Herpes simplex virus encephalitis: new infection or reactivation?

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Purpose of review

This review describes the pathogenesis, clinical presentation, course, and therapy of herpes simplex encephalitis (HSE), the most fatal viral encephalitis, in which prognosis is dependent on early diagnosis and effective therapy.

Recent findings

Herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2) are human neurotropic viruses that establish latent infection in dorsal-root ganglia for the entire life of the host. From this reservoir, they can reactivate to cause human morbidity and mortality. HSE is one of the most devastating disorders caused by these viruses. The biology of their ability to establish latency, maintain it for the entire life of the host, reactivate, and cause primary and recurrent disease is being studied in animal models and in humans. Of special interest is the question whether HSE is the result of primary infection or is it the outcome of reactivation. The present review covers the biological, medical, and neurological aspects of HSE, focusing among others on recent molecular findings of gene expression during latent infection of HSV-1.


Despite accumulating knowledge, there are still several issues regarding both pathogenesis and therapy of HSV-1 that currently defy understanding.

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