2018
DOI: 10.2105/ajph.2018.304631
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The Mother of All Pandemics Is 100 Years Old (and Going Strong)!

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Cited by 64 publications
(61 citation statements)
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“…The 1918 mortality curve, however, was "W-shaped," with an additional mortality peak in persons 20-40 years old ( Fig. 3; Morens and Taubenberger 2018), and an increased (although to a lesser degree than expected) mortality in elderly populations. The decreased mortality in the elderly could be attributed to nineteenth century exposure to then-prevalent influenza A viruses either containing an H1 HA or an N1 neuraminidase (NA), or to other conserved antigens in common with the 1918 virus (Taubenberger and Morens 2006;Viboud et al 2013).…”
Section: Influenza Virus Pathogenicitymentioning
confidence: 88%
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“…The 1918 mortality curve, however, was "W-shaped," with an additional mortality peak in persons 20-40 years old ( Fig. 3; Morens and Taubenberger 2018), and an increased (although to a lesser degree than expected) mortality in elderly populations. The decreased mortality in the elderly could be attributed to nineteenth century exposure to then-prevalent influenza A viruses either containing an H1 HA or an N1 neuraminidase (NA), or to other conserved antigens in common with the 1918 virus (Taubenberger and Morens 2006;Viboud et al 2013).…”
Section: Influenza Virus Pathogenicitymentioning
confidence: 88%
“…This suggests that the pandemic virus had already been seeded around the globe, but that fatal infections remained below the threshold of excess mortality detection, thereby epidemiologically obscuring its place of origin. Such indolent prepandemic transmission, likely beginning in or before 1918, eventually reached pandemic explosivity (and therefore recognition) only after exceeding critical excess mortality thresholds in multiple large urban populations around the globe (Morens and Taubenberger 2018). Among the first of these, in July-August 1918, were pandemic emergences identified by excess mortality, although presumably blunted by summer temperature and humidity, which are unfavorable to influenza virus spread, in China and India, and in parts of northern Europe including England, northern Germany, and Scandinavia (Jordan 1927;Andreasen et al 2008).…”
Section: Origin Of the 1918 Pandemic H1n1 Virusmentioning
confidence: 99%
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“…In the modern era, we have vaccines for only one of the major bacterial copathogens that routinely caused fatal influenza in 1918, S. pneumoniae , in the form of 2 vaccines that each contain immunogens of common but different circulating bacterial types. We have argued elsewhere that, hand in hand with improved influenza vaccine prevention, we need to develop better means of preventing deaths from secondary bacterial pneumonia [ 2 ]. The highest priorities are efficacious vaccines against the most important secondary pneumopathogens, such as S. aureus and S. pyogenes , and identification of early reliable biomarkers of impending bacterial pneumonia in people with influenza illnesses.…”
Section: Influenza Infection and The Human Hostmentioning
confidence: 99%
“…In 1918, the world experienced the deadliest single event in recorded human history [ 1 , 2 ]—the sudden emergence of an influenza virus of extraordinary lethality, unprecedented in more than a millennium of influenza pandemic observation ( Figure 1 ). In considering the rationale for and the desired characteristics of so-called “universal” influenza vaccines, we must, before any other consideration, look back from the vantage point of 2018 to that century-old tragedy and ask: What are we trying to prevent, and how do we expect a vaccine to prevent it?…”
mentioning
confidence: 99%