My question would be: Antiviral drugs N°5 would produce something mimicing a kind of abortive infection, so it may be interesting to test antibodies in patients after a course with this kind of anti-viral drug...To see if we can observe the same pattern...
Sounds plausible in principle, but I don't really understand enough about abortive infections to know whether it would work in practice.
Some time ago, I was pondering on whether the reverse approach might work: to develop a drug that converts non-permissive cells into permissive ones, so that the abortive viral infection in these cells can start replicating and produce virions, resulting in a fully-fledged productive infection in the tissues, which the immune system should then attack and destroy, as per normal.
In the case of enterovirus infections, when enterovirus enters cells in the body that are dividing cells (like liver cells, which are always multiplying and replicating themselves via cell division), the virus forms a normal productive infection, creating thousands of new virions in each cell.
However, when enterovirus enters non-dividing cells, the virus is not able to make many new virions, and so instead may set up a chronic non-cytolytic enterovirus infection in these non-dividing cells (as explained earlier, a non-cytolytic infection is a sort of abortive infection).
The reason non-dividing cells are non-permissive for enterovirus is because non-dividing cells lack a factor (called
hnRNPC1) which is crucial for successful viral replication and production of new virions (more details about this factor
here).
This hnRNPC1 factor appears only during times of cell division and replication (cell mitosis), so you don't get any hnRNPC1 in non-dividing cells. Thus I wondered if it might be possible to develop a drug which stimulates the production of hnRNPC1 in all cells, including non-dividing cells, which might then convert non-cytolytic infections into productive infections, which would be cleared by the immune system.
Incidentally, it occurred to me that this issue of non-cytolytic enterovirus infections only occurring in non-dividing cells might explain why ME/CFS rarely occurs in anyone younger than around 10 years old (the "
twin peaks" study showed that ME/CFS before the age of around 10 is pretty rare — see
Figure 1).
I think the reason why young children rarely get ME/CFS might be due to the fact that the bodies of young children are rapidly growing, so the cells in their body will be constantly undergoing cell division, making it hard for enterovirus to create any non-cytolytic infections. As children grow older, their rate of growth slows, and cell division slows down and eventually stops in many organs. So as children grow into adults, you now you have more non-dividing cells in the adult body, which enterovirus may infect and produce the non-cytolytic infections linked to ME/CFS.
