MODEL-BASED EVALUATION OF HIGHLY AND LOW PATHOGENIC AVIAN INFLUENZA DYNAMICS IN WILD BIRDS

Since the emergence of highly pathogenic (HP) H5N1 in southern China, there is growing interest in avian influenza (AI) epidemiology to predict disease risk in wild and domestic birds, and prevent further transmission to humans. However, understanding the epidemic dynamics of HPAI viruses remains challenging because they have rarely been detected in wild birds. We used modeling to integrate available scientific information from laboratory and field studies, evaluate AI dynamics in individual hosts and waterfowl populations, and identify key areas for future research.

We developed a Susceptible-Exposed-Infectious-Recovered (SEIR) model describing the course of the disease in a population of waterfowl. We used published laboratory challenge studies to estimate epidemiological parameters (rate of infection, latency period, recovery and mortality rates), considering the importance of age classes, and virus pathogenicity. We extended this model to wild bird populations by estimating the rate of infectious contact θ with virus using prevalence data from waterfowl surveys.

Infectious contact leads to infection and virus shedding within 1-2 days, followed by relatively slower period for recovery or mortality. Our sensitivity analysis demonstrated that the rate of infection plays a key role in AI epidemic dynamics. Therefore, additional laboratory challenges clarifying age-related differences in LPAI infection processes, the source of virus exposure (by direct bird-to-bird transmission or environmental transmission), and the level of exposure would expand our understanding of infection rates under various conditions.

We found a shorter infectious period for HPAI than low pathogenic (LP) AI, which may explain that HPAI has been much harder to detect than LPAI during surveillance programs. Our model predicted a rapid LPAI epidemic curve, with a median duration of infection of 50-60 days and no fatalities. In contrast, HPAI dynamics had lower prevalence and higher mortality, especially in young birds. Extensive surveillance programs for AI viruses have reported the presence of LPAI asymptomatic carrier birds all around the world but HPAI viruses have been detected in only a few healthy wild birds, and in most HPAI outbreaks, only a few dead individuals have been found. In a general sense, these observations agree with our model predictions of short epidemics for HPAI and much higher prevalence and longer duration of infection in birds with LPAI. Our model suggests increasing surveillance for HPAI in post-breeding areas, because the presence of immunologically naïve young birds is predicted to cause higher HPAI prevalence and bird losses during this season. Moreover, serological surveys to determine circulation of AI viruses in avian populations may effectively complement swab data, because immunity appears to last considerably longer than infection. Our results indicate a better understanding of immunity-related processes is required to refine predictions of AI risk and spread, improve surveillance for HPAI in wild birds, and develop disease control strategies to reduce potential transmission to domestic birds and/or humans.