Herpes simplex virus type 1 (HSV-1) infections are widespread in developed countries, with estimates of seropositivity exceeding 50% (54). Primary infections in immunocompetent individuals are usually mild or even asymptomatic and result in lifelong latent infections in sensory ganglia and the central nervous system (CNS) (5). Reactivated HSV-1 can result in recurrent diseases of mucous membranes (e.g., gingivostomatitis and herpes labialis) and herpes keratitis, an immunopathological disease that is a leading cause of blindness (39). Also, HSV-1 is the most common cause of fatal, sporadic encephalitis in immunocompetent individuals (40, 56). Improvements in diagnosis and antiviral drug treatment have dramatically reduced the morbidity and mortality of HSV-1 encephalitis (HSE) (55), although some patients fail to respond or subsequently suffer neurological relapses after completing a standard treatment course (18,55).Clinical and animal model studies have clearly demonstrated the importance of genetic makeup in resistance to a broad range of infectious agents (15,41). In regard to HSV-1, C57BL/6 (B6) and related B10 mouse strains are resistant, while other strains, such A/J, BALB/c, 129S6 (129), and DBA/ 2J, are susceptible to fatal infections (21,23,25). In these animal models, mortality results from CNS infection. In prior studies, we defined the herpes resistance locus (Hrl) on mouse chromosome 6 as a major determinant of resistance (22, 25); however, ongoing studies indicate that resistance to HSE is genetically very complex, involving multiple interacting loci, with tumor necrosis factor playing a critical role (26) (unpublished results). The mechanism by which HSV-1 CNS infection causes death has not been defined. Counterintuitively, necropsy virus titers of nervous system tissues do not correlate with mouse resistance or susceptibility genotype (25,26). These and other observations have led to the suggestion that variation of the host inflammatory response may play a major role in determining HSV fatality. Intense inflammatory responses in CNS tissues in a mouse model of HSE have been reported, with tumor necrosis factor and macrophage chemoattractant protein 1 being expressed prominently (43). Also, in vitro and in vivo studies have shown that human and mouse microglia nonproductively infected with HSV-1 express a variety of proinflammatory cytokines and chemokines, consistent with their involvement in

We report a seven‐year‐old girl who developed a hepatitis A viral infection and encephalitis. The patient developed fever, abdominal pains and jaundice. Five days later she became delirious, combative, and did not respond to verbal commands. Laboratory studies showed elevated liver enzymes and elevated serum immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies to hepatitis A virus. Cerebrospinal fluid contained IgG antibodies to hepatitis A virus but not IgM antibodies. Polymerase chain reaction, which amplifies a portion of the hepatitis A virus genome, did not demonstrate viral nucleic acid in cerebrospinal fluid. These studies suggest that the patient may have suffered from a post‐viral hepatitis A encephalitis from which she fully recovered.

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