Henipavirus Encephalitis: Recent Developments and Advances

The genus H enipavirus within the family P aramyxoviridae includes the Hendra virus ( HeV ) and N ipah virus ( NiV ) which were discovered in the 1990s in A ustralia and M alaysia, respectively, after emerging to cause severe and often fatal outbreaks in humans and animals. While HeV is confined to A ustralia, more recent NiV outbreaks have been reported in B angladesh, I ndia and the P hilippines. The clinical manifestations of both henipaviruses in humans appear similar, with a predominance of an acute encephalitic syndrome. Likewise, the pathological features are similar and characterized by disseminated, multi‐organ vasculopathy comprising endothelial infection/ulceration, vasculitis, vasculitis‐induced thrombosis/occlusion, parenchymal ischemia/microinfarction, and parenchymal cell infection in the central nervous system ( CNS ), lung, kidney and other major organs. This unique dual pathogenetic mechanism of vasculitis‐induced microinfarction and neuronal infection causes severe tissue damage in the CNS . Both viruses can also cause relapsing encephalitis months and years after the acute infection. Many animal models studied to date have largely confirmed the pathology of henipavirus infection, and provided the means to test new therapeutic agents and vaccines. As the bat is the natural host of henipaviruses and has worldwide distribution, spillover events into human populations are expected to occur in the future.