Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018
Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.
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Matos Aline R, Martins Jéssica S C C, Oliveira Maria de Lourdes A, Garcia Cristiana C, Siqueira Marilda M
Аннотация
BACKGROUND: Influenza is an acute and highly contagious viral respiratory infection that causes significant morbidity and mortality. The identification of host genetic factors associated with susceptibility and severity of influenza virus infection is of paramount importance. Previous studies evaluating the potential involvement of the CCR5Δ32 polymorphism (rs333), a 32 base pair deletion in CC motif chemokine receptor 5 (CCR5) gene, in severity and mortality of influenza A(H1N1)pdm09 infected individuals have been reported, but their results are quite conflicting.
OBJECTIVES: The aim of this study was the evaluation of the CCR5Δ32 frequency in individuals with mild, severe and fatal influenza A(H1N1)pdm09 infection and its putative association with clinical and epidemiologic data.
PATIENTS/METHODS: A total of 432 individuals were included in this study and classified according to their clinical status, into the following groups: influenza like illness (ILI) (n = 153); severe acute respiratory infection (SARI) (n = 173) and fatal (n = 106) cases. The samples were collected in the post pandemic period, from 2012 to 2018. Individuals were further stratified according to their clinical and epidemiological data. The CCR5Δ32 variant was genotyped by PCR amplification and a subset of samples was further submitted to Sanger sequencing.
RESULTS: The different clinical groups (ILI, SARI and fatal) presented similar distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 allele frequencies. Genotype Δ32/Δ32 was not detected in our study. Additionally, no association between wt/wt and wt/Δ32 genotypes and dyspnea, a clinical factor for influenza complications was found. Similarly, no significant differences in the distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 variant allele frequencies were observed in samples from the different Brazilian geographical regions.
CONCLUSIONS: The CCR5Δ32 variant does not influence the susceptibility to influenza A(H1N1)pdm09 severe disease or mortality in individuals from Brazil.
OBJECTIVES: The aim of this study was the evaluation of the CCR5Δ32 frequency in individuals with mild, severe and fatal influenza A(H1N1)pdm09 infection and its putative association with clinical and epidemiologic data.
PATIENTS/METHODS: A total of 432 individuals were included in this study and classified according to their clinical status, into the following groups: influenza like illness (ILI) (n = 153); severe acute respiratory infection (SARI) (n = 173) and fatal (n = 106) cases. The samples were collected in the post pandemic period, from 2012 to 2018. Individuals were further stratified according to their clinical and epidemiological data. The CCR5Δ32 variant was genotyped by PCR amplification and a subset of samples was further submitted to Sanger sequencing.
RESULTS: The different clinical groups (ILI, SARI and fatal) presented similar distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 allele frequencies. Genotype Δ32/Δ32 was not detected in our study. Additionally, no association between wt/wt and wt/Δ32 genotypes and dyspnea, a clinical factor for influenza complications was found. Similarly, no significant differences in the distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 variant allele frequencies were observed in samples from the different Brazilian geographical regions.
CONCLUSIONS: The CCR5Δ32 variant does not influence the susceptibility to influenza A(H1N1)pdm09 severe disease or mortality in individuals from Brazil.