Studentship: Analysis of the function of infectious bronchitis virus accessory proteins-towards better vaccines

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

A key area of research in animal disease is the development of more effective and efficient vaccines to prevent infection and transmission. To be able to achieve this objective, a better understanding of virus interaction with host cells and viral pathogenicity factors is required. The avian coronavirus infectious bronchitis virus (IBV) causes respiratory disease in chickens, and some strains cause pathology in the kidneys and reproductive tract. Virus infection results in significant losses to worldwide poultry industries due to reduced meat quality and reduced egg quality and production. Although both live attenuated and killed vaccines are available for IBV, there is poor cross protection between viral strains and the mechanism of attenuation of vaccine viruses is poorly understood. There is a real requirement for improved strategies for IBV vaccine design and understanding molecular aspects of virus replication will provide new insight for this. IBV encodes 5 accessory proteins, including the recently described gene 4b. The function of these accessory proteins is not understood, although they are known not to be required for virus replication in cell culture. The accessory proteins of other coronaviruses including mouse hepatitis virus (MHV) and SARS-coronavirus (SARS-CoV) have been shown to play a role in replication of viral RNA, evasion of host immune responses and modulation of host cell transcription. Although genetically distinct from the accessory proteins from MHV and SARS-CoV, it is possible that the function of the IBV accessory proteins may be similar. The objectives of this project will be to characterise more fully the function of accessory proteins 3a, 3b and 4b on virus replication and identify host cell and viral interaction partners. This will be achieved by virological, molecular biology and proteomic techniques, initially utilising existing recombinant viruses lacking these genes.

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