Abstract

Porcine reproductive and respiratory syndrome (PRRS) is one of the most ruinous diseases in pig production. Our previous work showed that Tongcheng pigs (TC) were less susceptible to PRRS virus (PRRSV) than Large White (LW) pigs. To elucidate the difference in PRRSV resistance between the two breeds, small RNA-seq and ribo-zero RNA-seq were used to identify differentially expressed non-coding RNAs (including miRNAs and lincRNAs) responded to PRRSV in porcine alveolar macrophages (PAMs) from TC and LW pigs. Totally, 250 known mature miRNAs were detected. For LW pigs, there were 44 down-regulated and 67 up-regulated miRNAs in infection group; while for TC pigs, 12 down-regulated and 23 up-regulated miRNAs in TC infection group were identified. The target genes of the common differentially expressed miRNAs (DEmiRNAs) in these two breeds were enriched in immune-related processes, including apoptosis process, inflammatory response, T cell receptor signaling pathway and so on. In addition, 5 shared DEmiRNAs (miR-181, miR-1343, miR-296-3p, miR-199a-3p and miR-34c) were predicted to target PRRSV receptors, of which miR-199a-3p was validated to inhibit the expression of CD151. Interestingly, miR-378 and miR-10a-5p, which could inhibit PRRSV replication, displayed higher expression level in TC control group than that in LW control group. Contrarily, miR-145-5p and miR-328, which were specifically down-regulated in LW pigs, could target inhibitory immunoreceptors and may involve in immunosuppression caused by PRRSV. This indicates that DEmiRNAs are involved in the regulation of the immunosuppression and immune escape of the two breeds. Furthermore, we identified 616 lincRNA transcripts, of which 48 and 30 lincRNAs were differentially expressed in LW and TC pigs, respectively. LincRNA TCONS_00125566 may play an important role in the entire regulatory network, and was predicted to regulate the expression of immune-related genes through binding with miR-1343 competitively. In conclusion, this study provides an important resource for further revealing the interaction between host and virus, which will specify a new direction for anti-PRRSV research.

Highlights

  • Virus, Porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) genome mutates with a high rate

  • With RNA-sequencing, we compared the transcriptome difference of porcine alveolar macrophages (PAMs) between TC and Large White (LW) pigs, which revealed that TC pigs may promote the extravasation and migration of leukocytes to defend against PRRSV infection[12]

  • Despite of the important roles of non-coding RNAs in immune response regulation, our previous work as well as other reported PRRSV-related transcriptome studies was focused on the function of protein-coding genes in PRRSV infection, less is known about the expression pattern of miRNAs and long intergenic non-coding RNA (lincRNA) in the process of PRRSV infection

Read more

Summary

Introduction

Virus, PRRSV genome mutates with a high rate. Due to the poor cross-protection of the traditional vaccine for PRRSV variants, clinical prevention of PRRS is quite difficult, host genetic improvement of PRRSV resistance would be a better choice. More artificial infection experiments were conducted within different pig breeds or populations with different backgrounds, which provides a strong evidence and support for the genetic contributions to PRRSV resistance. Despite of the important roles of non-coding RNAs in immune response regulation, our previous work as well as other reported PRRSV-related transcriptome studies was focused on the function of protein-coding genes in PRRSV infection, less is known about the expression pattern of miRNAs and lincRNAs in the process of PRRSV infection. RNA sequencing with small RNA, and total RNA of ribosomal RNA removal, from PAMs of both TC and LW pigs were performed to obtain profiles of miRNAs and lincRNAs, which we hope and believe will provide another perspective for revealing the PRRSV resistance mechanism

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call