By itself, the WNV-Cp protein can cause inflammation. Weiner and
his colleagues found that WNV-Cp drives apoptosis in cell
cultures through what is called the mitochondrial pathway. The
protein begins the process of cell suicide by somehow disrupting
the membrane potential of the cell's mitochondria, which then
leads to the activation of proteins such as caspase-9 and
caspase-3 that start a cascade of reactions to subsequently
cause the cell to digest itself. Since the protein enters the
nucleus of the cell, it is possible that WNV-Cp changes the host
cell's transcriptional machinery, resulting in an over
production of certain proteins related to an apoptotic program,
which consequently feed back to the mitochondria. Alternatively,
as WNV-Cp moves from the cytoplasm to the nucleus, it may
inactivate an important part of the cell's natural control
system that keeps apoptosis in check overpowering the guard as
it were thus inducing the cell suicide. "Overall, our data
suggest that WNV-Cp may interact with host