ArticleBMC research notes2014
The CCR5Δ32 allele is not a major predisposing factor for severe H1N1pdm09 infection.
Article in BMC research notes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- A systematic review and meta-analysis of host genetic factors associated with influenza severity.BMC genomics · 2021Pooled it
- The Dual Role of CCR5 in the Course of Influenza Infection: Exploring Treatment Opportunities.Frontiers in immunology · 2021Review
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Metabolomics as an Approach to Characterise the Contrasting Roles of CCR5 in the Presence and Absence of Disease.International journal of molecular sciences · 2020Review
- Influenza Pathogenesis: The Effect of Host Factors on Severity of Disease.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
- Host genetics of severe influenza: from mouse Mx1 to human IRF7.Current opinion in immunology · 2016Review
- Host genes and influenza pathogenesis in humans: an emerging paradigm.Current opinion in virology · 2015Review
- The CCR5Δ32 (rs333) polymorphism is not a predisposing factor for severe pandemic influenza in the Brazilian admixed population.BMC research notes · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHost genetic factors are thought to modulated the severity of disease caused by infection with the 2009 H1N1 pandemic influenza virus (H1N1pdm09). The human CCR5 gene encodes a cytokine receptor important for cell-mediated immune response against H1N1pdm09. A 32-bp polymorphic deletion in the coding sequence of CCR5, the so-called CCR5Δ32 allele, segregates in populations of European ancestry with a frequency of 8-15%. A high proportion of CCR5Δ32 heterozygotes was reported in a sample of white Canadian critically-ill H1N1pdm09 infected subjects, suggesting an association with disease severity.
methodsWe recruited 29 H1N1pdm09 infected subjects from Southern Europe (mostly Italians) with a wide clinical spectrum of disease symptoms; the sample included 7 subjects who developed acute respiratory distress syndrome requiring extracorporeal membrane oxygenation. The CCR5Δ32 variant was genotyped in all subjects.
resultsThe CCR5Δ32 allele was found in one single subject, who developed a very mild form and was not hospitalized.
conclusionsThe CCR5Δ32 allele was not found to be associated with the risk of H1N1pdm09 infection or with a severe disease course.
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Registered trials
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.