To my disappointment there was no significant improvement to any of my CFS/ME symptoms from Fluoxetine. So that pretty much rules out a CVB3/CVB4 infection in the brain for my side.
I was looking more closely at the anti-enteroviral mechanism of fluoxetine, and it occurred to me that fluoxetine's mechanism may not work for non-cytolytic enterovirus infections. In fact, fluoxetine might even promote non-cytolytic infections.
So given that the chronic enterovirus infections found in ME/CFS patients involve a non-cytolytic infection, as well as a normal lytic enterovirus infection, this could explain why fluoxetine may not help. Fluoxetine may work for the lytic infection, but not for the tricky non-cytolytic infection.
The technical details of why I think fluoxetine won't work for non-cytolytic enterovirus infections are as follows (bear in mind that I am not a virology expert, so this is just my own interpretation, and I may be wrong):
This study says that fluoxetine inhibits the 2C viral protein made by enterovirus. This viral protein is important for normal lytic replication.
This paper explains a bit more about the 2C protein: it says that enteroviral 2C protein "may be crucial for the synthesis of positive-strand RNA from the negative-strand RNA template".
The way enterovirus normally replicates is by making a small number of negative-sense viral RNA strands, containing the full the viral genome. Each negative RNA strand acts a template or "stamp", and this strand is able to create multiple positive RNA strand copies. These multiple positive RNA strands are then packed into new viral shells to make new viral particles. This is the normal lytic virus replication cycle.
In normal lytic enterovirus infections, you find that each single negative RNA strand is able to create around 100 positive RNA strands.
However, in non-cytolytic enterovirus infections, something goes wrong, and the negative RNA strand template is unable to make lots of positive RNA strands, because something blocks the production of positive strands. When you get this shortage of positive RNA strands, that's how a non-cytolytic infection arises (I won't explain the details here). Thus when something blocks the normal production of hundreds of positive strands in a lytic infection, that lytic infection is converted into a non-cytolytic infection.
So if we now go back to fluoxetine, we see that the 2C protein "may be crucial for the synthesis of positive-strand RNA from the negative-strand RNA template". Thus inhibiting this 2C protein will block the production of positive RNA strands, and is this way, may turn a lytic infection into a non-cytolytic infection. So fluoxetine might even increase levels of non-cytolytic infection.
And for existing non-cytolytic infection, fluoxetine may not have any antiviral effect at all, because as explained, in non-cytolytic infections, positive RNA strand production is already blocked, so fluoxetine's positive strand-blocking effects will be superfluous and ineffectual in non-cytolytic infections.
