Department of Veterinary and Biomedical Sciences, University of Minnesota, 1971 Commonwealth Ave., St. Paul, MN 55108, USA.
Vaccine. 2011 Jan 10;29(3):459-65. doi: 10.1016/j.vaccine.2010.10.074. Epub 2010 Nov 10.
Avian metapneumovirus subtype C (aMPV/C) causes a severe upper respiratory tract (URT) infection in turkeys. Turkeys were inoculated oculonasally with inactivated aMPV/C adjuvanted with synthetic double-stranded RNA polyriboinosinic polyribocytidylic acid (Poly IC). Immunized turkeys had elevated numbers of mucosal IgA+ cells in the URT and increased levels of virus-specific IgG and IgA in the lachrymal fluid and IgG in the serum. After 7 or 21 days post immunization, turkeys were challenged oculonasally with pathogenic aMPV/C. Immunized groups were protected against respiratory lesions induced by the challenge virus. Further, the viral copy number of the challenge virus in the URT were significantly lower in the immunized turkeys than in the unimmunized turkeys (P<0.05). These results showed that inactivated aMPV/C administered by the respiratory route induced protective immunity against pathogenic virus challenge.
禽偏肺病毒 C 型（aMPV/C）可引起火鸡严重的上呼吸道（URT）感染。火鸡通过眼鼻接种用合成双链 RNA 聚肌苷酸聚胞苷酸（Poly IC）佐剂化的灭活 aMPV/C。免疫火鸡的 URT 中有大量黏膜 IgA+细胞，并且泪液中病毒特异性 IgG 和 IgA 以及血清中 IgG 的水平升高。免疫后 7 或 21 天，火鸡通过眼鼻途径用致病性 aMPV/C 进行攻毒。免疫组可抵抗攻毒病毒引起的呼吸道病变。此外，免疫火鸡的 URT 中攻毒病毒的病毒拷贝数明显低于未免疫火鸡（P<0.05）。这些结果表明，呼吸道给予的灭活 aMPV/C 可诱导针对致病性病毒攻毒的保护性免疫。
