Biology Reference
In-Depth Information
pathway (Fig. 3 and Table 1) opens the possibility for vast effects on cellular physiology.
The resulting pathogenic effects could implicate HCMV as a subtle, and unex-
pected, cofactor in many maladies. For example, nearly every one of the targets
listed in Table 1 can be an oncoprotein when mutated, inappropriately activated or
inappropriately expressed. While not suggesting that HCMV is a frank transforming
agent, it is possible that the virus serves as a co-factor with other agents/mutations
to promote transformation. The effects of HCMV on oncoproteins such as PI3K,
Akt, mTOR, mTOR's effectors and eIF4E could increase the oncogenic potential
of a cell, serving as one factor among several which cause transformation, as
suggested by the Knudson multi-hit hypothesis (Knudson 1988). The understanding
of the means by which HCMV adapts cellular stress response signaling will provide
new insight into HCMV pathogenesis.
Acknowledgements
J.C.A. is funded by Public Health Service grants R01 CA28379-27 and R01
GM45773-15 from the National Institutes of Health and by the Abramson Family Cancer
Research Institute.
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