HERPES SIMPLEX VIRUS: PATHOGENESIS AND CLINICAL PRESENTATION

Herpes simplex virus (HSV) encephalitis due to HSV type 2 occurs in babies infected perinatally. However, HSV type 1 is the most common cause of acute non-epidemic viral encephalitis among healthy children (older than 6 months of age) and adults. The estimated frequency of HSV type 1 encephalitis in the United States is 1 in 250,000 to 1 in 500,00 persons per year. This encephalitis has no seasonal preference and can occur at any time of the year. In the absence of therapy, the mortality rate exceeds 70%, and only 2.5% of patients overall (11% of survivors) regain normal function. Early treatment is the most important factor in ameliorating the morbidity and mortality of this infection.

Pathogenesis
Encephalitis with HSV type 1 can be due either to reactivation of virus or to primary infection. Approximately one third of patients develop HSV type 1 encephalitis during primary infection, and approximately two thirds acquire the disease through reactivation. Reactivation of latent HSV type 1 in the trigeminal ganglion leads to active replication of virus with subsequent spread directly to the temporal cortex. Primary HSV type 1 encephalitis results from either intranasal inoculation with direct invasion of the olfactory tract or from oral inoculation with spread along the trigeminal nerve. Whether primary infection or reactivation, the clinical syndromes are identical, producing inflammation and necrotizing lesions in the inferior and medial temporal lobes arid orbital-frontal cortex.

Clinical Presentation
HSV type 1 encephalitis typically has an abrupt onset, although an insidious, subacute presentation has been reported.
Fever is almost always present, and headaches are prominent early in the disease course. More than 90% of patients have signs that suggest a localized lesion in one or both temporal lobes, and this localization often takes the form of intense personality changes. Seizures, hemiparesis, visual field defects, and paresthesias may also be present. Symptoms often take 2 to 3 weeks to reach maximal severity, and some patients can progress rapidly to coma and death. Coexistent oral herpetic lesions are rare in HSV type 1 encephalitis.
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Herpes