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

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.

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.

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