Laboratory of Arbovirology
Research on vector-borne viral diseases: molecular biology, molecular epidemiology, pathogenesis of viral diseases.
Current research projects
Differences in clinical course of tick-borne encephalitis in host, and their genetic determination.
Tick-borne encephalitis (TBE), a disease caused by tick-borne encephalitis virus (TBEV), represents a serious viral neuroinfection of humans. Despite the medical importance of this disease, some crucial steps in the development of encephalitis remain poorly understood. In humans, TBEV may produce a variety of clinical symptoms, from an asymptomatic disease to a fever and acute or chronic progressive encephalitis. This is influenced by a variety of factors, e.g. inoculation dose and virulence of the virus, age and immune status of the host, but also, as our preliminary results strongly suggest, by susceptibility based on host genetic background. Here, we propose a research project to study differences in clinical course of tick-borne encephalitis, and its genetical determination. As a model for TBE, recombinant congenic mouse strains will be used, since these mice develop TBE of various severity, and this correlates with the situation in humans. Results of this project should improve our understanding of the genetic basis of seriousness of this important infection.
Mechanisms of neuronal injury during tick-borne encephalitis virus infection of the CNS
The mechanisms of TBEV-induced injury to the central nervous system (CNS) are unclear. To address this issue we study interactions of TBEV with primary human neurons, mechanisms of their injury and antiviral defence, as well as the interaction of the infected neurons with other key cells in the CNS (astrocytes, pericytes, microglia and brain microvascular epithelial cells). We propose that the innate immune response is an important cause of neuron death during the acute infection.This is in contrast to the prevailing hypothesis that neuron loss is mediated solely by virus. The results of this project should provide new crucial data about the neuropathogenesis of TBE.