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Innate immune responses of domestic pigeons to the infection of pigeon paramyxovirus type 1 virus

Authors :
Yutong Hou
Zhanbang Ma
Deying Ma
Mengying Gao
Zongxi Han
Lili Zhang
Fangfang Wang
Source :
Poultry Science, Vol 100, Iss 2, Pp 603-614 (2021), Poultry Science
Publication Year :
2021
Publisher :
Elsevier, 2021.

Abstract

Pigeon paramyxovirus type 1 (PPMV-1) is a globally distributed, virulent member of the avian paramyxovirus type-1. The PPMV-1–associated disease poses a great threat to the pigeon industry. The innate immune response is crucial for antiviral infections and revealing the pathogenic mechanisms of PPMV-1. In this study, we evaluated the pathogenicity of a PPMV-1 strain LHLJ/110822 in one-month-old domestic pigeons, as well as the host immune responses in PPMV-1–infected pigeons. We observed typically clinical sign in infected pigeons by 3 dpi. The morbidity rate and the mortality in pigeons inoculated with the PPMV-1 strain were up to 100% and 30%, respectively. The virus could replicate in all of the examined tissues, namely trachea, lung, liver, spleen, and bursa of Fabricius. In addition, the infected pigeons had developed anti-PPMV-1 antibodies as early as 8 dpi; and the antibody level increased over the time in this study. The expression level of toll-like receptor (TLR) 2, TLR3 TLR15, IFN-γ, and IL-6 were significantly upregulated by the PPMV-1 infection in some tissues of pigeons. By contrast, PPMV-1 infection results in downregulation of IL-18 expression in most of investigated tissues except for bursa of Fabricius in this study. The current results confirmed that this virus could replicate in pigeons and induce host immune responses, then leading to produce serum antibody titers. Meanwhile, the PPMV-1 infection induces strong innate immune responses and intense inflammatory responses at early stage in pigeon which may associate with the viral pathogenesis.

Details

Language :
English
ISSN :
00325791
Volume :
100
Issue :
2
Database :
OpenAIRE
Journal :
Poultry Science
Accession number :
edsair.doi.dedup.....d831104361751b92d4e52def51fffda1