The first known human Nipah virus (genus Henipavirus,family Paramyxoviridae) outbreak was from 1998–1999in Malaysia and Singapore involving more than 350 peo-ple [1]. In Bangladesh and India there were several recur-ring Nipah virus (NiV) outbreaks starting 2001 affectingabout 120 people so far. The incubation period was a fewdays to 2 weeks. Clinical manifestations ranged fromfever, headache, drowsiness and cough to a fatal acuteencephalitic syndrome with a mortality rate of 40% to75% [1]. Human autopsy studies showed acute NiV infec-tion to be a systemic infection [2]. Blood vessels andparenchymal cells in most major organs were affected. Inblood vessels, the earliest lesion seemed to be theendothelial multinucleated syncytia, followed byendothelial ulceration, intramural inflammation andnecrosis. Viral antigens and nucleocapsids were localizedto endothelium, syncytia and tunica media. Associatedthrombosis and vascular occlusion was often observedand gave rise to microinfarction. The brain was mostseverely involved by disseminated vascular lesions.Around vasculitic vessels with or without microinfarction,surviving neurons or other parenchymal cells may revealviral inclusions, antigens/RNA and nucleocapsids. Vascu-litis, parenchymal lesions and viral antigens could also befound in the lung, kidney, heart and other organs. In thelung, fibrinoid necrosis, vasculitis, alveolar multinucle-ated giant cells were observed. Kidney pathology wascharacterized mainly by vasculitis and glomerular lesions.Multinucleated syncytia probably arising from podocyteswas occasionally noted.The golden hamster was reported to be a good model foracute NiV infection [3]. Infected hamsters developed neu-rological features and evidence of systemic vasculitis,multi-organ parenchymal and central nervous systeminfection confirming findings in human autopsies. Like inhuman cases, viral antigens/RNA and nucleocapsids weredemonstrable in blood vessels and susceptible parenchy-mal cells. This confirmed the unique double pathogeneticmechanism of tissue injury arising from infarction anddirect parenchymal infection. Successful intranasal inocu-lation suggested that oral and/or respiratory tract could bea major route of infection in humans via contaminatedpig or patient secretions.In infections of the pig and cat, the main pathology wasapparently in the respiratory system and meninges. Therewas evidence of pneumonia characterized by bronchialand alveolar inflammation, associated with multinucle-ated cells with viral inclusions and antigens. Vasculitisand meningitis was severe but encephalitis was rare ormild. In the pig, viral antigens were apparently moreprominent in glial cells than neurons, and were also dem-onstrated in cranial nerves, olfactory bulb and cerebralcortex.