It's kind of counterintuitive sometimes, that an agent that -- an infectious agent that is very good at killing its host is actually not a very well adapted infectious agent. That is, that bacteria that live on your skin or inside your colon are extremely adapted to living in humans. They don't cause disease. And so they have a nice relationship. They have set up shop and they live happily on your skin and you don't do anything about it, and occasionally there's even a mutually beneficial relationship that occurs. For example, some of the vitamin in your colon make a vitamin, vitamin K that we need.
In the case of bacteria or viruses that are not so well adapted, if they kill their host very quickly, they actually may limit their own ability to spread to other people. That is, if they kill people so quickly that they don't have time to replicate, they're kind of hurting their own chances of replication.
In this case, it was something in between. It was a virus that certainly killed a lot of people, but realistically only killed a small percentage, 2 to 5 percent of the people that were infected. So it was clearly a really good virus to infect humans. It spread amazingly well from person to person and spread all over the world. But probably in about a year's time, from 1918-19, practically every person on earth was at least exposed to this virus. So everyone formed an immune response against the virus in one degree or another. So that would put enormous pressure on the virus to mutate, to change its coat so that it could continue to infect humans.
Possibly what happened was that whatever caused this virus to be so unbelievably virulent changed when the virus mutated and the viruses that continued to circulate both in humans and in pigs after 1918 are probably actually mutated descendants of the virus but not the 1918 virus itself.