Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction

We determined the extent of neuronal and glial cell destruction in 13 patie nts with herpes simplex type 1 (HSV-1) encephalitis, 15 patients with tick- borne encephalitis (TBE), and 20 noninfectious controls by analyzing the ce rebrospinal fluid (CSF) concentrations of neurofilament protein (a marker o f neurons, mainly axons), neuron-specific enolase (a marker of neurons, mai nly somas), glial fibrillary acidic protein, and S-100 protein (markers of astrocytes). In addition, in patients with HSV-I encephalitis CSF samples w ere collected serially before 7, 8-14, and 18-49 days and 3-10 months after the onset of neurological symptoms. In the acute stage of HSV-1 encephalit is we found markedly higher CSF levels of the cell damage markers than in p atients with TEE. The concentration of cell damage markers in HSV-I encepha litis decreased within 45 days after acute infection, except for neurofilam ent protein. The CSF concentrations of neurofilament protein increased duri ng the second week, remained extremely high throughout the next month, and decrease thereafter. The changes in these markers of neuronal and glial des truction demonstrate the neuronal and astroglial cell damage during the fir st month after HSV-I encephalitis. In contrast, most patients with TEE had signs only of slight astrogliosis, except for two patients with paresis.