I'm trying to understand why transduction of cells with a viral gene under its viral promoter yields a different phenotype than when the same gene and promoter are incorporated into a viral vector (HSV1 in this case).
Ex: Transducing cells to express an essential protein for HSV1 viral lifecycle (ICP4) vs just having a wildtype ICP4+ virus. If the cells transduced and expressing ICP4 dont rescue the virus what could the reason be? Aside from a shutdown of the trans gene expression. General or specific answers/speculations appreciated.
LOOK FOR GLYCOSILATION SITES MOST PROTEINS ARE ANCHORED TO THE MEMBRANES BY CORBOHYDRATES.......YOU MAY FIND AN ALGORITHM FOR GLYCOSILATION SITES PREDICTION...
@Mr. Rosario-Cruz Thankyou for the response, but is your answer applicable if the sequences of the genes are identical, and translated in the host cell? If any post translational glycosylation were occurring wouldn't it occur on both proteins regardless of the genome they were transcribed from?
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