I think our differences on this are just generational. As the paper discusses below the idea that pathogens would evolve towards less virulence was widely believed and taught last century. The idea probably is still found in textbooks.
Oh Puhleese.
You think I read something in school years ago and never read anything since? Don't insult me. The difference is you don't have enough information about the state of genetic research on viruses like flu.
More modern views are that epidemics are associated with evolutionary pressures to increase virulence, (this is NOT that the epidemic is a consequence of increased virulence but it provides an opportunity to increase virulence).
Indeed the development of immunity in the host population may be an evolutionary driver to increased virulence.
Trade offs between host and parasite and environment may result in shifting of virulence both more and less. Viruses may evolve to be less virulent under some circumstances but other circumstances such as a well connected naive population favour increased virulence. There is no natural law that pathogens evolve to be less virulent.
Apologies if this is seen as pasting too much text, but I thought some might like to read the abstracts.
I did not say selection to milder strains was the
only selection pressure. It isn't. If that were true we'd never have incredibly virulent flu epidemics.
But when a virulent strain of flu does enter the human population, then there is a selection pressure toward attenuation. Otherwise we'd have the same number of mild and severe flu epidemics, randomly, and we don't.
What happened to the 1918 flu strain if it didn't become attenuated?
First, you can't lump all viruses together. So let's look at two examples: measles and flu.
Before measles vaccine, epidemics over baseline endemicity occurred every few years. Why? Because measles is so efficient that after a surge in cases, the host population develops a high degree of immunity. After a few years, a new crop of kids are born and at some point the threshold of population susceptibility is reached and we get a new surge of cases.
There is no mechanism for selecting either more or less virulent strains. And over time measles virulence remains about the same. Most people developed measles before they reached adulthood. (Antivaxxers have changed that and cases are occurring in all age groups, but that's a different subject.) Unlike flu, measles only infects people one time with rare exceptions. It evolved to infect a new crop of kids rather than evolving to get around the host immune system.
Now take influenza. It evolved multiple mechanisms of mutation. Milder and more severe epidemics occur quite randomly. However,
you don't see strains randomly developing more virulence through genetic drift. Rather most strains just drift toward avoiding recognition while severe strains drift toward milder disease.
New severe strains usually emerge from new species transfers or new recombinant strains.
If strains drifted randomly to more or less virulent strains then we would see that in the genetic history. But we don't. Strains with changes in the envelope evolve by being selected to avoid recognition thus they can reinfect a person who had flu a year or two ago.
IOW strains not selected by more or less virulence but rather
they are selected to avoid the initial immune response and reinfect the population:
Evolution of Influenza A Virus by Mutation and Re-Assortment
There are three main characteristics which contribute to the rapid evolution of these viruses: large populations, short generation times, and high mutation rates. Every mutation, which helps the virus to evade the host immune system, may be positively selected, passed on to the next generation, and distributed more widely.
Genetic drift.
Genetic shift:
Studies have shown that duck 3286/H7N9 virus PB2 gene mutation enhances polymerase activity and viral replication in human cells [63]. The data reveal that the E627K substitution in the PB2 polymerase protein appears to be one of main determinants of the avian influenza virus host range [64]. ...
In addition to mutation and re-assortment, IAVs still have another relatively rare means of evolution called recombination. Genetic recombination is one of the primary processes that produce the genetic diversity upon which natural selection acts.
So random mutations in a non-human species is one source of new human strains. Another is recombination and re-assortment.
Strains occur randomly but were not selected to be more virulent. But when a virulent strain emerges, it's not through genetic drift.
IOW the virus' genetics drift and after ~18 months (I don't know the range) it can circulate again in people previously infected.
So what happens to these highly virulent strains once they enter the population? They don't keep changing to avoid host immunity and recirculate.
Over the past 100 years, there have been four flu pandemics: 1918 H1N1 Spanish flu [6], which has been described as "the greatest medical holocaust in history" [7], 1957 H2N2 Asian flu, 1968 H3N2 Hong Kong flu, and 2009 H1N1 swine flu. The most serious pandemic occurred in 1918, killing more than 50 million people worldwide [8]. Since 1996, the highly pathogenic avian influenza (HPAI) virus (H5N1) has caused more than 1000 deaths, resulting in a mortality rate of about 55% [9]. Recently, a low-pathogenic avian influenza (LPAI) virus (H7N9) identified first in the East China region caused an outbreak in humans, with a mortality rate as high as 40% [10].
So where are those strains?
Highly virulent strains drift genetically toward attenuation. We know this from genetic analysis of flu mutations.
