Abstract
BackgroundGenotype VIId Newcastle disease virus (NDV) isolates induce more severe damage to lymphoid tissues, especially to the spleen, when compared to virulent viruses of other genotypes. However, the biological basis of the unusual pathological changes remains largely unknown.MethodsVirus replication, cytokine gene expression profile and cell death response in chicken splenocytes infected with two genotype VIId NDV strains (JS5/05 and JS3/05), genotype IX NDV strain F48E8 and genotype IV NDV strain Herts/33 were evaluated. Statistical significance of differences between experimental groups was determined using the Independent-Samples T test.ResultsJS5/05 and JS3/05 caused hyperinduction of type I interferons (IFNs) (IFN-α and -β) during detection period compared to F48E8 and Herts/33. JS5/05 increased expression level of IFN-γ gene at 6 h post-inoculation (pi) and JS3/05 initiated sustained activation of IFN-γ within 24 h pi, whereas transcriptional levels of IFN-γ remained unchanged at any of the time points during infection of F48E8 and Herts/33. In addition, compared to F48E8 and Herts/33, JS3/05 and JS5/05 significantly increased the amount of free nucleosomal DNA in splenocytes at 6 and 24 h pi respectively. Annexin-V and Proidium iodid (PI) double staining of infected cells showed that cell death induced by JS3/05 and JS5/05 was characterized by marked necrosis compared to F48E8 and Herts/33 at 24 h pi. These results indicate that genotype VIId NDV strains JS3/05 and JS5/05 elicited stronger innate immune and cell death responses in chicken splenocytes than F48E8 and Herts/33. JS5/05 replicated at a significantly higher efficiency in splenocytes than F48E8 and Herts/33. Early excessive cell death induced by JS3/05 infection partially impaired virus replication.ConclusionsViral dysregulaiton of host response may be relevant to the severe pathological manifestation in the spleen following genotype VIId NDV infection.
Highlights
Genotype VIId Newcastle disease virus (NDV) isolates induce more severe damage to lymphoid tissues, especially to the spleen, when compared to virulent viruses of other genotypes
At 12 and 24 h pi, F48E8 showed high replication efficiency in splenocytes, which is consistent with its high virus titer in chicken embryo fibroblasts (CEF) (Table 1)
These results suggest that high replication efficiency of genotype VIId NDV in splenocytes was isolate-specific and NDV replication may be partially associated with virus-induced cell death
Summary
Genotype VIId Newcastle disease virus (NDV) isolates induce more severe damage to lymphoid tissues, especially to the spleen, when compared to virulent viruses of other genotypes. Many pathological studies have revealed that genotype VIId NDV isolates induce the most severe necrosis in lymphoid tissues, especially in the spleen, when compared with virulent isolates of many viral determinants for pathogenicity of NDV have been identified [7,8,9], few mechanistic data regarding host response to NDV infection are available. Some recent studies have demonstrated that viral modulation of host innate immune response is associated with viral pathogenesis and pathological outcomes [4,10]. Numerous studies in animal and cell models have shown that robust host immune response contributes to the pathogenesis of highly pathogenic avian H5N1 influenza virus [11,12]. Harrison et al have shown that the degree of apoptosis in lymphoid tissues is correlated with the severity of disease caused by NDV strains of varying virulence [15]
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