Studentship: Identifying the role of viral protein 3A in FMDV replication

Lead Research Organisation: The Pirbright Institute
Department Name: UNLISTED

Abstract

Foot-and-mouth disease virus (FMDV) is one of the most significant animal pathogens in global agriculture, causing a highly infectious disease in multiple livestock and wildlife species. In endemic regions it continually causes enormous economic burden and contributes to food insecurity. Outbreaks in disease-free areas also incur costs in the £billions. FMDV is a non-enveloped, single-stranded, positive-sense RNA virus in the picornavirus family which also includes human pathogens such as poliovirus. New control measures for FMDV would have major economic and social value worldwide; however, the development of such measures will require a deeper understanding of the molecular mechanisms of viral replication. FMDV has a small genome and heavily relies on cellular factors to replicate; therefore identifying the host proteins that interact with viral proteins is crucially important to gain a comprehensive understanding of viral RNA replication. FMDV encodes a number of proteins (the non-structural proteins) involved in its replication. One of these proteins known as 3A has been shown to play a key role in the replication of other picornaviruses. FMDV 3A has not been extensively studied but naturally occurring mutations and deletions in 3A strongly support its involvement in replication, host tropism, attenuation and virulence. This PhD will undertake a detailed investigation of the role of the 3A protein in FMDV replication. The study will use an established reverse genetics system for engineering mutated viruses, sub-genomic reporter replicons to quantitate replication and state of the art proteomics and molecular biology techniques. This is an exciting and fundamentally important area for study as the results will give novel insight into how FMDV interacts with its host-cell to replicate its genome. Analysis of this critical stage of the viral life cycle is likely to identify novel targets for therapeutic control of FMDV.

Publications

10 25 50