Human viral infections as a contributor to failure of repair
This area of investigation is conducted in collaboration with Dr. David Mock.
Latency viral infections are commonplace in human brains but their role and impact of injury and repair events is for many virus not understood. Our interest is focus on the impact of human herpesvirus (HHV6) infection on the capacity of the CNS to engage in self repair. We have shown that viral infection of oligodendrocytes precursor cells (OPCs), the ancestors of oligodendrocytes and astrocytes, causes changes in morphology (see Figure 3), cell cycle arrest, loss of self-renewal, and premature differentiation in both human and murine OPCs (Dietrich et al, 2005 J of Neuroscience). We are now characterizing the molecular pathway by which the virus is achieving these impairments of precursor cell function and have identified a specific viral protein that is able to elicit the cell cycle disruption. Using a transfection approach we are now able to study viral function in a murine model, which allowed us to extend our observations from the in vitro experiments into an in vivo setting. Through a demyelinating transplantation model we can for the first time compare infected and control cells in their ability to migrate, proliferate and differentiation in a lesion environment and quantify their ability to contribute to repair of demyelinating lesions.
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