HHV-6A, HHV-6B, and HHV-7 in Encephalitis

Among etiological agents of sporadic viral encephalitis, human herpesvirus (HHV)-6A, HHV-6B, and HHV-7 have been identified. In immunocompetent individuals, exanthema subitum rarely associates with encephalitis and sequelae, whereas HHV-7 might induce serious encephalitis with generalized symptoms. Risk factors for reactivation of HHV-6 and HHV-7 and encephalitis are unrelated cord blood cell transplantation, repeated hematopoietic stem cell transplantation, young age, immunsuppressive and cytotoxic drugs, and chromosomally integrated HHV-6. The most severe manifestation is the syndrome of posttransplantation acute limbic encephalitis (PALE), which is associated with high morbidity. Posterior reversible encephalopathy syndrome (PRES) is associated with medical interventions in underlying disorders. HHV-6 enters the brain via the olfactory route, spreads to the brain stem, hippocampus, limbic tissue, and cerebrospinal fluid (CSF). Proinflammatory cytokines mediate inflammation. Early and serial quantitation of HHV-6A, HHV-6B, and HHV-7 in CSF is used to monitor disease course. Ganciclovir, valganciclovir, foscarnet therapy, and preemptive therapy can eliminate viruses in the majority of cases.