. "Workshop Overview." The Domestic and International Impacts of the 2009-H1N1 Influenza A Pandemic: Global Challenges, Global Solutions: Workshop Summary. Washington, DC: The National Academies Press, 2010.
The following HTML text is provided to enhance online
readability. Many aspects of typography translate only awkwardly to HTML.
Please use the page image
as the authoritative form to ensure accuracy.
The Domestic and International Impacts of the 2009-H1N1 Influenza a Pandemic: Global Challenges, Global Solutions - Workshop Summary
than 0.1 percent for other pandemic strains). As Morens et al. (2009) point out, all influenza pandemics since that time, and indeed most cases of influenza A worldwide (other than human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, as illustrated in Figure WO-2. These include the H2N2 (1957) and H3N2 (1968) viruses, which possessed key genes from the 1918 virus along with additional avian influenza genes. Hence, the 1918 H1N1 virus is truly the “mother” of all influenza pandemics.
In the spring of 1918, a “herald wave” of relatively mild influenza cases occurred in New York City. That fall, a second wave of severe disease (and in many places, a subsequent wave in early 1919) produced significantly higher rates of mortality among people between the ages of 20 and 34, and particularly among pregnant women, than is typical of seasonal influenza epidemics (Simonsen et al., 2005). Two conditions tended to occur (both individually and in combination) in these fatal H1N1 cases: bronchopneumonia, likely caused by a secondary bacterial infection, and severe acute respiratory distress, often leading to cyanosis (CIDRAP, 2009).
Despite its depiction as the “Spanish flu,”4 the geographic origin of the 1918 H1N1 strain of the influenza virus remains a mystery (CIDRAP, 2009). It is likely that the virus, which had previously infected birds, emerged as a human pathogen in the Midwestern United States and accompanied American troops to Europe during World War I. Some investigators believe that the avian virus jumped into swine at approximately the same time it began to infect humans (Morens et al., 2009; Zimmer and Burke, 2009). Others contend, based on viral phylogeny, that genetic components of the 1918 pandemic strain circulated among swine and humans as early as 1911, which in turn suggests that the pandemic virus was generated by reassortment over a period of years and not introduced directly from birds into humans (Smith et al., 2009). Swine are believed to act as a “mixing vessel” for the reassortment of avian and human viruses (Salomon and Webster, 2009). As noted earlier, such events in doubly infected pigs generated the 1957 and 1968 pandemic influenza strains.
1957: A Model for 2009?
Between 1957 and 1958, an estimated 25 percent of the U.S. population was infected with pandemic H2N2 influenza, resulting in nearly 70,000 fatalities out of an estimated 1 million deaths worldwide (CIDRAP, 2009; Henderson et
“America in 1918 was a nation at war. Draft call-ups, bond drives, troop shipments were all in high gear when the flu epidemic appeared. American soldiers from Fort Riley carried the disease to the trenches of Europe, where it mutated into a killer virus. The disease would later be dubbed, inaccurately, Spanish influenza. Spain had suffered from a devastating outbreak of influenza in May and June of 1918. The country, being a non-combatant in the war, did not censor news of the epidemic that was cutting through its population and was therefore incorrectly identified as its place of origin” (PBS, 2009).