Aren't epithelial cells a reservoir or a target of EBV? So killing some of those would perhaps be good?
In the cancer studies, as I understand them, the high-dose VC killed the cancer cells selectively and wasn't (very) cytotoxic for healthy cells. Could the same be the case for virus-infected cells? That could perhaps be an explanation why @@Learner1 felt a positive effect.
Epithelial cells make up your skin and the mucous membranes of your respiratory and gastrointestinal tract, etc; viruses which spread by respiratory secretions are usually able to infect epithelial cells in your respiratory or gastrointestinal tract, as that is how they establish the first infection in your body.
In the in vitro antiviral study above, they tested the effects of high dose vitamin C in a line of epithelial cells that were not virally infected, and at the concentration given, 50% of the cells were killed by vitamin C. The concentration at which 50% of the cells die is called the CC50 concentration.
It is normal for in vitro antiviral studies to measure the CC50. It is also normal for these studies to measure the concentration of the antiviral at which viral replication is inhibited by 50%, this is called the EC50 concentration.
For a good antiviral, you want the CC50 concentration to be much higher than the EC50 concentration. In other words, you want to be able to use the antiviral to kill the virus, without killing the cells.
In fact, that is how you measure the potency of an antiviral, by taking the ration of CC50 / EC50. That ratio is known as the selectivity index. For a potent and useful antiviral, you will find the selectivity index has a value around 10 to 50.
Bu in the case, of vitamin C, it's CC50 concentration is actually lower that its EC50 concentration in these epithelial cells.
I have been reading a lot of antiviral studies recently, so that's why I am familiar with this stuff.