4.7 Article

NDV related exosomes enhance NDV replication through exporting NLRX1 mRNA

Journal

VETERINARY MICROBIOLOGY
Volume 260, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.vetmic.2021.109167

Keywords

Newcastle disease virus; Exosomes; NLRX1; MAVS signal pathway; Exosome mediated exportation

Funding

  1. National Science Foundation of China [31772735]
  2. Youth Program of National Natural Science Foundation of China [32002321]
  3. Key Project of Jilin Provincial Programs for Research and Development [2020040237NC]

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This study reveals a novel mechanism by which NDV Ex facilitates NDV infection through exporting NLRX1 mRNA to reduce the antiviral capacity of host cells. The research indicates that NDV can manipulate host immune responses through the exosome pathway, utilizing the decrease of NLRX1 mRNA to promote viral replication.
Virulent Newcastle disease virus (NDV) is a violent infection in avian species. The understanding of its pathogenic mechanism is consistently evolving along with the development of molecular biological advancement. Exosomes derived from NDV infected cells (NDV Ex) were reported to promote virus replication through transportation of viral proteins and miRNAs. However, the function of mRNAs in NDV Ex remains unknown. In this study, a novel mechanism of NDV Ex to facilitate NDV infection was explored. Through transcriptome analysis, seven immune related genes were found to up-regulate in NDV Ex. Among them, NLRX1 mRNA was notably enriched in NDV Ex, and decreased inside the cells after virulent NDV infection. Further investigation suggested that NLRX1 mRNA decrease was in accordance with the NLRX1 protein expression reduction. This process can be reversed by the inhibition of exosome release. Therefore, NDV infection could utilize NDV Ex to export NLRX1 mRNA and reduce cellular NLRX1 protein. As NLRX1 is a crucial anti-viral protein of MAVS signal pathway, and NDV Ex transported NLRX1 cannot counteract its function in recipient cells, it can be concluded that NDV could benefit its replication through exporting NLRX1 mRNA to relieve the anti-viral pressure on its survival.

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