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HCMV needs to activate threshold levels of NFκ-B to initiate gene transcription
(cellular and/or viral), but because high levels of this host factor are detrimental to
the virus (generation of antiviral responses) and the host (pathogenic consequences),
the virus has a mechanism to balance and moderate this transcription factor, or in a
more general sense cellular signaling pathways; the virus thus walks a fine line by
activating the factors necessary to allow productive infection and life-long persist-
ence within the host with only minimal pathological consequences.
Acknowledgements A.D.Y. is supported by grants from the National Institutes of Health (AI56077
and 1-P20-RR018724). The author wishes to thank S. Adams and Drs. R.S. Scott and S.Μ. Karst for
careful reading of the review of the manuscript and Dr. E.S. Huang for inspiration and support.
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