Evidence map›Paper›PMID 33392111›Full record

ArticleFrontiers in cellular and infection microbiology2020

Fcγ Receptor IIa

María Pía Holgado, Silvina Raiden, Inés Sananez, Vanesa Seery, Leonardo De Lillo, Lucas L Maldonado, Laura Kamenetzky, Jorge Geffner, Lourdes Arruvito

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.1field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
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.

María Pía HolgadoInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, CONICET, Ciudad de Autónoma Buenos Aires, Argentina.
Silvina RaidenHospital General de Niños "Pedro de Elizalde", Ciudad Autónoma de Buenos Aires, Argentina.
Inés SananezInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, CONICET, Ciudad de Autónoma Buenos Aires, Argentina.
Vanesa SeeryInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, CONICET, Ciudad de Autónoma Buenos Aires, Argentina.
Leonardo De LilloHospital General de Niños "Pedro de Elizalde", Ciudad Autónoma de Buenos Aires, Argentina.
Lucas L MaldonadoIMPaM, CONICET, Facultad de Medicina, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina.
Laura KamenetzkyIMPaM, CONICET, Facultad de Medicina, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina.
Jorge GeffnerInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, CONICET, Ciudad de Autónoma Buenos Aires, Argentina.
Lourdes ArruvitoInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, CONICET, Ciudad de Autónoma Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARHospital Pedro de Elizalde · ARInstituto de Investigaciones Biomédicas en Retrovirus y Sida · ARUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Most patients with respiratory syncytial virus (RSV) infection requiring hospitalization have no risk factors for severe disease. Genetic variation in the receptor for the Fc portion of IgG (FcγR) determines their affinity for IgG subclasses driving innate and adaptive antiviral immunity. We investigated the relationship between FcγRIIa-H131R polymorphism and RSV disease. Methods: Blood samples were collected from 182 infants ≤24-month-old (50 uninfected, 114 RSV-infected with moderate course and 18 suffering severe disease). FcγRIIa-H131R SNP genotypic frequencies (HH, HR, RR) and anti-RSV IgG1, IgG2 and IgG3 levels were studied. Results: Genotypic frequencies for FcγRIIa-H131R SNP were comparable between uninfected and RSV-infected infants. In contrast, we found a significant higher frequency of HH genotype in severe RSV-infected children compared to moderate patients. Among severe group, HH infants presented more factors associated to severity than HR or RR patients did. Furthermore, compared to moderate RSV-infected infants, severe patients showed higher levels of anti-RSV IgG1 and IgG3. Conclusions: We found an association between an FcγRIIa (H131) polymorphism and severe RSV disease, which points towards a critical role for interactions between FcγRs and immune complexes in RSV pathogenesis. This genetic factor could also predict the worse outcome and identify those infants at risk during hospitalization.

Indexed as

Receptors, IgGRespiratory Syncytial Virus InfectionsChildHumansInfantPolymorphism, GeneticRespiratory Syncytial VirusesFc gamma receptor IIAFCGR2A protein, humanReceptors, IgGantibodiesFcγ receptorinfantsseverityvirus

Identifiers

PMID33392111
PMCPMC7775358
OpenAlexW3112651756

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.