Award details

Studies on peste des petits ruminants

Reference	BBS/E/I/00000252
Principal Investigator / Supervisor	Professor Thomas Barrett
Co-Investigators / Co-Supervisors
Institution	The Pirbright Institute
Department	The Pirbright Institute Department
Funding type	Research
Value (£)	50,201
Status	Completed
Type	Institute Project
Start date	01/04/1997
End date	31/03/2000
Duration	36 months

Abstract

The pathogenesis of morbillivirus infections is very poorly understood. The viruses are known to vary greatly in their pathogenic potential in any one host species and individual strains can show completely different pathogenic profiles depending on the host species infected. The basis for this restriction could be at the level of virus entry (receptor specificity / affinity) or could depend on intracellular factors required for efficient virus growth. The only morbillivirus receptor so far identified is that for measles virus (MV). This turned out to be the membrane co-factor protein (CD 46) which plays a role in protecting the hosts cells from complement lysis. Infection of cells with certain MV strains causes significant downregulation of this molecule on the cell surface and consequently increases lysis of the infected cells, thus limiting the virus pathogenicity. Many virulent, non-cell culture adapted MV strains do not cause this downregulation of CD 46 although they appear to use the molecule as a receptor. Rinderpest virus (RPV) is closely related to MV and it also causes significant downregulation of CD 46 from the surface of infected cells although it clearly does not use CD 46 as a cell receptor. In contrast to MV, both highly attenuated and highly pathogenic strains of rinderpest cause CD 46 downregulation. The phenomenon of downregulation is therefore quite independent of usage of CD 46 as a virus receptor and it does not appear to influence the pathogenicity of RPV infections. Other morbilliviruses, with the exception of peste des petits ruminants virus (PPRV) which causes a slight decrease in CD 46, have no effect on the level of expression in infected cells.

Summary

unavailable

Committee	Closed Committee - Animal Sciences (AS)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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