Abstract
The 1918 influenza pandemic was the deadliest in known human history. It spread globally to the most isolated of human communities, causing clinical disease in a third of the world’s population, and infecting nearly every human alive at the time. Determination of mortality numbers is complicated by weak contemporary surveillance in the developing world, but recent estimates put the death toll at 50 million or even higher. This outbreak is of great interest to modern day epidemiologists, virologists, global health researchers and evolutionary biologists. They ask: Where did it come from? And if it happened once, could it happen again? Understanding how such a virulent epidemic emerged and spread offers hope for prevention and strategies of response. This review uses historical methodology and evolutionary perspectives to revisit the 1918 outbreak. Using the American military experience as a case study, it investigates the emergence of virulence in 1918 by focusing on key susceptibility factors that favored both the influenza virus and the subsequent pneumococcal invasion that took so many lives. This article explores the history of the epidemic and contemporary measures against it, surveys modern research on the virus, and considers what aspects of 1918 human and animal ecology most contributed to the emergence of this pandemic.
Highlights
The 1918 influenza pandemic was the deadliest in known human history
As a physician with interests in evolutionary medicine, I weave evolutionary perspectives into this historical context, focusing on the American military experience as a case study to investigate the emergence of virulence in 1918 by focusing on key susceptibility ß The Author(s) 2018
It is important to realize that there were two linked epidemics—influenza and subsequent bacterial pneumonia—which together generated high case mortality rates
Summary
The 1918 influenza pandemic was the deadliest in known human history. It spread globally to the most isolated of human communities, causing clinical disease in a third of the world’s population and infecting nearly every human alive at the time. Han and Rambaut conclude, ‘We hypothesize that childhood exposure to an H3N8 virus may have made some young adults in 1918 a sort of temporal counterpart to highly vulnerable geographical isolated populations, inducing suboptimal immunity that tilted the odds in favor of secondary infection with the wide range of bacterial pathogens that cause most influenza-related mortality’.
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