The Transmission of Influenza

Leake, J. P.

doi:10.1056/nejm191912111812401

Cited by 4 publications

(3 citation statements)

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“…The model does not specify whether transmission occurs by direct or indirect contact, via droplets, fomites or aerosols, since the relative contribution of each mode of transmission is unclear for influenza [32,33,[43][44][45]. Unfortunately, there are very few experimental studies of human-to-human transmission; besides, existing studies are inconclusive and predate the discovery of the influenza virus [32,46,47]. Indirect evidence for influenza transmission between humans can nevertheless be found in observational studies in close contact settings, such as aeroplanes, hospitals, households, schools, and day-care centres [48][49][50][51][52][53].…”

Section: Discussionmentioning

confidence: 99%

Seasonal influenza in the United States, France, and Australia: transmission and prospects for control

2007

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SUMMARYRecurrent epidemics of influenza are observed seasonally around the world with considerable health and economic consequences. A key quantity for the control of infectious diseases is the reproduction number, which measures the transmissibility of a pathogen and determines the magnitude of public health interventions necessary to control epidemics. Here we applied a simple epidemic model to weekly indicators of influenza mortality to estimate the reproduction numbers of seasonal influenza epidemics spanning three decades in the United States, France, and Australia. We found similar distributions of reproduction number estimates in the three countries, with mean value 1.3 and important year-to-year variability (range 0.9-2.1). Estimates derived from two different mortality indicators (pneumonia and influenza excess deaths and influenza-specific deaths) were in close agreement for the United States (correlation = 0.61, P < 0.001) and France (correlation = 0.79, P < 0.001), but not Australia. Interestingly, high prevalence of A/H3N2 influenza viruses was associated with high transmission seasons (P = 0.006), while B viruses were more prevalent in low transmission seasons (P = 0.004). The current vaccination strategy targeted at people at highest risk of severe disease outcome is suboptimal because current vaccines are poorly immunogenic in these population groups. Our results suggest that interrupting transmission of seasonal influenza would require a relatively high vaccination coverage (> 60 %) in healthy individuals who respond well to vaccine, in addition to periodic re-vaccination due to evolving viral antigens and waning population immunity.

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Section: Discussionmentioning

confidence: 99%

Seasonal influenza in the United States, France, and Australia: transmission and prospects for control

2007

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“…However, according to Jordan's frightening monograph on the 1918 pandemic, there were five attempts to demonstrate sick-to-well influenza transmission in the desperate days following the pandemic and all were "singularly fruitless" [ 19 ]. (p. 441) Jordan reports that all five studies failed to support sick-to-well transmission, in spite of having numerous acutely ill influenza patients, in various stages of their illness, carefully cough, spit, and breathe on a combined total of >150 well patients [ 51 - 55 ].…”

Section: Human Studies Attempting Sick-to-well Human Transmissionmentioning

confidence: 99%

On the epidemiology of influenza

Cannell

Zasloff

Garland

et al. 2008

Virol J

181

170

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The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. 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. We identify -and attempt to explainnine 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. 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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“…However, according to Jordan's frightening monograph on the 1918 pandemic, there were five attempts to demonstrate sick-to-well influenza transmission in the desperate days following the pandemic and all were "singularly fruitless" [19]. (p. 441) Jordan reports that all five studies failed to support sick-to-well transmission, in spite of having numerous acutely ill influenza patients, in various stages of their illness, carefully cough, spit, and breathe on a combined total of >150 well patients [51][52][53][54][55]].…”

Section: Human Studies Attempting Sick-to-well Human Transmissionmentioning

confidence: 99%

The Epidemiology of Influenza

1922

Medicine

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The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. 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. We identify-and attempt to explainnine 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. 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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The Transmission of Influenza

Cited by 4 publications

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Seasonal influenza in the United States, France, and Australia: transmission and prospects for control

Seasonal influenza in the United States, France, and Australia: transmission and prospects for control

On the epidemiology of influenza

The Epidemiology of Influenza

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