Posted on 01/28/2006 1:29:23 PM PST by Termite_Commander
YEARS ago when I first started studying the avian influenza virus H5N1, it seemed highly unlikely that it would ever develop into pandemic status. I believed it might eventually trigger a conventional bout of flu, but certainly nothing to the degree of its H1N1 ancestor, the 1918 Spanish Flu that killed 50 to 100 million people.
I have followed this virus in its inexorable march towards a pandemic, seen how it kept surprising the experts by picking up more and more human-infectious traits, until now there is virtually no doubt that there will be a worldwide avian flu pandemic and that H5N1 will be responsible for it.
We have all heard the projections from avian influenza experts like Dr Michael Osterholm that in a single flu season as many as 360 million people could die. That figure is unimaginable. It's the total number of dead from the Boxing Day Tsunami every two hours, or a fully loaded 747 crashing every 13 seconds, around the clock for months on end. Three million dead in the UK alone or the equivalent of six Edinburghs.
The global integrated economy cannot survive a pandemic of this magnitude. Absenteeism rates of upwards of 75 per cent caused by illness and panic would cripple food distribution, utility access and virtually all other commerce. The bleak vision of surviving on canned food and bottled water in cold, dark homes, fearful of stepping outdoors for months on end, could happen right here in Scotland and around the world.
Do not make the error of assuming this cannot happen here. Migratory birds from Western China brought H5N1 to Turkey in early October where it lay undetected until people started dying a couple of weeks ago. Those migratory patterns continue into North Africa and Western Europe. When will H5N1 arrive in Scotland? Judging by the Turkish model, it may already be here. Let's not even consider what can happen when an infected individual arrives at Edinburgh Airport.
The 1918 pandemic started in an Army barracks in Kansas. Within one week the virus was present in all 48 contiguous United States in an era where the only modes of transport were trains and horses. The spread of this virus in the jet age is unimaginable. There likely would not be a corner of the Earth where this modern plague would not be present within weeks, maybe days.
The virus needs to pick up another trait or two to become as easily transmitted between humans as a common cold. That could happen at any time or it may already have begun.
Developing a vaccine against H5N1 is like targeting a clay pigeon. You have to shoot ahead of the target to allow the bullet and clay to intersect. Unfortunately H5N1 is a pigeon that does random, sudden 90 degree turns. It is the ultimate moving target. The time to develop and manufacture a global vaccine is six to eight months. By that time, the avian flu virus will likely have mutated into a form that is immune to the vaccine.
Current flu vaccines have no effect on H5N1, and although it is recommended that everyone be vaccinated, we should be clear in the knowledge that should a pandemic start, there is no protection from current vaccines or certainly from antiviral drugs. The antivirals of choice right now are Roche's Tamiflu and Glaxo's Relenza. The UK has ordered more than £200 million of Tamiflu, believing that it could help fend off the pandemic. Unfortunately, Tamiflu is fairly useless as an avian flu pandemic fighter.
In a recent Asian study Tamiflu was proven as ineffective as sugar pills against some H5N1 strains. The best use for these drugs is as a preventative, taking at least two doses per day from the moment the first virus arrives in your area and throughout all the months of the flu wave.
To provide everyone in the world with this albeit minor preventative measure would require, in a conservative calculation, 650 billion pills or the equivalent to the total weight of the Queen Elizabeth II fully loaded with passengers and cargo just in pure Tamiflu! All we have to do is write a cheque to Roche for one trillion pounds. And it still wouldn't stop the pandemic.
Thorough hygiene and other common-sense precautions are the only ways to blunt the impact of this pandemic. Raw poultry must be considered as a biohazard. Surfaces and clothing must be disinfected with bleach. It's time to rediscover the "disinfect everything" policy of the NHS matrons of the 1950s.
H5N1 could surprise us all and evolve into a squirrel or koala virus, sparing humanity. However, the chances of that occurring are next to zero. The world is fully unprepared. The onus must shift from wasting billions on "magic bullet" drugs that don't work to preparation and survivability.
bump
"That's just rose-colored speculation, right?"
Considering that Dr. Edwin Kilbourne is an emeritus professor of immunology at New York Medical College I would put a bit more credibility into his assessment than a random poster on FR.
"In any event, it hasn't much mitigated the effect on those thus far infected."
The point he's made, and apparently your missing, is that thousands may have already been infected with mild symptoms. If true, it paints a much different picture than what is being currently portrayed. Observational data from Turkey would certainly suggest a lower mortality rate than what the UN has advertised and it suggests that Kilbourne's hypothesis might be credible.
Many observers have speculated such. Little hard evidence has been presented that this is the case. If you are in possession of the smoking gun I know numerous immunologists, epidemiologists, and virologists would love to see it. The point you, and apparently he, are missing, is that widespread human infections would be a bad thing, even mild ones, as many additional opportunities for recombination and, especially, reassortment would occur.
It appears that this Ed Kilbourne has his posterior glued to his rocking chair and doesn't venture out in the field much these days. A brief Goggle on his name and H5N1 will show that many have already dismissed his comments, such as this poster:
It seems to me that Dr. Kilbourne makes several statements based on old paradigms. Yet a lot of the public are going to accord him expert status on the basis of being an emeritus professor.
Would you be included in that group?
In light of the fact that no seroprevalence studies have been published, a study was recently completed and published in Archives of Internal Medicine that supports the "more widespread and mild symptom theory".
http://archinte.ama-assn.org/cgi/content/abstract/166/1/119
Additionally, commentary from Dr. Henry Niman (Dr. Doomsayer some say) last June that suggests the same:
“Although the positive western blot data has not been confirmed, positive data would be consistent with more clusters in the north which are large and extend over a longer time period. The alarming increase in admission is further cause for concern because the admitted cases have mild disease, suggesting an even larger number of unreported cases with slightly milder disease.
This H5N1 is silently spreading mild disease in human and asymptomatic infections in poultry, which would move the pandemic to phase 6. The seeding of the human population with H5N1 sets the stage for further recombination in the fall when migratory birds bring in new sequences, which will cause new problems.”
http://www.recombinomics.com/News/06260502/H5N1_Silent_Spread_Vietnam.html
If you want me to dig a bit deeper and find more for you, let me know.
Do you believe the situation merits classification as Phase 6, as the Niman quote suggests?
Increasing Lethality of H5N1 Seroprevalence and Animal Studies Agree
31 January 2006
Monotreme – at 22:34
There was much speculation in the news recently suggesting that H5N1 may be becoming less lethal. WHO case reports did not support this idea. However, cases that had not been confirmed by the WHO affiliated lab in Mill Hill were often cited as proof that H5N1 was now less lethal. However, it now appears that many of the apparent cases were in fact not infected with H5N1. The tentative case fatality rate in Turkey is now thought to be 33%, similar to what has been reported in some southeast asian countries. The issue of seroprevalence studies came up when discussing the “real” case fatality rate. DemFromCT added a table from the WHO that appeared in the New England Journal of Medicine summarizing some of the seroprevalence studies. I noticed that there was some evidence of mild cases from the samples collected from the 1997 outbreak, but almost none from the 2004 outbreak. What could this mean? One interpretation is that the virus became more lethal between 1997 and 2004. Is there any other information that would support this idea? Indeed there is. Animal studies were conducted with H5N1 strains collected from 1997 and 2004. The results? Rapid disease progression and high lethality rates in ferrets distinguished the highly virulent 2004 H5N1 viruses from the 1997 H5N1 viruses. Thus both seroprevalence and animal studies suggest the same conclusion, H5N1 became more lethal to mammals, including humans, from 1997 to 2004. There is no evidence that H5N1 has become less lethal since 2004. There may be evidence that it is becoming easier to transmit (more and larger clusters) but we must wait for proper documentation from the WHO to be sure. There is no data to suggest that H5N1 is becoming less lethal or that it must do so before becoming a pandemic strain. Fact-based planning should include the possibility that a pandemic strain of H5N1 may kill 30% or more of its victims, as terrible as that is to contemplate.
Is that available online?
“When we get a positive, we’re sure,” Alan Hay at the NIMR told New Scientist. “But when we get a negative, we aren’t.” One problem is getting a sample with virus in it. The amount of virus present during the course of bird flu in humans varies more than with human flu. And test samples are usually mucus from the nose or throat. But because H5N1 is a bird virus, it prefers the higher temperatures – and the more bird-like cell-surface molecules – of the lower lungs.
From a NewScientist RSS feed,
I'm not using false negatives as evidence of a broader spread of a milder disease, rather suggesting that a number of patients who died presumably of other causes actually died of bird flu.
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