Award details

Studentship: Characterisation of inhibition of the innate apoptotic response by classical swine fever virus

Reference	BBS/E/I/00002121
Principal Investigator / Supervisor	Dr Julian Seago
Co-Investigators / Co-Supervisors	Dr Elizabeth Reid
Institution	The Pirbright Institute
Department	The Pirbright Institute Department
Funding type	Research
Value (£)	46,570
Status	Completed
Type	Institute Project
Start date	05/10/2015
End date	31/03/2017
Duration	17 months

Abstract

Upon viral infection host cells recognise and respond to pathogens through innate immune responses. However, in order to infect target host cells and produce infectious progeny, viruses have developed various strategies to circumvent such responses. For example, classical swine fever virus (CSFV) antagonises both the production of type-1 IFN and the initiation of apoptosis. CSFV is the causative agent of classical swine fever (CSF), an economically important disease of pigs. Our research group is involved in characterising the multiple functions of a CSFV non-structural protein termed Npro. We and others have shown that Npro contributes towards the observed CSFV antagonism of both the IFN and apoptotic responses (Johns et al., 2010; Seago et al., 2007), however the underlying mechanisms have not been fully determined. The proposed project will further investigate the ability and mechanism by which Npro facilitates evasion of apoptosis. Initially, the student will characterise the repertoire of porcine cell types in which Npro can antagonise the apoptotic response. Npro will be expressed in these different cell types using lentiviral constructs that the student will make using established techniques. Apoptosis in the respective cells will be monitored using a variety of molecular and immunological assays. In order to identify the functions of Npro through its physical interactions with host proteins our group has previously performed yeast-two-hybrid screens. One host protein identified in the screen was TID1. TID1 has recently been shown to participate in mitochondrial-mediated apoptosis (Ahn et al., 2010). This part of the project will further characterise the putative Npro/TID1 interaction and investigate its role in apoptosis.

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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