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Virus interference between H7N2 low pathogenic avian influenza virus and lentogenic Newcastle disease virus in experimental co-infections in chickens and turkeys
- Costa-Hurtado, Mar, Afonso, Claudio L, Miller, Patti J, Spackman, Erica, Kapczynski, Darrell R, Swayne, David E, Shepherd, Eric, Smith, Diane, Zsak, Aniko, Pantin-Jackwood, Mary
- Veterinary research 2014 v.45 no.1 pp. 1
- Influenza A virus, Newcastle disease virus, chickens, pathogenicity, poultry diseases, receptors, turkeys, viral shedding, virus replication, viruses
- Low pathogenicity avian influenza virus (LPAIV) and lentogenic Newcastle disease virus (l NDV) are commonly reported causes of respiratory disease in poultry worldwide with similar clinical and pathobiological presentation. Co-infections do occur but are not easily detected, and the impact of co-infections on pathobiology is unknown. In this study chickens and turkeys were infected with a l NDV vaccine strain (LaSota) and a H7N2 LPAIV (A/turkey/VA/SEP-67/2002) simultaneously or sequentially three days apart. No clinical signs were observed in chickens co-infected with the l NDV and LPAIV or in chickens infected with the viruses individually. However, the pattern of virus shed was different with co-infected chickens, which excreted lower titers of l NDV and LPAIV at 2 and 3 days post inoculation (dpi) and higher titers at subsequent time points. All turkeys inoculated with the LPAIV, whether or not they were exposed to l NDV, presented mild clinical signs. Co-infection effects were more pronounced in turkeys than in chickens with reduction in the number of birds shedding virus and in virus titers, especially when LPAIV was followed by l NDV. In conclusion, co-infection of chickens or turkeys with l NDV and LPAIV affected the replication dynamics of these viruses but did not affect clinical signs. The effect on virus replication was different depending on the species and on the time of infection. These results suggest that infection with a heterologous virus may result in temporary competition for cell receptors or competent cells for replication, most likely interferon-mediated, which decreases with time.