Hendra virus and Nipah virus comprise the Henipavirus genus within Paramyxovirinae (Wang et al. 2001). Hendra has a nonsegmented, negative stranded, 18.2 kb RNA genome with long untranslated regions at the 3’ end. Rinderpest virus reacts weakly to HeV-infected cells in immunofluorescence and immunoblot tests (Selleck unpub., cited in Murray et al. 1995), and NiV and HeV cross-react under ELISA, immunohistochemistry, and immunofluorescence (Barclay and Paton 2000, Wang et al. 2001). Unlike NiV, HeV has 10- and 18 nm surface projections that give it a “double fringe” appearance under electron microscopy (Murray et al. 1995). Like other paramyxoviruses, HeV is easily destroyed by heat, lipid solvents, non-ionic detergents, formaldehyde, and oxidizing agents (Barclay and Paton 2000).
HeV is unique in its ability to grow in cell cultures from birds, reptiles, amphibians, fish, and many mammals (Westbury et al. 1995). Electron microscopy, PCR, indirect immunofluorescence and peroxidase tests for antigens in infected tissues, microtiter assays, serum neutralization tests, and ELISA were traditionally used to identify HeV (Crameri et al. 2002); ELISA replaced serum neutralization tests after the Brisbane outbreak (Daniels et al. 2001), though Black et al. (2001) used SN in their study. They report >95% sensitivity and 100% specificity; sensitivity is apparently 100% in animals that have been infected a sufficient time to mount an antibody response (Daniels unpub., reported in Black et al. 2001). Recently, Crameri et al. (2002) have developed a rapid immune plaque assay for HeV and NiV that allows for virus and antibody detection in non-BSL4 conditions.
Author: S. Cobey.