Detection of viral components in exosomes derived from NDV-infected DF-1 cells and their promoting ability in virus replication

Exosomes are micro messengers encapsulating RNA, DNA, and proteins for intercellular communication associated with various physiological and pathological reactions. Several viral infection processes have been reported to pertain to exosomal pathways. However, because of the difficulty in obtaining a...

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Veröffentlicht in:Microbial pathogenesis 2019-03, Vol.128, p.414-422
Hauptverfasser: Xu, Xiaohong, Qian, Jing, Ding, Jiaxin, Li, Jindou, Nan, Fulong, Wang, Weiqi, Qin, Qi, Fei, Yidong, Xue, Cong, Wang, Jianzhong, Yin, Renfu, Ding, Zhuang
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Sprache:eng
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Zusammenfassung:Exosomes are micro messengers encapsulating RNA, DNA, and proteins for intercellular communication associated with various physiological and pathological reactions. Several viral infection processes have been reported to pertain to exosomal pathways. However, because of the difficulty in obtaining avian-sourced exosomes, avian virus-related exosomes are scarcely investigated. In this study, we developed a protein A/G-correlated method and successfully obtained the Newcastle disease virus-related exosome (NDV Ex). These exosomes promoted NDV propagation, proven by both GW4869-mediated deprivation and exosomal supplementation. Viral structural proteins NP and F were detected in the NDV Ex and further investigation indicated that the NP protein can be transferred to DF-1 cells through exosomes. The intracellular NP protein exhibited viral replication-promoting and cytokine-suppressing abilities. Therefore, NDV infection produces exosomes, which transfer viral NP protein and promote NDV infection, emphasizing the importance of exosomes in an NDV infection. •Avian source exosomes were successfully separated (NDV Ex).•NDV Ex promoted NDV replication and suppressed cytokine secretion.•NP and F proteins were detected and NP protein is pivotal for NDV Ex mediated NDV replication enhancement.
ISSN:0882-4010
1096-1208
DOI:10.1016/j.micpath.2018.12.047