From nasal to basal: single-cell sequencing of the bursa of Fabricius highlights the IBDV infection mechanism in chickens
文献类型: 外文期刊
作者: Shah, Abid Ullah 1 ; Li, Yuchen 2 ; Ouyang, Wei 3 ; Wang, Zhisheng 4 ; Zuo, Jinjiao 1 ; Shi, Song 5 ; Yu, Qinghua 2 ; Lin, Jian 1 ; Yang, Qian 2 ;
作者机构: 1.Nanjing Agr Univ, Coll Life Sci, Wei Gang 1, Nanjing 210095, Jiangsu, Peoples R China
2.Nanjing Agr Univ, Coll Vet Med, Wei Gang 1, Nanjing 210095, Jiangsu, Peoples R China
3.Jiangsu Acad Agr Sci, Inst Vet Med, Minist Agr, Key Lab Vet Biol Engn & Technol, Nanjing 210014, Peoples R China
4.Jiangsu Acad Agr Sci, Natl Res Ctr Engn & Technol Vet Biolog, Inst Vet Immunol & Engn, Nanjing 210014, Peoples R China
5.Shanghai OE Biotech Co Ltd, Shanghai 201114, Peoples R China
关键词: Nasal cavity; Infectious bursal disease virus; Bursa of Fabricius; Single cell RNA-sequence; RNA interference
期刊名称:CELL AND BIOSCIENCE ( 影响因子:9.584; 五年影响因子:8.113 )
ISSN:
年卷期: 2021 年 11 卷 1 期
页码:
收录情况: SCI
摘要: Background: Chickens, important food animals and model organisms, are susceptible to many RNA viruses that invade via the nasal cavity. To determine the nasal entry site of the virus and clarify why avians are susceptible to RNA viruses, infectious bursal disease virus (IBDV) was selected because it is a typical avian RNA virus that infects chickens mainly via the nasal route. Results: First, we found that IBDV infected the posterior part of the nasal cavity in chickens, which is rich in lymphoid tissue and allows the virus to be easily transferred to the blood. Via the blood circulation, IBDV infected peripheral blood mononuclear cells (PBMCs) and was transferred to the bursa of Fabricius to damage the IgM+B lymphocyte population. Subsequently, the single-cell RNA sequencing (scRNA-seq) results suggested the more detailed response of different bursal cell populations (B cells, epithelial cells, dendritic cells, and fibroblasts) to IBDV. Regarding B cells, IBDV infection greatly decreased the IgM+B cell population but increased the IgA+B cell population in the bursal follicles. In contrast to B cells, bursal epithelial cells, especially basal cells, accumulated a large number of IBDV particles. Furthermore, we found that both innate RNA sensors and interferon-stimulated genes (ISGs) were highly expressed in the IBDV-infected groups, while dicer and agog expression was largely blocked by IBDV infection. This result suggests that dicer-related RNA interference (RNAi) might be an effective antiviral strategy for IBDV infection in avian. Conclusion: Our study not only comprehensively elaborates on the transmission of airborne IBDV via the intranasal route and establishes the main target cell types for productive IBDV infection but also provides sufficient evidence to explain the cellular antiviral mechanism against IBDV infection.
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