tetano
Editor, Senior Moderator
BMC Res Notes. 2015 Jul 30;8:326. doi: 10.1186/s13104-015-1299-1.
[h=1]The CCR5Δ32 (rs333) polymorphism is not a predisposing factor for severe pandemic influenza in the Brazilian admixed population.[/h] Maestri A[SUP]1[/SUP], Dos Santos MC[SUP]2[/SUP], Ribeiro-Rodrigues EM[SUP]3[/SUP], de Mello WA[SUP]4[/SUP], Sousa RC[SUP]5[/SUP], Dos Santos SE[SUP]6[/SUP], Sortica VA[SUP]7[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Recent studies have tried to identify host genetic variants that could explain severe cases and deaths in infection with Influenza A(H1N1)pdm09, especially among children and young adults. CCR5 is a chemokine receptor expressed on T cells, macrophages and dendritic cells, which is an important mediator of leukocyte chemotaxis during the immune response. A deletion mutation (Δ32) in this gene interferes with the response of immune cells, impairing viral clearance. We evaluated the CCR5Δ32 polymorphism (rs333) in individuals of the Brazilian admixed population with a diagnosis of Influenza A(H1N1)pdm09 infection.
[h=4]METHODS:[/h] A total of 330 subjects with a diagnosis of Influenza A(H1N1)pdm09, evaluated at health services in the northern and northeastern regions of Brazil between June 2009 and August 2010, were genotyped for the Δ32 deletion (rs333). The cases were classified according to the progression of infection into a group of hospitalized patients (n = 156) and a group of non-hospitalized patients (n = 174).
[h=4]RESULTS:[/h] No significant differences in the allele or genotype frequencies of the CCR5Δ32 polymorphism were observed between non-hospitalized and hospitalized patients (p = 0.289 and p = 0.431, respectively).
[h=4]CONCLUSION:[/h] The Δ32 deletion in the CCR5 gene is not associated with an unfavorable outcome in patients infected with Influenza A(H1N1)pdm09 in the Brazilian admixed population.
PMID: 26223981 [PubMed - in process] PMCID: PMC4520097 Free PMC Article
[h=1]The CCR5Δ32 (rs333) polymorphism is not a predisposing factor for severe pandemic influenza in the Brazilian admixed population.[/h] Maestri A[SUP]1[/SUP], Dos Santos MC[SUP]2[/SUP], Ribeiro-Rodrigues EM[SUP]3[/SUP], de Mello WA[SUP]4[/SUP], Sousa RC[SUP]5[/SUP], Dos Santos SE[SUP]6[/SUP], Sortica VA[SUP]7[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Recent studies have tried to identify host genetic variants that could explain severe cases and deaths in infection with Influenza A(H1N1)pdm09, especially among children and young adults. CCR5 is a chemokine receptor expressed on T cells, macrophages and dendritic cells, which is an important mediator of leukocyte chemotaxis during the immune response. A deletion mutation (Δ32) in this gene interferes with the response of immune cells, impairing viral clearance. We evaluated the CCR5Δ32 polymorphism (rs333) in individuals of the Brazilian admixed population with a diagnosis of Influenza A(H1N1)pdm09 infection.
[h=4]METHODS:[/h] A total of 330 subjects with a diagnosis of Influenza A(H1N1)pdm09, evaluated at health services in the northern and northeastern regions of Brazil between June 2009 and August 2010, were genotyped for the Δ32 deletion (rs333). The cases were classified according to the progression of infection into a group of hospitalized patients (n = 156) and a group of non-hospitalized patients (n = 174).
[h=4]RESULTS:[/h] No significant differences in the allele or genotype frequencies of the CCR5Δ32 polymorphism were observed between non-hospitalized and hospitalized patients (p = 0.289 and p = 0.431, respectively).
[h=4]CONCLUSION:[/h] The Δ32 deletion in the CCR5 gene is not associated with an unfavorable outcome in patients infected with Influenza A(H1N1)pdm09 in the Brazilian admixed population.
PMID: 26223981 [PubMed - in process] PMCID: PMC4520097 Free PMC Article