Integrated time-serial transcriptome networks reveal common innate and tissue-specific adaptive immune responses to PRRS
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RESEARCH ARTICLE
Open Access
Integrated time‑serial transcriptome networks reveal common innate and tissue‑specific adaptive immune responses to PRRSV infection Byeonghwi Lim1, Sangwook Kim1, Kyu‑Sang Lim2, Chang‑Gi Jeong3, Seung‑Chai Kim3, Sang‑Myeong Lee4, Choi‑Kyu Park5, Marinus F. W. te Pas6, Haesu Gho7, Tae‑Hun Kim7, Kyung‑Tai Lee7*, Won‑Il Kim3* and Jun‑Mo Kim1*
Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) infection is the most important viral disease caus‑ ing severe economic losses in the swine industry. However, mechanisms underlying gene expression control in immunity-responsible tissues at different time points during PRRSV infection are poorly understood. We constructed an integrated gene co-expression network and identified tissue- and time-dependent biological mechanisms of PRRSV infection through bioinformatics analysis using three tissues (lungs, bronchial lymph nodes [BLNs], and tonsils) via RNA-Seq. Three groups with specific expression patterns (i.e., the 3-dpi, lung, and BLN groups) were discovered. The 3 dpi-specific group showed antiviral and innate-immune signalling similar to the case for influenza A infection. Moreover, we observed adaptive immune responses in the lung-specific group based on various cytokines, while the BLN-specific group showed down-regulated AMPK signalling related to viral replication. Our study may provide com‑ prehensive insights into PRRSV infection, as well as useful information for vaccine development. Keywords: adaptive immunity, gene co-expression network, innate immunity, integrated transcriptomes, porcine reproductive and respiratory syndrome virus Introduction Porcine reproductive and respiratory syndrome (PRRS) is one of the most important diseases affecting commercial pig productivity in the swine industry worldwide [1]. PRRS is caused by the PRRS virus (PRRSV), a single-stranded RNA virus [2, 3], resulting in severe *Correspondence: [email protected]; [email protected]; [email protected] 1 Department of Animal Science and Technology, Chung-Ang University, Anseong, Gyeonggi‑do 17546, Republic of Korea 3 College of Veterinary Medicine, Jeonbuk National University, Iksan, Jeollabuk‑do 54596, Republic of Korea 7 Animal Genomics and Bioinformatics Division, National Institute of Animal Science, RDA, Wanju 55365, Republic of Korea Full list of author information is available at the end of the article
reproductive losses for breeding pigs and respiratory problems for growing pigs [4]. Vaccination—a solution for this problem—is still limited because of the high mutation rate in the viral proteins and the intrinsic characteristics of PRRSV that impede innate immune responses [5–7]. Therefore, to date, several studies have been performed to identify host factors that confer resistance to PRRSV infection. Some mutations in the guanylate-binding protein 1 and cluster of differentiation 163 (CD163) genes were reported to be associated with PRRSV susceptibility [8, 9], and also CD163 knockout was proved to show full resistance for PRRSV infect
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