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AIM: To explore the relationship between the TaqI restriction fragment length polymorphism (RFLP) in the 3’-untranslated region (UTR) of IL-12p40 gene or the length polymorphism in the promoter of IL-12p40 gene and the clinical phenotype of infantile RSV infection. METHODS: One hundred and fifty-seven infants with RSV lower respiratory infection (106 bronchiolitis and 51 pneumonia, of them 53 were severe) and 48 healthy children as control were enrolled in the study. Direct immunofluorescence technique was utilized to identify RSV antigen in the respiratory epithelium cells. The Taql restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene was detected by polymerase chain reaction (PCR), followed by TaqI digestion, agarose gel electrophoresis and sequencing, and the IL-12p40 gene promoter polymorphism by PCR, followed by polyacrylamide gel electrophoresis (PAGE) and sequencing. RESULTS: 1) The TaqI restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene was confirmed by PCR, TaqI enzyme digestion and/or sequencing, defined as allele A without Taql digestion site, allele B with TaqI digestion site, and allele AB (heterozygote). 2) No significant differences in the TaqI restriction enzyme site potymorphism in the 3’-UTR of IL-12p40 gene were found among RSV bronchiolitis, RSV pneumonia and control groups. 3) Mild RSV infection infants showed no difference in the TaqI restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene from that of severe cases. 4) The 1L- 12p40 gene promoter polymorphism was confirmed by PCR, PAGE and/or sequencing, defined as allele 1.1 with the PCR production of 162 base pairs, allele 2.2 with the PCR production of 158 base pairs and allele 1.2 (heterozygote). 5) No significant differences in the IL-12p40 gene promoter polymorphism were found among RSV bronchiolitis, RSV pneumonia and control groups. 6) Heterozygosity (allelel.2) for the IL-12p40 promoter polymorphism was observed in a much higher rate (71.7％) in severe RSV infection patients than those with mild RSV infection (43.3％) and control groups (47.9％), while no differences were found between the latter two groups. CONCLUSIONS: 1) No relationship between the TaqI restriction enzyme site polymorphism in the 3’-UTR of IL- 12p40 gene and the clinical phenotypes of infantile RSV infection was found. 2) The IL-12p40 gene promoter polymorphism is associated with the severity of RSV infection, with a much higher rate of heterozygosity (allele 1.2) in severe RSV infection patients than those with mild infection.
AIM: To explore the relationship between the TaqI restriction fragment length polymorphism (RFLP) in the 3’-untranslated region (UTR) of IL-12p40 gene or the length polymorphism in the promoter of IL-12p40 gene and the clinical phenotype of infantile RSV METHODS. One hundred and fifty-seven infants with RSV lower respiratory infection (106 bronchiolitis and 51 pneumonia, of them 53 were severe) and 48 healthy children as control were enrolled in the study. Direct immunofluorescence technique was utilized to identify RSV antigen in the respiratory epithelium cells. The Taql restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene was detected by polymerase chain reaction (PCR), followed by TaqI digestion, agarose gel electrophoresis and sequencing, and the IL-12p40 gene promoter polymorphism by PCR, followed by polyacrylamide gel electrophoresis (PAGE) and sequencing. RESULTS: 1) The TaqI restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene was confi rmed by PCR, TaqI enzyme digestion and / or sequencing, defined as allele A without Taql digestion site, allele B with TaqI digestion site, and allele AB (heterozygote). 2) No significant differences in the TaqI restriction enzyme site potymorphism in the 3 ’-UTR of IL-12p40 gene were found among RSV bronchiolitis, RSV pneumonia and control groups. 3) Mild RSV infection infants showed no difference in the TaqI restriction enzyme site polymorphism in the 3’-UTR of IL-12p40 gene from that of severe cases. 4) The 1L-12p40 gene promoter polymorphism was confirmed by PCR, PAGE and / or sequencing, defined as allele 1.1 with the PCR production of 162 base pairs, allele 2.2 with the PCR production of 158 base pairs and allele 1.2 ( 5) No significant differences in the IL-12p40 gene promoter polymorphism were found among RSV bronchiolitis, RSV pneumonia and control groups. 6) Heterozygosity (allelel.2) for the IL-12p40 promoter polymorphism was observed in a much higher rate (71.7% )in severe RSV infection patients than those with mild RSV infection (43.3%) and control groups (47.9%), while no differences were found between the latter two groups. CONCLUSIONS: 1) No relationship between the TaqI restriction enzyme site polymorphism in the 3 ’-UTR of IL-12p40 gene and the clinical phenotypes of infantile RSV infection was found. 2) The IL-12p40 gene promoter polymorphism is associated with the severity of RSV infection, with a much higher rate of heterozygosity (allele 1.2) in severe RSV infection patients than those with mild infection.