Eight herpesviruses cause human disease: herpes simplex virus 1 (HSV-1), herpes simplex virus 2 (HSV-2), cytomegalovirus (CMV), varicellazoster virus (VZV), Epstein-Barr virus (EBV), human herpesvirus 6 and 7, and simian herpesvirus B. All of these except HSV-7 can cause devastating central nervous system (CNS) disease. All herpesviruses contain double-stranded DNA, located at a central core with a size of 120–300 nm, average molecular weight of 80–150 million, consisting of 120 000–130 000 base pairs. HSV-1 and HSV-2 have approximately 50% homology. The most common herpesviruses causing herpes encephalitis in human beings belong to the alpha subclass of herpes-viruses, namely HSV-1, HSV-2, and VZV. They are characterized by a very short reproductive cycle, prompt destruction of the host cell, and the ability to establish latency, usually in sensory ganglia. During replication different gene classes are expressed, the immediate early gene such as thymidine kinase being particularly important for virus replication and current antiviral chemotherapy. Latency is characteristic for all herpesviruses. Persisting in an apparently inactive state for a variable duration of time, their reactivation occurs by provocative stimuli such as physical (e.g., surgery in trigeminal neuralgia) or emotional stress, fever, and exposure to ultraviolet light. Reactivation appears to be dependent upon an intact anterior pathway and peripheral pathway. Latent virus has been isolated from trigeminal, sacral, and vaginal ganglia in human beings. In animals HSV can become latent directly within the brain; so far this has not been found in human beings. Neurovirulence is the consequence of peripheral multiplication, invasion of the CNS, and growth in the CNS, but HSV isolated from encephalitic brains often differs genetically from HSV isolated from peripheral blood.
KeywordsNeurol Meningitis Thymidine Hydrocephalus Astrocytoma
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