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ARS Home » Research » Publications at this Location » Publication #262930
Title: Deletion of the M2-2 Gene from Avian Metapneumovirus Subgroup C (aMPV-C) Impairs Virus Replication and Immunogenicity in Turkeys

Author
item Yu, Qingzhong
item Estevez, Carlos
item Roth, Jason
item HU, HAIXIA - Jilin University
item Zsak, Laszlo

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/1/2011
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: The second matrix (M2) gene of avian metapneumovirus subgroup C (aMPV-C) virus contains two overlapping open reading frames (ORFs), encoding two putative proteins, M2-1 and M2-2. Both proteins are believed to be involved in either viral RNA transcription or replication. To further characterize the function of the M2-2 protein in virus replication, the non-overlapping region of the M2-2 ORF was deleted from an infectious aMPV-C cDNA clone and a viable virus was rescued using reverse genetics technology. The recombinant virus, raMPV-C 'M2-2, was characterized in vitro and in vivo. In Vero cells, raMPV-C 'M2-2 replicated less efficiently, 10-fold reduction, than the parental virus during the first 48 hours post-infection. raMPV-C 'M2-2 induced typical cytopathic effects (CPE) that were indistinguishable from those seen with the parental virus infection. In specific-pathogen-free (SPF) turkeys, raMPV-C 'M2-2 was attenuated and caused no clinical signs of disease. Less than 20% of the inoculated birds shed detectable virus in tracheal tissue during the first five days post-infection, and no virus shedding was detected afterwards. Forty percent of infected birds produced a weak antibody response, log2 6.0, at 14 days post-infection. Upon challenge with virulent aMPV-C strain, more than 80% of the raMPV-C 'M2-2-inoculated birds showed typical disease signs and virus shedding in tracheal tissue. These results suggest that the M2-2 protein of aMPV-C virus is not essential for virus replication in vitro, but is required for sufficient virus replication to maintain pathogenicity and immunogenicity in the natural host.