NIAID CEIRS | Research Publication Commentary
Smith, J. et al. A comparative analysis of host responses to avian influenza infection in ducks and chickens highlights a role for the interferon-induced transmembrane proteins in viral resistance. BMC Genomics (2015).
The recent highly pathogenic avian influenza (HPAI) H5 outbreak continues to have significant economic impacts on the international and domestic poultry industries and presents a potential public health concern. Avian influenza infects numerous avian hosts, including chickens and ducks. Reducing the spread of avian influenza requires an understanding of how the virus interacts with its avian hosts. However, it remains unclear why some species are more susceptible than others to certain strains of influenza. For instance, although ducks are infected they show minimal signs of disease to most HPAI viruses, while chickens are highly susceptible and quickly succumb to HPAI infections. Determining which genes are activated in chickens and ducks following infection with avian influenza viruses can shed light on the difference in susceptibility between the two species.
In mammals, the family of interferon induced transmembrane proteins (IFITM) is known to play a role in limiting influenza infection. The precise role of IFITM proteins during infection is not known, though they have been shown to be involved in preventing the early stages of infection. However, IFITM genes have not previously been examined in avian species and their role in avian influenza virus infections is unknown. Here, Drs. Jacqueline Smith, Nikki Smith, and colleagues from St. Jude CEIRS are the first to examine differences in the expression of IFITM genes in chickens and ducks following an infection with low or highly pathogenic avian influenza viruses.
Chickens and ducks were infected with either the low pathogenic strain A/Mallard/British Columbia/500/2005 (H5N2) or the highly pathogenic strain A/Vietnam/1203/2004 (H5N1) and monitored for disease progression. Both chickens and ducks survived infection with the low pathogenic H5N2 virus. However, the HPAI H5N1 virus proved fatal to all chickens, while some of the ducks survived the infection.
Genetic material was harvested from infected tissues to determine which genes were expressed following infection and specifically, whether IFITM genes were activated. Analysis of all genes indicated that although chickens mounted an immune response to H5N1 HPAI viruses, the response was short-lived and inadequate to confer protection. Conversely, HPAI infections in ducks with H5N1 caused a robust and sustained immune response. When the authors investigated the expression of the IFITM genes specifically, the IFITM response in chickens was almost non-existent while ducks initiated and maintained high expression of IFITM genes following H5N1 HPAI infection. Analysis indicated significant differences in host antiviral responses between chickens and ducks and the difference in IFITM response could play a crucial role in the ability of ducks to survive HPAI infection where infection is highly lethal to chickens.
The authors also performed a phylogenetic analysis to determine the evolutionary relationships of IFITM genes in avian species. Evolutionary patterns show that among all bird species the IFITM genes appear to be evolving more rapidly in ducks compared to chickens. Further research is needed to identify the specific genes that are activated in response to influenza infections in avian species. Understanding of these biological pathways and mechanisms could lead to potential mitigation or treatment strategies that could reduce or prevent the economic and public health consequences of avian influenza.