I don't know what that means or what your source is. It sounds like you're maybe saying that orthodox evolution theory doesn't apply when humans are involved. Why, what is the mechanism?
And how exactly do you get from the idea of a pathogen evolving to be less virulent to "artificial" selection? Stipulating that somehow artificial selection is different, what would make it artificial? It seems obvious that human behavior would factor in, but what is the definition that makes the evolution artificial?
https://en.wikipedia.org/wiki/Directed_evolution
...and this means directed selection is not an natural process by definition. natural evolution doesnt proceed toward a defined end, [bipedal primates with large cerebrum] [or from highly lethal-->moderately lethal-->nonlethal]
virus do not start from day one as very lethal and become progressively less lethal over successive replications.
communicability is an advantage to host to host transmission. breaking linkage between traits allows differing selective factors to act on these traits.
when a virus doesnt kill you or make you ill until after you have infected others then that virulence is not subject to the same selective factors as it previous partner [communicability]
It's a matter of degree, not a binary thing. You can't be 100% sure of anything, but as long as people are aware of something and act accordingly, there will be selection pressure. Reduced social contact has an effect regardless of whether specific carriers are identified.
are virus always absolutely lethal and then lose lethality as they evolve?
or do virus of non lethal character spontaneously become more lethal?
So, specifically in answer to your question, it seems obvious to me that "lethal characteristics" are context dependent, so they come from random chance when an organism (or virus) encounters a new environment that it can replicate in way easier.
when a virus has infected a host, replicated, passed to a secondary host, then symptoms appear, then X occurs,
You have a situation where X has no influence on reproduction, replication or transmission, it just is not even on the same blackboard as that equation.
here is some suggested reading for you, not everyone understands evolution or natural selection very well so it is a bit of a TLDR
It is true that a basic law of reality/nature is that causes must precede effects, so in a sense, I think I agree your statement is technically correct regarding the exact cycle you describe.
But when talking about evolution in a population, the cycle happens a huge number of times. So "X" will influence all of the instances of replication that in fact happen after it. It would be silly to talk about evolution in a context of one and only one reproduction event.
I don't think we are debating anything that has to do with specialist knowledge of viruses.
directional selection is a very different thing it exists, it is part of evolutionary theory, it means there is a bias toward a particular allele [natural selection is a form of directional selection.
selection does not lead to a path of improvements, it leads to changes in frequencies of phenotypes.
there are other ways of enhancing spread, and retaining lethality, such as being communicable before symptoms become debilitating, this removes selective pressure that is based on communicability. If the host does not get sick enough to to be bedridden, they can contact other hosts. If the symptoms are mild or unseen there is no behavioral basis for other hosts to avoid the infected host. so by delaying expression of characteristics the virus may be highly communicable and highly lethal at the same time. high lethality is not subject to selective pressure in this case and will remain.