Abstract
Viral encephalitis occurs in epidemic settings or is sporadic. New encephalitis patterns reflect the roles that biologic reservoirs and vectors play in determining virus-human interactions. "New" viral encephalitis can also result from human host modifications that increase susceptibility to neuroinvasive viral infection.
Three human viruses, Nipah virus, Human Herpesvirus-6, and West Nile virus, present examples of how "new" viral encephalitides emerge in a specific geographic region or clinical setting. Nipah virus encephalitis emerged after the molecular evolution of a new zoonotic viral genus within the Paramyxovirinae family. Human herpesvirus-6 encephalitis has emerged in the immune suppressed human host harboring this ubiquitous but typically benign herpesvirus. West Nile virus encephalitis has emerged in the Western hemisphere after apparent abrupt translocation of this mosquito-borne virus to a distant geographic region with immunologically naive avian and human hosts.
While the clinical features of these viral encephalitides are somewhat distinct, they each emerged as the result of human-derived factors that altered the biologic dynamic between humans and their viral pathogens.
