Looking more closely at this
CVB4 Arbidol study, and mechanism by which Arbidol (umifenovir) reduces the IL-10 secretion caused by CVB4, the full paper says that:
CVB4 virus infection reduced p38 phosphorylation, while phosphorylation of the downstream MK2 was increased. However, treatment with Umifenovir significantly promoted p38 phosphorylation and reduced MK2 phosphorylation. Therefore, we speculated that CVB4 virus infection induced IL-10 expression was mainly through the p38MAPK pathway.
So if we can further
boost p38 phosphorylation (p38 activation) and
reduce MK2 phosphorylation (MK2 activation) by other means as well, that may help even more to shift from Th2 to Th1 in the case of chronic coxsackievirus B4 infection.
MK2 = MAPK-activated protein kinase 2.
Seems that
insulin boosts p38 activation in smooth muscle cells (so perhaps the intranasal insulin I was experimenting with might have an antiviral effect in the brain), as does
follicle stimulating hormone. And
genistein (a dietary supplement) reduces MK2 activation (ref:
1); but unfortunately genistein also reduces p38 activation, which is the opposite of what we want (ref:
1).