If one is to believe that depression is a type of illness behavior to avoid further pathogens, I'd invite members to recognize the importance of indoleamine 2,3-dioxygenase (IDO) activity in the manifestation of depression. I see very little discussion by the lay media with regards to this molecule, mainly because research is sparse. One is to also assume the tail suspension test, sucrose and other tests are adequate models of depression for the following to take hold.
In short, IDO is activated when an infectious process is encountered and shunts tryptophan (serotonin precursor) and instead creates an anti-pathogenic molecule called N-formylkynurenine, thus leaving a void of serotonergic activity. Specifically, it induces IFN-y, which is essentially the gold standard depressive. So, an IDO inhibitor may help "resolve" this, to unknown consequences at this point.
Minocycline has been known for two decades to be an antidepressant although the mechanisms suspected in the initial trials didn't have the correct immuonlogical foundation.
My point is 1-methyl-l-tryptophan would hypothetically have better tolerability than minocycline, even though recent evidence indicates minocycline pretty well-tolerated.