Dengue and Japanese encephalitis

Abstract

This article summarizes recent research at the molecular and host population level for the two major mosquito-borne flaviviral pathogens, dengue and Japanese encephalitis. Although the flavivirus genome is completely known and complete RNA genomes have been synthesized which are capable of replicating whole viruses, the function of most genes is unclear. Current work focuses on understanding non-structural genes. These 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 inserting a small piece of negative strand dengue RNA into a mosquito. This 'antisense' RNA prevents normal replication. Meanwhile, dengue fever continues to expand as a human disease problem; outbreaks were reported as soon as US troops landed in both Somalia and Haiti. Reasons why dengue hemorrhagic fever occurs in some but not all persons infected with a second dengue virus continue to puzzle researchers. It is now clear that epidemics of dengue hemorrhagic fever in the American tropics are not caused by indigenous viruses but by viruses which were imported from Southeast Asia. Japanese encephalitis has spread to Bali, Indonesia. The good news for travellers is that a new live-attenuated Japanese encephalitis vaccine produced in China has been shown to be 98% protective against naturally occurring disease and, unlike the current mouse brain-derived vaccine, has very low rates of side reactions