In 1996, the parental virus (A ⁄ Goose ⁄ Guangdong ⁄ 1 ⁄ 96; A ⁄ Gs ⁄ GD ⁄ 1 ⁄ 96) of currently circulating H5N1 HPAI viruses emerged in southern China. Genetic evidence revealed that this virus originated from H5 LPAI viruses carried from northern Japan by wild ducks or other migratory birds. 15, 35 A reassortant H5N1 HPAI virus subsequently emerged in poultry at farms and live animal markets in Hong Kong in 1997. Genetic analyses showed that the H5 HA gene of the reassortant virus was derived from an A ⁄ Gs ⁄ GD ⁄ 1 ⁄ 96-like virus, while the remaining gene segments were derived from low-pathogenic viruses: the N1 NA gene came from A ⁄ Teal ⁄ Hong Kong ⁄ W312 ⁄ 97 (H6N1) virus, and the internal genes from A ⁄ Quail ⁄ Hong Kong ⁄ G1 ⁄ 97 (H9N2) virus. 36 The reassortant virus caused the first lethal infection in humans (6 deaths among 18 known cases) by direct bird-to-human transmission. 37 Between 1999 and 2002, H5N1 HPAI viruses with the H5 HA gene of A ⁄ Gs ⁄ GD ⁄ 1 ⁄ 96-like viruses but with a diversity of genotypes in the other genes, re-emerged multiple times in Hong Kong. 37 The first indication of the spread of H5N1 HPAI viruses from domestic to wild species of aquatic birds occurred in Kowloon and Penfold Park in Hong Kong, 38 where 19 different duck species were infected. Some species, including the Red-Crested Pochard (Netta rufina), were highly susceptible (19 ⁄ 20 died), whereas others, including the Bahama Pintail (Anas bahamensis), were less susceptible (4 ⁄ 21 died).