Abstract

There is growing interest in avian influenza (AI) epidemiology to predict disease risk in wild and domestic birds, and prevent transmission to humans. However, understanding the epidemic dynamics of highly pathogenic (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 and 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. Infectious contact leads to infection and virus shedding within 1–2 days, followed by relatively slower period for recovery or mortality. 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. Based on field data from LPAI studies, our model suggests to increase 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. Our results indicate a better understanding of the transmission, infection, and 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.

Highlights

  • Avian influenza (AI) became a significant human and domestic animal health issue in 1996 when highly pathogenic (HP) H5N1 virus was isolated from domestic geese in southern China

  • Susceptible birds exposed by contact to LPAI-inoculated birds became infectious at a slower rate compared with highly pathogenic (HPAI)-inoculated birds (0.76 day)

  • Subtracting the latent time (i.e. ERI) from the time for susceptible individuals to become infectious (SRI), we estimated the median time required for susceptible birds to become exposed/infected (SRE), which was slightly longer for HP than low pathogenic (LP) viruses (0.48 vs. 0.28 day, respectively)

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Summary

Introduction

Avian influenza (AI) became a significant human and domestic animal health issue in 1996 when highly pathogenic (HP) H5N1 virus was isolated from domestic geese in southern China. Since 2002, HPAI H5N1 strains have emerged in both wild and domestic birds and spread throughout the Old World [1,2]. HPAI viruses in domestic poultry, and subsequently humans, likely arose by the introduction and mutation of low pathogenic (LP) AI strains from wild birds. Extensive field surveys reported the continuous worldwide circulation of LPAI in wild birds, primarily Anseriformes and Charadriiformes, which are considered the natural reservoir of all 16 HA and 9 NA subtypes of influenza A viruses [3,4,5]. Prevalence and distribution of LPAI virus subtypes markedly differ among species, years, and places. Epidemic dynamics may be influenced by ecological factors that influence habitat use by waterfowl species, species differences in susceptibility, age- and species-related differences in virus shedding, environmental conditions that influence virus persistence in wetlands [10], and immunity (or cross-immunity) from a previous exposure to influenza viruses [11]

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