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Clipboard (0)  Related Articles  1.  The C-Terminal 42 Residues
of the Tula Virus Gn Protein Regulate Interferon Induction▿ 
Journal of Virology  2011;85(10):4752-4760. Hantaviruses
primarily infect the endothelial cell lining of capillaries and
cause two vascular permeability-based diseases. The ability of
pathogenic hantaviruses to regulate the early induction of
interferon determines whether hantaviruses replicate in
endothelial cells. Tula virus (TULV) and Prospect Hill virus
(PHV) are hantaviruses which infect human endothelial cells but
fail to cause human disease. PHV is unable to inhibit early
interferon (IFN) responses and fails to replicate within human
endothelial cells. However, TULV replicates successfully in
human endothelial cells, suggesting that TULV is capable of
regulating cellular IFN responses. We observed a >300-fold
reduction in the IFN-stimulated genes (ISGs) MxA and ISG56
following TULV versus PHV infection of endothelial cells 1 day