Vindication—of Sorts II

Thursday I snuck in my Viral Tsunami theory when most weren’t looking. Today I’d like to expound on it a bit. I realize that by just tossing it “out there” it looks even loonier than what it is, although I admit, it’s still pretty loony by the standards of accepted wisdom.


See my post Vindication—of Sorts for the accepted wisdom of Pandemic Influenza if you are unfamiliar with it (though I find that impossible).


A/H1N1 was, as best we can determine, an Avian Influenza A virus that had somehow gained the ability to infect humans and be transmitted to other humans, all the genes were avian in origin. It was not a “human” influenza A virus, the sort we get every year, year in—year out. It had an average CFR (Case Fatality Ratio) of 2.5% as best we can determine (yep, there’s that phrase again, one I use with regularity).


A/H5N1 is an Avian Influenza virus; all genes are avian in origin. See the Taubenberger paper mentioned a bit farther down for why this is an important distinction when it comes to pandemic influenza.

J Gen Virol 88 (2007), 3094-3099; DOI 10.1099/vir.0.83129-0

Origin of highly pathogenic H5N1 avian influenza virus in China and genetic characterization of donor and recipient viruses

Muhammad Mahmood Mukhtar et al.



Genetic analysis of all eight genes of two Nanchang avian influenza viruses, A/Duck/Nanchang/1681/92 (H3N8-1681) and A/Duck/Nanchang/1904/92 (H7N1-1904), isolated from Jiangxi province, China, in 1992, showed that six internal genes of H3N8-1681 virus and five internal (except NS gene) genes of H7N1-1904 virus were closely similar to A/Goose/Guangdong/1/96 (H5N1) virus, the first highly pathogenic avian influenza (HPAI) virus of subtype H5N1 isolated in Asia. The neuraminidase (NA) gene of Gs/Gd/1/96 had the highest genetic similarity with A/Duck/Hokkaido/55/96 (H1N1-55) virus. The haemagglutinin (HA) gene of Gs/Gd/1/96 virus might have originated as a result of mutation of H5 HA gene from A/Swan/Hokkaido/51/96 (H5N3-51)-like viruses. The PA gene of H5N3-51 virus had the highest similarity with Gs/Gd/1/96. This study explains the origin of first Asian HPAI H5N1 virus in Guangdong by the reassortment of Nanchang (close to Guangdong) and Hokkaido (Japan) (H1N1-55 and H5N3-51) viruses. Genetic characteristics of donor and recipient viruses were also studied.


A graphic representation of the author’s conclusions on where the genes for HP H5N1 came from (credit: the above paper and authors)

As shown, the genetic makeup of HP A/H5N1 is entirely avian at this time, coming from ducks, swans, and geese via reassortment events.


No one knows the why behind HP A/H5N1′s incredible virulence, that’s a mystery they are still trying to figure out. Of the WHO confirmed human cases ~60% die, many of them with medical attention. Unfortunately, we are struggling to try to understand while being hobbled with lack of autopsy findings. When we do get news of autopsies the news is far from comforting, as these new findings out of China published in The Lancet attest:

The Lancet 2007; 370:1106-1108



Pathology of human H5N1 infection: new findings

Wai Fu Ng and Ka Fai To 


The pathogenic mechanisms of this highly fatal infection remain unclear. The concentrations of inflammatory mediators related to an innate immune response in fatal cases were higher than in non-fatal cases. High concentrations of cytokines in the blood and the innate immune responses might contribute to pathogenesis.3,4,9 In the adult patient who died on day 9 of disease in Gu and colleagues’ report, the finding of sparse infected pneumocytes in the lungs contrasted with the severe and widespread histopathological changes of diffuse alveolar damage, which is consistent with a late phase of viral eradication in an immunocompetent host. [Emphasis added]


Though viral load was far less than expected damage from the human immune response was massive. Whatever it is about HP H5N1 the human lungs do not like it at all, even small amounts of infected pneumocytes appeared to trigger the cytokine storm leading to ARDS which is highly fatal, as it was in this case. The body kills itself in the attempt to kill the viral invader.

We have a highly lethal virus, no questioning that. Many believe, even many experts, that for H5N1 to gain human-to-human transmission it must give up most of its lethality, but there is no sound scientific basis to believe it, much less officially act upon it.


September 2006 WHO report:

Influenza Research at the Human and Animal Interface


One especially important question that was discussed is whether the H5N1 virus is likely to retain its present high lethality should it acquire an ability to spread easily from person to person, and thus start a pandemic. Should the virus improve its transmissibility by acquiring, through a reassortment event, internal human genes, then the lethality of the virus would most likely be reduced. However, should the virus improve its transmissibility through adaptation as a wholly avian virus, then the present high lethality could be maintained during a pandemic.


We may not understand the why behind the lethality but that does not change the fact that it is highly lethal. And while there is no way of knowing with certainty what the properties of a pandemic strain of H5N1 would be, it is foolish, in the extreme, to ignore the possibility that a wholly avian H5N1 , though adapted to humans, would retain much of its current lethality.


So, that’s the support for my supposition of a highly lethal PanFlu H5N1. Why do most experts believe otherwise? Mostly because 1918 H1N1 had an average CFR of 2.5%, although variable by location and cohort, the overall average is estimated at 2.5%. Logically the expert assumption does not make sense, do we assume all cars perform like a 1966 Volkswagon Beetle? Perhaps if that were all we have ever been exposed to but I’m sure Lamborghini and Ferrari would argue the validity of the measure. A Straw man argument to be sure, but how else to make the point: you cannot judge all by one.


To use the phrase that has gained some traction in Flublogia: When you quantify all severe influenza pandemics by 1918 you judge all future events by a data set consisting of one datum. Should your curiosity be piqued and you are not yet familiar with why 1957 and 1968 influenza pandemics are not valid comparisons see 1918 Influenza: The Mother of All Pandemics Taubenberger et al.


In my previous post I stated that the UK SAG report chose to base their recommendations on the one wave model, not the more generally accepted three-wave model. Again, three waves is often viewed as de rigueur for modeling and planning purposes. I have always discounted the three wave model because of our three times greater world population, mass transit, and the existence of large-to-mega-cities.


The only way I can see a multi-wave pandemic is if we can mitigate the effects down to 5 – 10% of the population being infected, known as AR, or Attack Rate.


Again, drawing upon the UK’s SAG modeling, they model the CAR at 50%. However, buried in their findings paper OVERARCHING GOVERNMENT STRATEGY TO RESPOND TO PANDEMIC INFLUENZA ANALYSIS OF THE SCIENTIFIC EVIDENCE BASE

Issued by: Civil Contingencies Secretariat Cabinet Office
is this little gem:


4.35 The value of the basic reproduction number R0 currently being used by other countries planning for a pandemic ranges from 1.4 – 3.5, although the scientific basis for the value selected is not always clear. Pandemic modelling has tended to work on the basis of R0 1.8 to 2.534. Based on expert views in SAG, the UK’s assumption for R0 has been close to 2. The general consensus is that a future pandemic would be expected to have an R0 in the range 1.4 – 2.2. Depending on the detailed model used, this could lead to a national infection attack rate of the order of 80%.



4.36 The combination of an 80% infection attack rate and a figure of 67% for the proportion of these showing clinical symptoms (based on the higher estimates from surveys of those in previous pandemics and outbreaks of seasonal influenza) suggest an upper limit for the national clinical attack rate of the order of 50%35. While such a figure would be extreme for the national epidemic, planning to this figure also allows for variation in local infection transmission rates which may generate local attack rates in excess of the national average in some areas.


32 Assuming that in a pandemic situation initial immunity in the population is negligible.

33 Based on comparisons with the epidemic in the United States.

34 Because models are fitted to actual historical data, the variation in different model results for different estimates of Ro is less than might be assumed given the spread in the numerical estimates of Ro. The range of Ro-s used within a particular model is, however, significant.

35 In special circumstances however, for example enclosed communities, a much higher figure closer to 90% has been observed in previous pandemics.

But above these two paragraphs is this one:

4.26 This case fatality ratio is based only on cases that have come to medical attention, and medical intervention has often been late. Theoretically, there might be cases of infection without serious symptoms that therefore go undetected. This would reduce the case fatality rate. However, as more countries institute monitoring of people in the vicinity of an avian outbreak of H5N1 and fail to detect asymptomatic infections and as more population surveys from H5N1 endemic areas fail to reveal asymptomatic infections, this seems so far unlikely.


It the last paragraph they admit to the unsettling fact that we just haven’t found the number of asymptomatic infected H5N1 people that were assumed to be out there. Not that they aren’t out there, somewhere, we just haven’t found but a few, and they have been aggressively searched for.


Therefore, if the UK’s scientific findings support the assumption of a CAR of between 50 and 85% then it’s safe to further assume those will be sick people, and thus far, a majority of the sick have died.


For my reasoning of an AR of 70 – 90% and the supporting R0 I will expound in the next posting as this one is already far too long, even for me.


As succinctly as I could manage for a mish-mash of supporting data my Viral Tsunami theory, which is made up of following:

  • One wave of infection
  • An AR of 70 – 90%
  • A CFR that remains high, although ~1/2 of its current 60%.


So, while I may be a LOON, I am not the only one who has lain out the evidence for the possible horror this would visit upon humanity. However, even though I do feel a certain vindication that others have spotted the discrepancies of official statements, assumptions and plans, I take no comfort in my vindication.



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