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.
Page #16
The 1957 pandemic, during an era with much less globalization, spread to the US within 4-5 months of its detection in China, and the 1968 pandemic spread to the US from Hong Kong within 2-3 months. Now we live in the era of “overnight” delivery – and that speed of travel might well come to do us harm.
I am sure you understand that we were able to stop the SARS outbreak by rigidly enforcing “barrier nursing techniques”. However, many of the public health interventions that successfully contained SARS will not be effective against a disease that is far more contagious, has a very short incubation period, and can be transmitted prior to the onset of symptoms.
We have a roughly 20-24% divergence of this novel 2009 H1 from the seasonal influenza H1 virus. This antigenic shift will play itself out with the novel virus replacing the seasonal influenza as the dominate strain. As that happens you should look for new risk groups to emerge and for the tracking of classical period doubling episodes in the infection rates.
In phase transitions there are three universal routes:
• Period doubling
• Intermittency
• Quasiperiodicity
But as an epidemic moves from its initial introduction into a population to mass infection - it is period doubling that best defines that route. At some point along that transition the health authorities will cease to count cases and use macro metrics to measure the disease penetration.
We are very near that phase.
Q: Do you believe that this virus (H1N1) will lead to the type of deaths and disruption that the 1918 flu caused?
MA: In the field of medicine anything is possible, but on balance I would have to say no. In fact, there is some evidence that this influenza A (H1N1) might even be less lethal than our seasonal flu.
That does not mean that there will not be problems. When you have a virus that targets the young, pregnant and those with asthma, respiratory illness and compromised immune systems- then there will be suffering.
But we have fought this battle many times.
However, because of the level of transmission in this pandemic we must be prepared for a huge spike in the fall.
We can’t completely prevent its spread, but we can minimize it through simple measures: frequent handwashing, covering our mouths with the crook of our elbows when we cough, and staying home from work or school when we’re sick.
For people who are exposed and at high risk from influenza, medications such as oseltamavir (TamiFlu) are still effective against H1N1, although there is always a risk that widespread resistance to these drugs could develop.
A vaccine for H1N1 influenza is under development, and people at high risk of illness from infection (such as the elderly) or at high risk to transmit the infection (such as schoolchildren) should be strongly recommended to receive it.