The Spanish flu as a worst case scenario?

Abstract

For preparation of pandemic plans for the H5N1 bird flu virus, it has been common practice among health authorities in several countries to use crude death figures from the Spanish flu pandemic as a worst case scenario. This has been done without taking into consideration either what is known about the molecular biology of malignant influenza viruses or the detailed statistical information that is available about the Spanish flu pandemic, as regards the variation of death risk as a function of age and also as regards the different behavior of the virus during successive pandemic waves. There is no scientific basis for the assumption that a new pandemic influenza virus cannot be worse than the Spanish flu virus. However, if we hypothetically assume recurrence of a pandemic influenza virus with virulence and transmissibility properties identical to the Spanish flu virus, but belonging to a subtype other than those that have been circulating in human populations since 1918, it will be unrealistic to assume that the older part of the population will be immune against a type of virus that their immune system has never encountered before. Therefore we have attempted to estimate what might have happened by counterfactually assuming that individuals in 1918 had not been immunized earlier against H1 (or H1N1) influenza viruses that were circulating before 1890. An overview is given of age-related changes in immunological factors that may affect the age-specific mortality in different age groups, and also expected consequences for the mortality in different age groups of mitochondrial DNA aging per se. Extrapolations for age-specific death rate have been made for four different scenarios, giving lower and upper boundaries for what might have happened if nobody had been immune when the 1918Á1920 pandemic started. For the first (lower boundary) scenario the age-specific death rate is increasing up to the age of 30 and is assumed (very unrealistically) to be constant thereafter. For the second scenario the age-specific death rate is monotonically increasing as a function of age according to an almost cubic functionality. For the third (upper boundary) scenario the agespecific death rate is increasing exponentially with age. For the third scenario the mortality of the world population becomes 0.3. Thus 30% of the world population could have been killed by the Spanish flu virus, had nobody been immune when the pandemic started. For the fourth scenario the mortality by age due to the virus mimics the traditional mortality by age in a population. The fifth scenario is identical with scenario 3, except that it is also counterfactually assumed that the wave 2 virus came first. For this scenario, it is found that as much as 80% of the total world population in 1918 might have been killed by the Spanish flu virus.

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“…I have earlier written some survey articles together with a nutrition scientist from the Norwegian University of Life Sciences and a physicist from the Norwegian Defence Research Establishment, where we discuss how this hopefully may be achieved in cases of hypervirulent influenza (such as H5N1 avian influenza and the Spanish Flu), as well as about the reasons (with obviously important implications for therapy) why the lethality (risk of dying when one is infected) among patients suffering from hypervirulent influenza is strongly influenced both by the nutritional status (with the average surplus mortality being about 10 times higher in British India than it was in Norway in 1918, and also much higher in other poor countries than in those countries that in 1918 were more affluent) and the age of the patient (due to changes in the secretion of various immunostimulatory and immunosuppressive hormones as a function of age, as well as mitochondrial DNA aging) (520, 532, 533). …”

“…The sensitivity of C-fibres is also regulated by protein kinase C (PKC), with PKC activation leading to enhancement of the sensitivity of the C-fibres (533). They contain several different PKC isozymes that all can be activated by oxidative stress (533).…”

“…They contain several different PKC isozymes that all can be activated by oxidative stress (533). There is strong reason to expect that glutathione depletion, e.g .…”

“…This may be expected to lead to mutations in the mitochondrial DNA of the C-fibres, which will lead to enhancement of mitochondrial production of reactive oxygen species (ROS) similarly as normal aging does (533), with the ROS coming from the mitochondria next causing oxidative PKC activation, which will lead to enhancement of the sensitivity of the C-fibres (533) and therefore more pain and more neurogenic inflammation, including enhanced risk of asthma (534–534). …”

“…This would be expected not only to lead to reduced extravasation of blood plasma proteins through pores in the venules, as earlier explained, but also less stimulation of leukocytes ( i.a . macrophages) by peptides secreted from the C-fibres, as well as reduction of the centrally mediated reflex leading to enhanced ACTH secretion (533) and hence enhanced glucocorticoid secretion as a result of enhanced C-fibre activity (533). …”