1922, exacting a heavy toll on a territory already coping with other infectious disease problems including malaria, tuberculosis, plague, smallpox, cholera, and measles (e.g., Starling, 2007) (Box A12-1).
The 2009-H1N1 influenza A virus was recognized in the United States and Mexico in mid-April. Airplane travel could quickly seed the virus worldwide, more so than in previous pandemics, catching the Southern Hemisphere winter and summer in the Asian tropics at the usual time of peak influenza activity there (see below). Hong Kong, with its experience of dealing with influenza, was able to react with sound public health measures and diagnostic services. The first case was recognized on May 1st and 4 months later there were around 15,000 cases, a figure that is probably an underestimate. The vast majority of cases were mild. At the time of the Institute of Medicine (IOM) workshop (mid-September 2009), the numbers of cases in mainland China, Taiwan, and Macao were trickling in. Elsewhere in tropical Asia, reported numbers were also low (SEARO/WHO 2009).
Brief Overview of the Origin of the 1918 Pandemic H1N1 Virus and the Classical H1N1 Swine Flu Virus
Origin of the 1918 Pandemic Virus
Differing times of yearly influenza occurrence in temperate and tropical zones may be a key factor, something not appreciated until the late 1980s (see later discussion). Economic migrants from the southestern part of the influenza epicenter would have carried the H1N1 virus to Western Europe and the United States prior to 1918. Outbreaks there occurred in late winter and early spring 1918 before later doing so that year in the Canton area and in Hong Kong in summer, the usual time of peak occurrence (Shortridge, 1999b).
Origin of Classical Swine Flu Virus
Outbreaks of influenza in pigs followed the spread of the virus northward of Canton and were recorded at the time of human infection in the far northeast (Chun, 1919), suggesting initial human-to-pig transmission. Could there have been a similar occurrence in pigs in the United States around 1918 resulting in endemicity? Infection of piglets experimentally with the reconstructed 1918 pandemic virus is of interest (Weingartl et al., 2009). Phylogenetic studies on the hemagglutinins (HAs) from a range of H1N1 viruses suggest that the classical swine/Iowa/15/30 virus was not a direct descendant of the 1918 pandemic virus, rather from a common ancestral virus around 1905 (Kanegae et al., 1994). It seems that much activity was taking place in southern China involving an H1 or H1-like virus from around the turn of the century until 1918. While much must be conjectured, we may overlook it to our peril.