Page #15
As to your question of the two mixing and somehow acquiring the lethality of H5N1 and infectiousness of H1N1 - it is of course possible.
Antigenic shift between avian influenza and human influenza is not something unheard of. The "Asian" flu pandemic of 1957 and the "Hong Kong" flu pandemic of 1968 both introduced novel strains.
The H2 that appeared in 1957 and the H3 that appeared in 1968 came from influenza viruses circulating in birds.
So when we consider that the human population has absolutely no immunity against any H5 viruses the red flags go very high indeed.
Will H5N1 reassort with H1N1 or with H3N2, or will it "drift" into another host like pigs and then move to other mammals?
It has failed over the last few years to combine with H3N2 and has yet to find a non-avian host.
When novel H1N1 becomes ubiquitous, as it certainly appears headed, will the increased opportunity for antigenic shift finally create a specific case of reassortment or viral shift that confers a phenotypic change?
I don't know. No one does, but we can use our experience and make educated calculations as to the possibilities. I would rate the chance of H1 acquiring a polybasic cleavage site at nil, but the odds of H1 picking up lethal genes or polymorphisms at >5%.
There are, in my opinion, far greater risks on the horizon
Q. When you speak of “far greater problems” what are your concerns
MA. There are several. In recent pandemics, a second wave of influenza activity occurred 3 to 12 months after the first wave. We must anticipate this pandemic to do the same.
In 1957 the second wave began 3 months after the peak of the first wave, while in 1968 the second wave began 12 months after peak of the first wave.
The first wave of the 1918 flu occurred in the spring of that year ending in March. That flu was very severe by usual standards but the second wave beginning 6 months later in September was the most fatal.
During the 1918 pandemic, the deadly second wave was responsible for more than 90% of the deaths for the entire pandemic. The third wave occurred more than a year later, during the following 1919-1920 winter/spring, and was the mildest of all.
So when we think of the fall of 2009 and the children returning to classes we must be cognizant of this huge potential for a second wave of flu infections.
In the previous century, pandemics traveled from continent to continent along sea lanes, with global spread complete within six to eight months.
I went back and started reading from the start. SOmehow, in the midst of prepping for a well, and all the associated work deploying to location, I missed this post.
This, however, jumped out at me, perhaps becaus3e I was talking with a friend who had been a few states south and west of here, who said wild pigs were everywhere...there. He saw them as a potential food source in tough times, but this presents a different face:
Pigs are seen as a possible intermediate host that can help in that adaptation because the epithelial cells in pigs' trachea can be infected by both avian and human flu. Where, in the event of co-infection, viral reassortment might occur.