DENGUE AND JAPANESE ENCEPHALITIS

This article summarizes recent research at the molecular and host popu lation level for the two major mosquito-borne flaviviral pathogens, de ngue and Japanese encephalitis. Although the flavivirus genome is comp letely known and complete RNA genomes have been synthesized which are capable of replicating whole viruses, the function of most genes is un clear. Current work focuses on understanding non-structural genes. The se are translated into enzymes which cleave the polyprotein, replicate RNA, and then wind and package it into viral particles, A remarkable breakthrough in host defence against viruses has been achieved by inse rting a small piece of negative strand dengue RNA into a mosquito. Thi s 'antisense' RNA prevents normal replication. Meanwhile, dengue fever continues to expand as a human disease problem; outbreaks were report ed as soon as US troops landed in both Somalia and Haiti. Reasons why dengue hemorrhagic fever occurs in some but not all persons infected w ith a second dengue virus continue to puzzle researchers. It is now cl ear that epidemics of dengue hemorrhagic fever in the American tropics are not caused by indigenous viruses but by viruses which were import ed from Southeast Asia. Japanese encephalitis has spread to Ball, Indo nesia. The good news for travellers is that a new live-attenuated Japa nese encephalitis vaccine produced in China has been shown to be 98% p rotective against naturally occurring disease and, unlike the current mouse brain-derived vaccine, has very low rates of side reactions.