Transcriptome Profiling Identifies Immune Response Genes Against Porcine Reproductive and Respiratory Syndrome Virus and Co-infection in the Lungs of Piglets

Overview

Journal J Vet Sci

Specialty Veterinary Medicine

Date 2021 Dec 21

PMID 34931503

Citations 4

Authors

Jing Zhang

Jing Wang

Xiong Zhang

Chunping Zhao

Sixuan Zhou

Chunlin Du

Ya Tan

Yu Zhang

Kaizhi Shi

Affiliations

Soon will be listed here.

Abstract

Background: Co-infections of the porcine reproductive and respiratory syndrome virus (PRRSV) and the (HPS) are severe in Chinese pigs, but the immune response genes against co-infected with 2 pathogens in the lungs have not been reported.

Objectives: To understand the effect of PRRSV and/or HPS infection on the genes expression associated with lung immune function.

Methods: The expression of the immune-related genes was analyzed using RNA-sequencing and bioinformatics. Differentially expressed genes (DEGs) were detected and identified by quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC) and western blotting assays.

Results: All experimental pigs showed clinical symptoms and lung lesions. RNA-seq analysis showed that 922 DEGs in co-challenged pigs were more than in the HPS group (709 DEGs) and the PRRSV group (676 DEGs). Eleven DEGs validated by qRT-PCR were consistent with the RNA sequencing results. Eleven common Kyoto Encyclopedia of Genes and Genomes pathways related to infection and immune were found in single-infected and co-challenged pigs, including autophagy, cytokine-cytokine receptor interaction, and antigen processing and presentation, involving different DEGs. A model of immune response to infection with PRRSV and HPS was predicted among the DEGs in the co-challenged pigs. Dual oxidase 1 () and interleukin-21 () were detected by IHC and western blot and showed significant differences between the co-challenged pigs and the controls.

Conclusions: These findings elucidated the transcriptome changes in the lungs after PRRSV and/or HPS infections, providing ideas for further study to inhibit ROS production and promote pulmonary fibrosis caused by co-challenging with PRRSV and HPS.

Citing Articles

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