Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 2, 2009
Publication Date: February 1, 2010
Citation: Ramirez-Nieto, G., Shivaprasad, H.L., Kim, C., Lillehoj, H.S., Song, H., Osorio, I.G., Perez, D.R. 2010. Susceptibility And Adaptation Of A Mallard H5N2 Low Pathogenic Influenza Virus In Chickens Infected With Infectious Bursal Disease Virus. Avian Diseases. 54*1):513-521.
Interpretive Summary: Logical control of infectious diseases like avian influenza will depends on the comprehensive basic knowledge on how virus adapts to the host and how host makes innate immune response. Influenza type A viruses are members of the Orthomyxoviridae family and are subdivided into subtypes based on the antigenic properties of the two major surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA). To date, 16 HA subtypes and 9 NA subtypes have been characterized in influenza strains in many different combinations. The factors that determine interspecies
transmission and virulence of influenza viruses in both avian and mammalian species are generally poorly understood. In this paper, ARS scientists collaborated with scientists at University of Maryland and University of California to investigate antigenic evolution of different pathotypes of avian influenza strains. Using a virus which suppress host antibody response, these scientists demonstrated that immunosuppression of host facilitated the evolution of less pathogenic avian influenza strain to a more pathogenic type. More importantly, after adaptation,
avian influenza virus becomes more virulent in both immunosuppressed and immunocompetent chickens. These new findings will provide enhanced knowledge on avian influenza virus pathogenicity and important information for developing new control strategies against avian influenza virus.
The influenza A/Mallard/Pennsylvania/12180/1984 (H5N2) virus is unable to replicate in 2 to 4-week old normal, immunocompetent specific-pathogen-free (SPF) chickens. In contrast, this mallard virus shows limited replication in chickens that had been previously infected with the immunosuppressive agent infectious bursal disease virus (IBDV). This limited replication in IBDV-infected chickens allowed for the serial adaptation of the mallard virus in chickens. After 22 passages (P22) in IBDV-infected chickens, the resulting chicken-adapted virus replicated in both normal and IBDV-infected chickens more efficiently than the parental mallard virus. Analysis of the outcomes of infection and the lesions caused by the two viruses at the microscopic level in a time-point study showed that the P22 virus is more virulent than the parental mallard virus in both normal and IBDV-infected chickens. Our studies provide evidence that a previous history of IBDV infection in chickens may render them more susceptible to AI infections allowing for the potential introduction of AI in an otherwise resistant population.