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Even when aging of the population is accounted for, death rates of the most immunized age group did not decline. For example, influenza mortality and hospitalization rates for older Americans significantly increased in the 80's and 90's, during the same time that influenza vaccination rates for elderly Americans dramatically increased. If influenza is highly infectious, why doesn't direct inoculation of a novel virus cause universal illness in seronegative volunteers?Ī ninth conundrum evident only recently is that epidemiological studies question vaccine effectiveness, contrary to randomized controlled trials, which show vaccines to be effective. Similar studies by Beare et al on other H 1N 1 viruses found 46 of 55 directly inoculated volunteers failed to develop constitutional symptoms. Intranasal administration of various wild viruses to sero-negative volunteers only resulted in constitutional symptoms 60% of the time inoculation with Fort Dix Swine virus (H 1N 1) – a virus thought to be similar to the 1918 virus – in six sero-negative volunteers failed to produce any serious illness, with one volunteer suffering moderate illness, three mild, one very mild, and one no illness at all. Only three of eight subjects without pre-existing antibodies developed illness after aerosol inhalation of A 2/Bethesda/10/63. The percentage of subjects sickened by iatrogenic aerosol inoculation of influenza virus is less than 50%, although such experiments depend on the dose of virus used. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?Īn eighth conundrum – one not addressed by Hope-Simpson – is the surprising percentage of seronegative volunteers who either escape infection or develop only minor illness after being experimentally inoculated with a novel influenza virus. What explains the frequent coincidental timing of epidemics in countries of similar latitudes?
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Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?
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Nevertheless, he parsimoniously used latent asymptomatic infectors and an unidentified "season stimulus" to fully or partially explain seven epidemiological conundrums. Unfortunately, the mechanism of action of the "seasonal stimulus" eluded him in life and his theory languished. Realizing that solar radiation has profound effects on influenza, he added an unidentified "seasonal stimulus" to the heart of his radical epidemiological model. Edgar Hope-Simpson not only questioned that assumption, he went much further. Arguably, the most universally accepted assumption about influenza is that it is a highly infectious virus spread by the sick. It is useful, at times, to question our assumptions. We hypothesize that two factors explain the nine conundrums: vitamin D's seasonal and population effects on innate immunity, and the presence of a subpopulation of "good infectors." If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.
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#Vitamin r simpsons serial
We identify – and attempt to explain – nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns." Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson.