Award details

The Molecular Biology of FMDV

Reference	BBS/E/I/00001151
Principal Investigator / Supervisor	Dr Terry Jackson
Co-Investigators / Co-Supervisors
Institution	The Pirbright Institute
Department	The Pirbright Institute Department
Funding type	Research
Value (£)	382,566
Status	Completed
Type	Institute Project
Start date	01/04/2003
End date	30/06/2009
Duration	75 months

Abstract

The Picornavirus Structure Group carries out novel research aimed at improving knowledge of the cellular mechanisms of infection by FMDV. FMD is recognized by the OIE as the most economically important disease of livestock worldwide. The UK would greatly benefit from a new, fast-acting emergency measure for controlling the disease that blocks a critical step of the viral replication cycle without relying on the adaptive immune response. Currently, there are no anti-viral products that can be used to block infection in animals at risk of exposure or reduce excretion of virus from newly infected animals. To develop such reagents will require a deeper understanding of the molecular biology of the virus. Our main research interests are the receptors used to initiate infection, and the mechanisms of intracellular virus replication. We have identified four of the five known receptors used by FMDV. This information is allowing us to investigate the molecular determinates of receptor recognition, how FMDV enters its host cell, the mechanisms of membrane penetration by the viral genome, and the regulated expression of FMDV receptors on the epithelial cells target by the virus in the animal host. FMDV receptors are also being developed as "universal" virus-capture ligands in a number of different detection assays employed for FMDV diagnosis. Following entry into the cytosol, the viral RNA functions as a template for the synthesis of the viral proteins and the complementary negative-strand genome copies which are, in turn, used as a template for the synthesis of new progeny genomes. FMDV replication takes place on virus-induced vesicles which are believed to function as "platforms" to facilitate assembly of the viral replication complex. Here, we are interested in identifying the viral and cellular proteins that trigger host-cell membrane rearrangements and the cellular origin of the vesicles induced on infection, and to characterise the replication complex.

Summary

unavailable

Committee	Closed Committee - Biomolecular Sciences (BMS)
Research Topics	Animal Health, 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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