Ducks are members of the subfamily Anatinae, which contains most species of anserine birds. This subfamily is nearly cosmopolitan in distribution, and its members occupy almost all aquatic habitats. The ecology of these birds, summarized in Figure 1 , facilitates the maintenance and spread of avian influenza viruses. Although human influenza A isolates and the currently circulating H5N1 HPAI viruses typically infect the upper respiratory tract, the primary site of infection in ducks is the intestine. 6 Avian influenza viruses enter the environment when the host defecates or drools, and they then infect susceptible hosts as they feed and drink. Avian influenza virus replication has been observed in the respiratory tract, 6 but the contribution of this site to maintenance of infection in the population is unresolved. Specifically, fecal shedding of H4N7, H7N3, and H11N9 virions from experimentally infected mallard ducks persists longer and at higher titers than tracheal shedding. 6 When a large number of birds roost on a small pond (for example, in the staging ⁄ marshalling areas), as many as 10 10 EID 50 •g )1 •d )1 infectious virions are estimated to enter the environment in the fecal matter of each infected duck. 6 Further, avian influenza viruses are stable in water 1,7 and have been isolated from the surface of ponds containing a large number of waterfowl. 8, 9 Although aerosol transmission cannot be dismissed, the larger number of positive cloacal than tracheal swabs, the high fecal virus titer, and the stability of the virions in water suggest that lowpathogenic avian influenza (LPAI) viruses persist in duck populations through fecal-oral transmission. 1 This mechanism could partially explain the higher prevalence of infection in surface-feeding (dabbling) ducks than in diving ducks that typically feed in deeper water. 10 Surveillance data suggest year-round transmission of avian influenza viruses within duck populations. The prevalence of infection exhibits an annual cyclical pattern in both North American 1,11 and Eurasian 12 duck populations (Figure 1 ), peaking before and during the fall migration as a result of the influx of immunologically naïve juveniles. 1, 9, 10, 13 Experi-mentally infected white Pekin ducks have shed virus for more than 3 weeks after inoculation. 3, 14 Coupled with limited morbidity and serum antibody response, 3 infected birds are likely to shed virus during the first few weeks of the fall migration, dispersing it along their numerous migration corridors. However, the prevalence of infection is much lower along the migration routes and at the wintering grounds than at the marshalling areas. 9, 12, 15, 16 This disparity may reflect the development of immunity to circulating virus subtypes within the duck population or a decline in transmission because of population dispersal. 13 In general, prevalence of infection is higher at the wintering grounds and spring nesting sites in duck populations from Europe than in North American populations (Figure 1 ). The most likely explanation for this difference is random variation, since surveillance studies from multiple areas in North America and in Europe often obtain slightly different prevalence values in the duck populations. Many factors can affect prevalence including, but not limited to, the size of the duck population, sampling location, and time of collection. Thus, the few multi-year studies that exist likely exemplify the variation that one would observe if additional sampling sites were included in the studies, and not the differences in geography between Europe and North America. 16 Prevalence is at its lowest Figure 1 . Overview of the annual movement and behavior of migratory ducks and their role in interspecies transmission. During spring and fall migration, the ducks rest and feed for a few days to weeks at numerous stopover sites (wetlands, lakes, or ponds) along the migration route. The length of stay and the aquatic habitat allows the transmission of influenza viruses to and from the domestic duck populations. Domestic ducks that become infected are likely to maintain the virus locally and increase the probability of its spread to other species. In the diagram, solid arrows indicate confirmed routes of transmission of LPAI and ⁄ or HPAI viruses between species. The dashed line represents a probable but unconfirmed route of transmission. The graphs indicate the average prevalence of low-pathogenic avian influenza in North American and European duck populations during 3 stages of the annual migration. 10, 16 during the spring migration but increases again after the breeding season, when the ducks have moved to the molting and staging areas. 11, 13, 16 It is not clear how the duck population acquires avian influenza viruses during the spring of every year. Infectious virions may persist through the winter in the frozen waters of the breeding areas and reinfect the ducks when they return in the spring. 1, 6 Alternatively, the duck populations may carry the viruses throughout the entire migration. Year-round prevalence in the ducks supports the latter, although persistence in the frozen habitats could play a role in the perpetuation of the viruses. 10 Some virus subtypes are isolated more frequently than others. 10, 11 Three HA subtypes, H3, H4, and H6, are common in both North American and European ducks, 11, 12 and the most prevalent subtype combinations in both areas are H4N6 and H6N2. 16 Explanations vary for why certain HA and NA subtypes (and combinations) are common or rare in wild birds. The general hypothesis is that these subtypes likely have the highest fitness, with replication rates balanced by a level of virulence that sufficiently increases transmission probability to the level where infection in the next cohort of birds is almost guaranteed. It is speculated that this could be largely influenced by the functional balance between HA binding affinity and NA enzymatic activity. 17 Although the H6 gene is of Eurasian origin and is widely distributed in North American ducks, genomic analysis of viruses suggests limited intercontinental exchange between Eurasia and the Americas. 18 Therefore, novel viral genotypes must arise via mutation and reassortment of the genomes in circulation within a specific geographic area. The marshalling areas provide such an opportunity by attracting populations of ducks from various breeding areas and migration corridors, with each population harboring a potentially different combination of subtypes. 16 Coinfection of ducks with two or more virus subtypes is common, 19 as is reassortment, 14 and emergent strains that are most virulent to gallinaceous poultry can have low pathogenicity in the duck hosts. 20 However, the role of ducks in the maintenance and spread of influenza viruses, and especially in the emergence of novel genotypes, appears to depend on their migratory behavior. Specifically, ducks that migrate annually are likely to spread influenza viruses along the migration routes, primarily by exposing the resident and domestic duck populations at the numerous stopover sites. 10, 16, 21 In contrast, domestic and resident ducks maintain the viruses in close proximity to other species and have been implicated in the spread of both LPAI and HPAI viruses to domestic poultry and terrestrial birds. 20, 22, 23 