Aims Herpetic infection (HSV 1, 2) is the major problem of the paediatrics. The purpose of the study: detection of new pathogenetic mechanisms of development of the generalised herpetic infection in newborn children.
Methods 48 newborns were examined in the early neonatal period. 22 children had generalised herpetic infection. The control group was comprised of 26 clinically healthy newborns. The expression of TLR-2(CD14+CD282+) on monocytes was determined by the method of laser flow cytofluorometry (Beckman Coulter, USA). Polymorphism of allelic variants of TLR genes was studied by the PCR method with the subsequent restriction analysis using test systems for molecular genetic analysis developed by the State Scientific and Research Institute for Genetics and Selection of Industrial Microorganisms GENETIKA (Moscow).
Results The clinical presentation was characterised by meningoencephalitis – 4.6%, hepatitis – 13.6%, hypotrophy – 9.1%, pneumonia – 31.8%, central nervous system suppression syndrome – 45.5%, convulsive disorder – 40.9%, lymphadenitis – 27.3%.
A definitive reduction of TLR–2 expression (CD14+CD282+) on monocytes of the peripheral blood (43.8 ± 8.3% against 76.2 ± 5.6%) was detected in the basic group as compared with the control group. The reduction of TLR-2 expression explains high sensitivity of newborns to the herpetic infection. It is established that newborns with the generalised herpetic infection had definitively higher frequency (26.3% and 3.8%, correspondingly, p < 0.05) of Arg753Gln genotype of TLR-2 gene as compared with the control group. Thus, allelic variants of TLR gene in the points of Arg753Gln polymorphism may be genetic risk markers of the development of the generalised form of infection caused by HSV of type 1, 2 in newborns.
Conclusion In case of the generalised herpetic infection there is a reduction of TLR-2 expression on monocytes and Arg753Gln polymorphism of TLR-2 gene is detected which results in the disturbance of interrelation between the inborn and adaptive immune response and is one of the mechanisms of the generalised herpetic infection development.
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