Title: Previous infection with a mesogenic strain of newcastle disease virus prevents infection with a highly pathogenic avian influenza virus in chickens Authors
|Costa-Hurtado, Mar -|
Submitted to: International Poultry Scientific Forum
Publication Type: Abstract Only
Publication Acceptance Date: November 19, 2013
Publication Date: January 27, 2014
Citation: Costa-Hurtado, M., Afonso, C.L., Miller, P.J., Shepherd, E.M., Smith, D.M., Pantin Jackwood, M.J. 2014. Previous infection with a mesogenic strain of newcastle disease virus prevents infection with a highly pathogenic avian influenza virus in chickens [abstract]. International Poultry Scientific Forum, January 27028, 2014, Atlanta, GA. CDROM. Technical Abstract: Avian influenza virus (AIV) and Newcastle disease virus (NDV) are two of the most important viruses affecting poultry worldwide. Co-infections of poultry with AIV and NDV are a problem from both the clinical point of view and the diagnosis of these viruses, but little is known on the interactions between these two viruses when infecting poultry. AIV and NDV can produce from mild to moderate upper respiratory diseases in their low pathogenic forms (lentogenic or mesogenic NDV and low pathogenicity AIV), to severe systemic diseases with high mortality in their more virulent forms (velogenic NDV and highly pathogenic AIV). Our former co-infection studies have shown that previous infection of chickens with mesogenic and velogenic NDV strains can affect HPAIV replication in tissues, but the clinical outcome depended on the timing of the infections and the virulence of the NDV strain. To further evaluate the dynamics of AIV-NDV co-infections, two and four-week-old specific pathogen free (SPF) white leghorn chickens were co-infected with a mesogenic strain of NDV (mNDV) (Pigeon 84) and with highly pathogenic (HP) AIV (A/chicken/Jalisco/CPA-12283-12/2012 H7N3) by simultaneous or sequential inoculation. We observed that previous infection of chickens with mNDV can prevent infection with HPAIV 3 days later, consequently protecting against disease and mortality due to HPAIV. Similar protection was observed in both age groups. These results suggest that when mNDV has replication advantage is able to interfere with a second virus infection, most likely by inducing an antiviral state due to the activation of innate immune mechanisms that prevent host cells from being infected by a second virus. In conclusion, previous infection with mNDV can interfere with HPAIV infection; however the timing of the infections will determine the outcome observed.