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Viral evasion gene reveals new targets for eliminating chronic infections
Date:1/5/2011

68, which establishes chronic infections in mice and provides a model of the workings of the human gamma herpesvirus Epstein-Barr Virus, commonly known to cause infectious mononucleosis, or 'kissing disease'. Their results, which have been published in the Journal of Immunology show that a viral gene called K3 rapidly disables the antigen-processing machinery normally used by dendritic cells to alert the immune system to infections.

"This gene quickly helps the virus to hide from the immune system by subverting normal antigen presentation to T cells, which have the critical task of destroying virally-infected cells," Dr Belz said. "The virus carries out a top-secret operation. It shuts down the normal mechanisms that allow the immune system to recognise an infection and then boards the antigen-presenting cells which ferry the virus through the blood and tissues, allowing it to spread throughout the body and establish system infection."

Dr Belz said the study could change conventional views on the best way to generate an immune response to combat chronic infections.

"Our research shows that viral evasion of the immune system in chronic infections happens incredibly early," Dr Belz said. "Dendritic cells are compromised long before they have the chance to interact with T cells for the next phase of the immune response, so the T cells are never really activated properly. If we want to make an effective vaccine, we need to look at these early escape points used by the virus as the first target for trying to generate a more efficient immune response that will contain the virus and prevent it establishing a systemic infection."


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Contact: Penny Fannin
fannin@wehi.edu.au
61-393-452-345
Walter and Eliza Hall Institute
Source:Eurekalert  

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