Table 1.

Potential ecological drivers of AIV prevalence in wild birds derived from experimental and empirical findings of the ecological interactions between AIV and wildfowl.

mechanisms	epidemiological predictions1 and experimental2 or empirical3 findings	ecological factors of potential influence on AIV transmission
environmental transmission	1bird could be infected from long-lived virus persisting in the environment by drinking or feeding; infection rate depends on the virus concentration and persistence in the environment, and bird consumption rate [9]	local climate may influence the environmental persistence of AIV
	2AIV can remain infectious for several months in water under experimental conditions. Warmer temperatures, radiation and desiccation reduce the duration of AIV infectivity [10,11]
	3mathematical models of environmental transmission capture some patterns of AIV infection dynamics in wildfowl [9,12]
	2ducks can be successfully infected by contact with contaminated water [13]	species foraging behaviour may influence exposure to environmental infection
	3higher prevalence is commonly reported in Anas species of dabbling ducks compared with diving or grazing wildfowl [3,5]
	3morphological trait associated with filtration of food particles (density of lamellae) has been positively associated with variations in AIV prevalence and diversity of subtypes shed in dabbling ducks [14]
inter-individual transmission	1both transmission via airborne droplets or short-lived viruses shed in the environment are considered as essentially direct because they occur on the same time scale and rely on the proximity of hosts [9,12]	host density and seasonal patterns of social aggregation may influence contact rate and transmission
	3seasonal peak in prevalence in a wildfowl species that forage mainly on land [8], and higher AIV detection rate in respiratory than intestinal tract, support the existence of a direct airborne transmission via the respiratory route [4,8,15]
	1inter-individual transmission is expected to be density-dependent since the contact rate scales with host density [16]
	3northern autumn peak in AIV prevalence in ducks coincides with a seasonal social aggregation during pre-migration and migration that likely promotes contact rate and viral transmission [5,10,17,18]
host receptivity	1difference in prevalence between species may result from a difference in intrinsic receptivity to AIV infection [19]	taxonomic group may influence receptivity to infection
	3the spectrum of AIV receptors on host cell surface vary substantially among different bird species [20]
host susceptibility	2natural and experimental AIV infection stimulates the production of long-lasting AIV specific antibodies in ducks; subsequent exposure to AIV produce a boost in AIV antibody titers [21,22]	geographical range associated with migratory behaviour and age may influence previous AIV exposure hence susceptibility to re-infection
	2prior exposure to homo- or heterosubtypic AIV reduces the duration and concentration of viral shedding in consecutive infections, demonstrating the existence of a partial cross-protective immunity against re-infection [21,23]
	3natural consecutive infections with different AIV subtypes have been reported in ducks providing evidence that a prior exposure does not fully protect against a subsequent AI virus infection with a heterosubtypic AIV [6,24]
	3higher prevalence in hatch-year birds compared with after-hatch-year birds is consistently reported [5,8]
	3the duration of virus shedding decreases during the northern autumn in wild ducks [6]
population immunity	1the transmission rate depend on the proportion of susceptible individuals in the host population and the rate at which they experience their first infection [1,2,16]	demographic rates and seasonal peaks in prevalence may influence the turnover of susceptible hosts
	3prevalence strongly decline during northern autumn and winter as the proportion of immunologically naive hatch-year birds progressively decreases through infection or as result of a greater mortality rate compared with adults [5,17,18,25]
host dispersal	1infected hosts shedding virus may disperse AIV as they move [2,10]	timing and range of migration may influence period and origin of virus introduction
	2,3experimentally [21,26] and naturally infected wildfowl [6] generally excrete AIV for one to three weeks without clinical signs or lesions
	3migratory wildfowl are able to perform long-distance movements within the time frame of AIV infection [27]
	3phylogenetic analysis confirms the occurrence of inter-continental exchange of AIV [28]
	3phylo-geographical clusters of AIV in wildfowl across North America suggest a dominance of introduction over persistence in the interannual perpetuation of AIV [29]