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Although considered by many in the west to be a rare and exotic infection, Japanese encephalitis is numerically one of the most important causes of viral encephalitis worldwide, with an estimated 50 000 cases and 15 000 deaths annually.1 2 About one third of patients die, and half of the survivors have severe neuropshychiatric sequelae. Most of China, Southeast Asia, and the Indian subcontinent are affected by the virus, which is spreading at an alarming rate. In these areas, wards full of children and young adults afflicted by Japanese encephalitis attest to its importance.
Epidemics of encephalitis were described in Japan from the 1870s onwards. Major epidemics were reported about every 10 years, with more than 6000 cases reported in the 1924 epidemic.3 The term type B encephalitis was originally used to distinguish these summer epidemics from von Economo's encephalitis lethargica (sleeping sickness, known as type A), but the B has since been dropped. In 1933 a filterable agent was transmitted from the brain of a fatal case to cause encephalitis in monkeys; the prototype Nakayama strain of Japanese encephalitis virus was isolated from the brain of a fatal case in 1935. The virus was later classed as a member of the genus Flavivirus (family Flaviviridae) named after the prototype yellow fever virus (Latin; yellow=flavi). Although of no taxonomic significance, the ecological term arbovirus is often used to describe the fact that Japanese encephalitis virus is insect (arthropod) borne.
NEUROTROPIC FLAVIVIRUSES: A GLOBAL PERSPECTIVE
Japanese encephalitis virus is transmitted between animals by Culex mosquitoes, and occurs across eastern and southern Asia and the Pacific rim. However, related neurotropic flaviviruses are found across the globe (fig 1); they share many virological, epidemiological, and clinical features.2 Molecular virological studies suggest that all flaviviruses derived from a common ancestor some 10–20 000 years ago, and …
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