transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings. Influenza can also be transmitted by saliva, nasal secretions, and feces. Infections occur through contact with these bodily fluids or with contaminated surfaces. Influenza viruses can remain infectious for about one week at human body temperature, for more than 30 days at 0°C (32°F), and indefinitely at very low temperatures (such as lakes in northeast Siberia). They can be inactivated easily by disinfectants and detergents.
Box WO-1 provides a general overview of influenza virus classification, structure, and life cycle. For a complete overview on this topic and an extensive reference list please see Treanor (2010).
The scientific and public health response to the 2009-H1N1 influenza A pandemic was both informed and influenced by observations of past pandemics and seasonal influenza epidemics, by the response to an abortive pandemic threat from H1N1 swine influenza in 1976, and from ongoing efforts to address the pandemic threat posed by the highly pathogenic H5N1 avian influenza, following its emergence in humans in 1997. In this section, we review these events in order to establish the 2009-H1N1 influenza A pandemic within a historic and scientific context.
Ten apparent influenza pandemics, five of which occurred during the nineteenth century, have been recorded over the past 300 years. The three twentieth-century pandemics—presented in Table WO-1—which began in 1918, 1957, and 1968, respectively, are known to have been caused by three different antigenic subtypes3 of the influenza A virus, denoted H1N1, H2N2, and H3N2 in order of their emergence (Morens et al., 2009). While these pandemics varied widely in terms of their geographic origins and epidemiological characteristics, all gave warnings of their arrival, featured significant increases in mortality among younger age groups (a phenomenon known as “pandemic age shift”), and continued to cause morbidity and mortality months to years beyond their peaks (Simonsen et al., 2005) as will be discussed in greater detail, below.
Beginning in the spring of 1918, the H1N1 influenza virus that infected approximately one-third of the world’s population was exceptionally virulent (IOM, 2005; Taubenberger and Morens, 2006). It caused an estimated 50–100 million deaths, with a case-fatality rate of greater than 2.5 percent (compared with less
Every influenza A virus has a gene coding for 1 of 16 possible hemagglutinin (HA) surface proteins and another gene coding for 1 of 9 possible neuraminidase (NA) surface proteins. HA facilitates viral attachment to host tissues; NA is involved in the release of viral progeny from the host. Of the 144 possible combinations of H and N genes, only 3 (H1N1, H2N2, and H3N2) have ever been found in truly human-adapted viruses (Morens et al., 2009).