ArticleAnimals : an open access journal from MDPI2023
Role of Macrophages in the Pathogenesis of Genotype VII Newcastle Disease Virus in Chickens.
Article in Animals : an open access journal from MDPI, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Emergence and characterization of historically extinct virulent genotype IV Newcastle disease virus in wild and domestic birds: genetic insights, pathogenicity, and vaccine efficacy.Journal of virology · 2025Article
- Macrophages are the target cells of genotype VII Newcastle disease virus and promote the infection and apoptosis of chicken splenic T cells.Veterinary research · 2025Article
- Exploring the genetic basis of Newcastle disease virus in chickens: a comprehensive review.Frontiers in immunology · 2025Review
- mRNA Profiling and Transcriptomics Analysis of Chickens Received Newcastle Disease Virus Genotype II and Genotype VII Vaccines.Pathogens (Basel, Switzerland) · 2024Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Long-term evolution of Newcastle disease virus (NDV) results in substantial alteration in viral pathogenesis. NDVs of genotype VII, a late genotype, show marked tropism to lymphoid tissues, especially to macrophages in chickens. However, the role of macrophages in the pathogenesis of genotype VII NDV is still unclear. Herein, NDV infectivity in macrophages and the role of macrophages in the pathogenesis of genotype VII NDV in chickens were investigated. We reported that NDV strains of genotype VII (JS5/05) and IV (Herts/33) can replicate in the adherent (predominantly macrophages) and non-adherent cells (predominantly lymphocytes) derived from chicken peripheral blood mononuclear cells (PBMCs), and significantly higher virus gene copy was detected in the adherent cells. In addition, JS5/05 had significantly higher infectivity in PBMC-derived adherent cells than Herts/33, correlating with its enhanced tropism to macrophages in the spleen of chickens. Interestingly, the depletion of 68% of macrophages exerted no significant impact on clinical signs, mortality and the systematic replication of JS5/05 in chickens, which may be associated with the contribution of non-depleted macrophages and other virus-supportive cells to virus replication. Macrophage depletion resulted in a marked exacerbation of tissue damage and apoptosis in the spleen caused by JS5/05. These findings indicated that macrophages play a critical role in alleviating tissue damage caused by genotype VII NDV in chickens. Our results unveiled new roles of macrophages in NDV pathogenesis in chickens.
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