Pathogenicity of duck plague and innate immune responses of the Cherry Valley ducks to duck plague virus

Abstract

Duck plague caused by duck plague virus (DPV) is an acute and contagious disease. To better understand the pathogenic mechanism of duck plague virus in ducklings, an infection experiment was performed. Our results showed that typical symptoms were observed in the infected ducklings. DPV could replicate quickly in many tissues, leading to pathological lesions, especially on the spleen. Real-time quantitative PCR demonstrated that expression of many innate immune-related genes was mostly up-regulated in the brain, and the antiviral innate immune response was established, but not sufficient to restrict viral replication. In contrast, although the expression of many major pattern recognition receptors (PRRs) increased in the spleen, the expression of most cytokines was declined. Our study indicates that DPV is a pantropic virus that can replicate rapidly in tissues, causing serious pathological lesions but the immune responses are different in the spleen and brain. To our knowledge, this is the first report to systematically explore the expression profiles of the immune genes in the DPV-infected ducks. Our data provide a foundation for further study of the pathogenicity of duck plague.

Duck virus enteritis (duck plague) – a comprehensive update

“…In duck plague virus (DPV) infected ducklings, antiviral immunity comprised of noticeable presence of pattern recognition receptors (PRRs) significantly appears along with observable typical pathological lesions and symptoms. Study based on realtime quantitative PCR and TaqMan TM fluorescent quantitative real-time PCR with specific primers and probes also confirmed hike in the protective innate immune response and is helpful in finding the break points during pathogenesis to lower the establishment of infection of DPV/DEV in ducks (Zou et al 2010;Li, Hong, et al 2016). Even though differences in virulence have been observed among DEV strains, antigenic nature remains identical for most of the isolates (Kisary & Zsak 1983;Akter et al 2004).…”

“…DEV was also used in producing recombinant vaccines (rDEVs) as rDEV-N, rDEV-S and rDEV-S1 expressing the N, S, and/or S1 protein of infectious bronchitis virus (IBV). Such vaccines generated significant humoral and cellular immunity post-vaccination in terms of lowered CD4(+)/CD8(+) Tlymphocytic ratio, improved antibody titer, decreased viral shedding and reduced mortality in chickens even when challenged with virulent IBV strain than the use of any single recombinant vaccine (Li, Wang, et al 2016). Researchers have prepared oil emulsified inactivated vaccine against Salmonella Typhimurium (ST), DP and Duck Hepatitis Virus (DHV) which was found safe, potent and capable of protecting ducklings against ST, DP and DHV infections effectively (Hanan et al 2014;.…”

“…However, there was no elevation of pro-inflammatory cytokines in the spleen. Authors postulated that the virus has evolved ways to escape from the host immunity (Li, Hong, et al 2016). In convalescent birds, the virus undergoes latent infection in trigeminal ganglion where it, upon re-activation, results in shedding into the environment (Shawky & Schat 2002).…”

“…The lining epithelial cells and lymphocytes of these organs are the principal sites for replication of DEV (Xuefeng et al 2008). Since DEV can replicate quickly in many cell types and tissues, it is considered as a pantropic virus that leads to pathological lesions in many different organs (Li, Hong, et al 2016). Herpes virus attaches to host-cell receptors by virion glycoprotein spikes (Boehmer & Nimonkar 2003).…”

Isolation and Selection of Duck Primary Cells as Pathogenic and Innate Immunologic Cell Models for Duck Plague Virus

“…Infection with virulent DPV strains causes gross lesions in ducks in most tissues, including the heart, liver, spleen, bursa, and brain (15,16), where the virus has been detected (12,17). Upregulation of PRRs and ISGs expression has been reported, indicating that DPV exhibits broad organ tropism and activates the innate immune system (18,19). Differing basal and induced levels of PRRs and ISGs among different cell types and organs are important factors in determining the organ tropism of viruses such as poliovirus, reovirus, and murine coronavirus (20)(21)(22).…”