the case of the H5N1/HK/97 virus (Shortridge, 1999a) and civet cat⁸⁰ for the SARS coronavirus (Guan et al., 2003), prevented further zoonotic spread. The Bird Flu incident provided the foundation for dealing with SARS. There is still much to be learned about influenza toward improving pandemic preparedness. This will require renewed vigor across a range of influenza studies and public health measures. It cannot be denied that our goal must be to the vision of no more pandemics. The 2009-H1N1 influenza A pandemic has rekindled this vision and is seen, in part, against a background of 30 years in Hong Kong, a place that in effect functioned as an influenza sentinel post. This informal designation followed the hypothesis that southern China is an epicenter for the emergence of pandemic influenza viruses (Shortridge and Stuart-Harris, 1982), a hypothesis that was the anchor for subsequent thinking and goals considered here.

Should we have been surprised?

Simple epidemiological information based on the ages of those initially infected by the pandemic H1N1 virus in 1918 in Canton (now Guangzhou) in southeastern China suggests that an H1N1-like virus had been active in the area for about 11 years prior to 1918 (Shortridge, 1999b). Molecular evolutionary studies indicate that such a virus had circulated from as early as 1911 (Smith et al., 2009a). These data, seroarcheological studies, and virus isolation suggest that H1N1 or H1-like viruses circulated in humans four times over the last 120 or so years. Indeed, the H1N1 lineage may have extended back to the 1830s (Gammelin et al., 1990), a dating in accord with the emergence of a pandemic in China, possibly southern China, in 1830-1831 (Patterson, 1985). Thus, it is clear that this subtype of virus has an affinity for the human host. This includes the 1950-like H1N1 virus that reappeared in 1977 (Kendal et al., 1978; Nakajima et al., 1978) whether or not it is a rogue virus. And now, in 2009 another H1N1 virus has been able to establish a niche in humans—and doing so with pandemic gusto—in the face of a global population seemingly well protected with H1 antibodies. Whereas the pandemic viruses of the last century arose in southern China (see below about the 1918 virus) and were of Eurasian genetic extraction, the H1N1 2009 virus arose in North America and was of mixed geographical and host extractions.

The answer to the question posed is both “no” and “yes.” There is much to learn about the epidemiology, ecology, and science of H1N1 viruses.

While the 1918 pandemic seemingly manifested in Western Europe and the United States in late winter and early spring, it did not apparently do so in China