Award details

IAH-funded studentship: Role of Rinderpest virus non-structural proteins in blockade of Interferon signalling pathway

Reference	BBS/E/I/00001368
Principal Investigator / Supervisor	Dr Michael Baron
Co-Investigators / Co-Supervisors
Institution	The Pirbright Institute
Department	The Pirbright Institute Department
Funding type	Research
Value (£)	69,518
Status	Completed
Type	Institute Project
Start date	22/02/2008
End date	21/02/2012
Duration	48 months

Abstract

The aim of this project is to discover how a virus (rinderpest virus, a close relative of measles virus, though causing disease in cattle) gets around one of the main host defenses against viral infection: programmed cell death (apoptosis), the deliberate suicide of an infected cell to reduce viral replication and spread to neighbouring cells. We have found that rinderpest-infected cells do not undergo apoptosis, and wish to find out if the virus is blocking this process, or somehow avoiding triggering it. Whichever method the virus is using, we wish to find out which viral protein is responsible and to establish the mechanism by which it acts. We have already observed that one of the viral proteins has a direct effect on certain nuclear protein complexes that are a link point for several mechanisms of apoptosis induction, and we wish to further characterise the effects of virus infection and individual viral protiens on the structure of these complexes. These studies will increase our knowledge of how this important group of viruses interacts with host cell proteins. By comparing the relative ability of the virus to interfere with apoptosis in bovine and human cells, we hope also to cast light on why people don't get rinderpest disease. and cows don't get measles.

Summary

unavailable

Committee	Not funded via Committee
Research Topics	Animal Health, Immunology, Microbiology
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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