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Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245

Infections of the Endothelium

Issue: 2009: 102/6 (Dec) pp. 1007–1291
Pages: 1014-1023

Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro

Andrea Maisner1; James Neufeld2; Hana Weingartl2

1Institute of Virology, Philipps University, Marburg, Germany; 2National Centre for Foreign Animal Disease, Winnipeg, Canada


endothelial cells, Nipah virus, cell tropism, organ tropism, ephrin-B2


Nipah virus (NiV) is a highly pathogenic paramyxovirus that was first isolated in 1999 during an outbreak in Malaysia. In contrast to other paramyxoviruses NiV infects many mammalian species. Because of its zoonotic potential, the high pathogenicity and the lack of therapeutic treatment, NiV was classified as a biosafety level 4 pathogen. In humans NiV causes a severe acute encephalitis whereas in some animal hosts respiratory symptoms are predominantly observed. Despite the differences in the clinical outcome, microvascular endothelial cell damage predominantly underlies the pathological changes in NiV infections in all susceptible host species. NiV generally induces a pronounced vasculitis which is primarily characterised by endothelial cell necrosis and inflammatory cell infiltration. For future developments of specific antiviral therapies or vaccines, a detailed understanding of the molecular basis of NiV pathogenesis is required. This article reviews the current knowledge about natural and experimental infections in different mammals, focusing on the main organ and cell tropism in vivo, and summarises some recent studies in cell culture on the role of ephrin-B2 and -B3 receptors in NiV infection of endothelial cells.

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