4.3 Article

MicroRNA transcriptome analysis of poly I:C-stimulated and PRRSV-infected porcine alveolar macrophages

Journal

JOURNAL OF APPLIED GENETICS
Volume 60, Issue 3-4, Pages 375-383

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s13353-019-00500-3

Keywords

PRRSV; Poly I; C; Innate immune; Apoptosis; miR-27b

Funding

  1. National Natural Science Foundation [31501924]
  2. Hubei Natural Science Foundation [2015CFA105, 2018CFA014]
  3. Hubei Province Technical Innovation Project [2016ABA117, 2017ABA134]
  4. Hubei Agricultural Science and Technology Innovation Center [2016-620-000-001-022]

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Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe reproductive failure in sows, respiratory diseases, and high mortality in piglets, which results in serious economic losses to the swine industry worldwide. Previous studies have described that PRRSV could suppress the host immune system and had antiapoptotic activity in its initial phase of infection. Polyinosinic-polycytidylic acid (poly I:C), a synthesized analogue of viral double-strand RNA, activates innate immunity responses and induces apoptosis in cells. Therefore, we performed miRNA transcriptome analysis of poly I:C-stimulated and PRRSV-infected porcine alveolar macrophages (PAMs) using deep sequencing technology, to compare the different miRNA profiles between the statuses of innate immune activation and inactivation. After sequencing, 267 known mature miRNAs and 64 novel miRNAs were observed in PAMs, and a total of 197 miRNAs were significantly differently expressed in poly I:C-stimulated PAMs, compared with mock control cells. Thirty-three of them were also significantly alerted in PRRSV-infected PAMs. This indicated that PRRSV only slightly alerted the miRNA expression profile of host cells compared with poly I:C-stimulated PAMs, which confirmed that PRRSV could suppress host innate immune responses during the early stages of infection. Among the differentially expressed miRNAs, we found that ssc-miR-27b-3p could significantly inhibit PRRSV RNA and protein replication in MARC-145 cells and PAMs. Its antiviral mechanism needs further research in the future.

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