Immunopatological and genetic aspects of pathogenesis of CNS lesions in VZV infection

Abstract

The review article provides information about the features of the Varicella-zoster virus (VZV), about the clinical manifestations of CNS damage in acute and chronic VZV infection in children and adults, about the mechanisms of interaction of the pathogen with the immune system during the development of the disease. The question of whether to consider neurological disorders in VZV infection as a complication or manifestation of the disease caused by a defective virus or the presence of subclinical immunodeficiency is discussed, which is confirmed by modern scientific studies. The critical mechanisms of immune defense against VZV, which are the main reason for the penetration of the virus into the CNS and the development of neurological disorders, as well as the relationship between VZV genotypes, the presence of mutations in the gE gene and the nature of the course, the identification of rare variants of the POLR3A, POLR3C, POLR3E and POLR3F genes associated with violation of IFNs induction, and the development of severe VZV infection, in which vasculopathy also occurs, which is the basis for the use of vascular drugs of complex action, such as Cytoflavin, the effectiveness of which has been proven by the authors. A special place is given to the analysis of intrathecal immunopathogenesis, which is likely to be associated with the presence and severity of neurological manifestations, their relapses. The issue of the causes of the development of a severe course of the disease in patients vaccinated against chickenpox, as well as the issue of resistance to specific antiviral drugs, probably associated with the presence of mutations responsible for the resistance of the virus to therapy, is discussed.