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Immune suppression by morbilliviruses

ReferenceBBS/E/I/00000721
Principal Investigator / Supervisor Professor Thomas Barrett
Co-Investigators /
Co-Supervisors
Institution The Pirbright Institute
DepartmentThe Pirbright Institute Department
Funding typeResearch
Value (£) 153,554
StatusCompleted
TypeInstitute Project
Start date 01/10/1997
End date 30/09/2000
Duration36 months

Abstract

A major factor influencing mortality following morbillivirus infections is their ability to cause transient immune suppression in the host. This enables secondary pathogens to flourish in the host. The mechanism whereby morbilliviruses cause immune suppression is not well understood. In this study immune suppression induced by all the known morbilliviruses (MV, RPV, PPRV, DMV, PDV and CDV) is being examined in the light of several mechanisms that have recently been proposed. These include CD46 (the putative MV receptor) which, when cross-linked to MV, results in a reduction in cytokine (IL12) production by monocytes. This cytokine is critical for the generation of a cell-mediated immune response and other cell ligands also produce this effect. RPV binds to and downregulates CD 46 in a similar way to MV, PPRV causes a very slight downregulation, while the other morbilliviruses have no effect on its expression and so this may not be a universal means whereby morbillivirus cause immune suppression. Another mechanism shown to be operating in MV infections is the inhibition of proliferative responses in peripheral blood lymphocytes (PBLs) when incubated with MV infected, UV-irradiated autologous peripheral blood lymphocytes (presenter cells) or with UV-irradiated virus. Similarly, these presenter cells or UV-irradiated virus can inhibit growth of BJAB cells in culture. This phenomenon has now been shown to occur with all other morbilliviruses and work is ongoing to show which virus proteins are involved in this suppression and the mechanism whereby the cells are induced to die.

Summary

unavailable
Committee Closed Committee - Animal Sciences (AS)
Research TopicsX – not assigned to a current Research Topic
Research PriorityX – Research Priority information not available
Research Initiative X - not in an Initiative
Funding SchemeX – not Funded via a specific Funding Scheme
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