Abstract
The role of vitamin D in innate and adaptive immunity is recently under investigation. In this study we explored the potential association of genetic variances in vitamin D pathway and infections in infancy. Τhis prospective case–control study included infants 0–24 months with infection and age-matched controls. The single nucleotide polymorphisms of vitamin D receptor (VDR) gene (BsmI, FokI, ApaI, TaqI), vitamin D binding protein (VDBP) (Gc gene, rs7041, rs4588) and CYP27B1 (rs10877012) were genotyped by polymerase chain reaction-restriction fragment length polymorphism. In total 132 infants were enrolled, of whom 40 with bacterial and 52 with viral infection, and 40 healthy controls. As compared to controls, ΤaqI was more frequent in infants with viral infection compared to controls (p = 0.03, OR 1.96, 95% CI 1.1–3.58). Moreover, Gc1F was more frequent in the control group compared to infants with viral infection (p = 0.007, OR 2.7, 95% CI 1.3–5.6). No significant differences were found regarding the genetic profile for VDR and VDBP in infants with bacterial infection compared to the controls and also regarding CYP27B1 (rs10877012) between the studied groups. Genotypic differences suggest that vitamin D pathway might be associated with the host immune response against viral infections in infancy.
Highlights
ΤaqI polymorphism, t allele, was more frequent in infants with viral infection compared to controls (p = 0.03, odds ratio (OR) 1.96 95% CI 1.1–3.58)
We demonstrated that polymorphisms of the vitamin D receptor (VDR) gene, in particular TaqI, are associated with viral infections and in particular with viral respiratory tract infections, in infants
The aforementioned studies support the results of our study since group- specific component 1 fast (Gc1F) was more frequent in the control group compared to infants with viral infections and may explain the protective effect that may confer against viral infections since Gc1F may enhance the host response against viral infections
Summary
Initial heating at 94 °C for 3 min 35 cycles of: 94 °C for 30 s, 59 °C for 30 s, 72 °C for 30 s Final extension step at 94 °C 10 min Initial heating at 94 °C 3 min 35 cycles of: 94 °C for 30 s, 57 °C for 30 s, 72 °C for 30 s Final extension step at 72 °C for 10 min Initial heating at 94 °C 3 min 36 cycles of: 94 °C for 30 s, 58 °C for 30 s, 72 °C for 30 s Final extension step at 72 °C for 10 min Initial heating at 95 °C for 15 min 35 cycles of: 94 °C for 45 s, 51 °C for 45 s, 72 °C for 45 s Final extension step at 72 °C for 7 min Initial heating at 94 °C for 5 min 30 cycles of: 94 °C for 45 s, 58 °C for 45 s, 72 °C for 45 s Final extension step at 72 °C for 7 min the VDR gene: FokI (rs2228570) G/A change in exon 2, TaqI (rs731236) T/C change in exon 9, BsmI (rs1544410) A/G and ApaI (rs7975232) G/T change in intron 816–18. The two most common SNPs of Gc gene are rs7041 T/G change (Asp416Glu) and rs4588 C/A change (Thr420Lys) in exon 11 (six haplotypes are observed); the composite genotype of these two SNPs results in the three variants of the Gc gene (rs7041T-rs4588C, rs7041G-rs4588C and rs7041T-rs4588A) that encode the three major electrophoretic variants of VDBP (allozymes), termed group- specific component 1 fast (Gc1F), Gc1 slow (Gc1S) and Gc2 r espectively[19,20,21]. Up to date data regarding the role of vitamin D pathway in susceptibility to infections in this age group are limited
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