009 influenza pandemic.

methodsLeukocyte surface activation markers were studied in serum from peripheral blood samples, collected from the 1(st) (April-May, 2009) and 2(nd) (October 2009-February 2010) pandemic waves. Patients with confirmed influenza A(H1N1)pdm2009 virus infection (H1N1), influenza-like illness (ILI) or healthy donors (H) were analyzed.

resultsSerum IL-6, IL-4 and IL-10 levels were elevated in H1N1 patients from the 2(nd) pandemic wave. Additionally, the frequency of helper and cytotoxic T cells was reduced during the 1(st) wave, whereas CD69 expression in helper T cells was increased in the 2(nd) wave for both H1N1 and ILI patients. In contrast, CD62L expression in granulocytes from the ILI group was increased in both waves but in monocytes only in the 2(nd) wave. Triggering Receptor Expressed on Myeloid cells (TREM)-1 expression was elevated only in H1N1 patients at the 1(st) wave.

conclusionsOur results show that during the 2009 influenza pandemic a T cell activation phenotype is observed in a wave-dependent fashion, with an expanded activation in the 2(nd) wave, compared to the 1(st) wave. Conversely, granulocyte and monocyte activation is infection-dependent. This evidence collected at the pandemic epicenter in 2009 could help us understand the differences in the underlying cellular mechanisms that drive the wave-related immune profile behaviors that occur against influenza viruses during pandemics.

Indexed as

AdolescentAdultAgedAntigens, CDAntigens, Differentiation, T-LymphocyteBiomarkersCD4 Lymphocyte CountCD69 AntigensFemaleHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanInterleukin-10Interleukin-4Interleukin-6Lectins, C-TypeAntigens, CDAntigens, Differentiation, T-LymphocyteBiomarkersCD69 AntigensIL10 protein, humanIL4 protein, humanIL6 protein, humanInterleukin-10Interleukin-4Interleukin-6Lectins, C-TypeL-SelectinMembrane GlycoproteinsReceptors, ImmunologicTREM1 protein, humanTriggering Receptor Expressed on Myeloid Cells-1Immune profilesPandemic A(H1N1)pdm2009 influenzaPandemic waves

Identifiers

PMID26696552
PMCPMC4914610
OpenAlexW2219842640

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.