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.
Page #17
This vaccine will be in addition to the regular seasonal influenza vaccine.
Again, people over 65 years of age, young children, pregnant women, and people with diseases of the heart or lungs should all receive these vaccines assuming they are not allergic to some component of the vaccine.
Q: If that is true, then why are you so worried about this new virus?
MA: Just as it is often not the seminal event that results in huge problems but the ensuing poor decisions (think Watergate)- thus it might be with this outbreak.
What we can safely assume is that (baring some very profound discovery) when fall arrives in the Northern Hemisphere and school resumes there will be a second wave of novel H1N1 cases flooding the world.
We can also reasonably infer that by then there will be a huge storehouse of neuraminidase inhibitors stockpiled and ready for distribution to millions of patients.
Individuals are buying these products online and with prescriptions just to have them ready for the first small symptom of the flu.
So what you will most certainly see in the next few months is a massive introduction into the human species of a mixture of novel H1N1 virus, a rapidly developed flu vaccine and million and millions of doses of neuraminidase inhibitors - many self-administered and many given long after the brief window where they might have helped.
We as scientists owe everyone a calm and reasoned examination of the effects of such a cocktail.
Have we evaluated the repercussions of these actions?
Are there any potential contraindications of which we should be aware?
I would like to discuss these issues with you.
Q. Please go ahead.
MA. Influenza viruses multiply by gaining entry into a host cell and upon entering these cells they commandeer the host machinery to produce new viral progeny. And they do this very well. So, if we may, let us spend a bit of time visualizing exactly how this event occurs.
The virion is generally a circular entity enveloped in a lipid membrane with two different types of spikes emerging from this surface. These spikes are proteins – actually glycoproteins - because they consist of protein linked to sugars – and are known as HA (hemagglutinin) and NA (neuraminidase).
One of the spikes, a triangular rod-shaped molecule, has haemagglutinin activity, while the other spike, a mushroom-shaped molecule, with a square box-like head sitting on top of long thin stalk, is the enzyme, neuraminidase.
Hemagglutinin is the method by which the flu virus takes hold on the infected cell whereas the neuraminidase is the enzyme that clips off the newly formed virus, so that the ‘free’ virus will infect another cell. But we can discuss that later. For it is neuraminidase and it's association with virulence that will be the focus of our discussion after we review the basics.
Q: (I did not know, at the time, that the review would take all winter)