Pathogenesis of HSE

HSV is the most commonly identified cause of acute, sporadic viral encephalitis in the United States, accounting for 10-20% of all cases (Corey, 2005). It is estimated that there are about 2.3 cases per million individuals per year. There are peaks at 5-30 years of age and at more than 50 years of age. Since the 1940s, HSV-1 and HSV-2 have been implicated in the causation of acute necrotizing encephalitis in infants, children, and adults. Encephalitis due to HSV-2 in newborn infants is a widespread disease in the brain and commonly involves a variety of other organs in the body, including the skin, eyes, and lungs (Stanberry et al., 2004). 

In general, HSE is associated with necrotic cell death resulting from virus replication and inflammatory changes secondary to virus-induced immune response (DeBiasi et al., 2002). However, there is not a perfect correlation between virus burden in the brain and the severity of histological changes and neurological symptoms. Furthermore, a small number of HSE patients are negative for HSV-1 DNA early in 

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