Comprehensive analysis of lncRNAs and mRNAs expression profiles unveils antiviral roles of lncRNAs and regulatory pathways in LSDV-infected MDBK cells

Author:

Liao Kai1,Wang Hao1,He Wei1,Qian Bingxu1,Jia Xiaoran1,Cao Yuying1,Wen Yuan1,Liu Cong1,Zeng Dexin2,Tang Fang1,Dai Jianjun3,Li Chao4,Xue Feng1

Affiliation:

1. Nanjing Agricultural University

2. Technology Center of Hefei Customs

3. China Pharmaceutical University

4. China Animal Health and Epidemiology Center

Abstract

Abstract

The lumpy skin disease virus (LSDV), a member of the Poxviridae family, is primarily characterized by the formation of skin nodules in cattle. In our study, RNA sequencing was employed to investigate LSDV-infected Madin-Darby bovine kidney (MDBK) cells. At 4 hours post-infection (hpi), 108 differentially expressed long non-coding RNAs (delncRNAs) were identified. A co-expressed functional analysis indicated that lncRNAs may influence cellular glycometabolic processes. Additionally, we observed 798 differentially expressed mRNAs (demRNAs), predominantly associated with lipopeptide-induced immune response pathways in enrichment analyses. These findings indicate an active cellular defense against the poxvirus at this early stage. At 24 hpi, 1101 delncRNAs were identified, impacting cell metabolism, especially glycometabolism. Notably, two LncRNAs, which interacted with MAPK3, emerged as potential central regulators in the lncRNA-mRNA cis-regulation network. The number of demRNAs surged to 5295, with KEGG pathway enrichment analysis revealing associations with various diseases. This late phase marked a critical juncture, as the virus inflicted near-total cellular destruction, resulting in severe pathological conditions. Moreover, two of the demRNAs at 4 hpi, AV5191 and AV15574, were shown to inhibit LSDV replication in MDBK cells. The LSDV-induced host lncRNA/mRNA profiles reveal intricate regulatory dynamics, providing a foundational and robust public resource for understanding the nuanced mechanisms in poxvirus-host interactions.

Publisher

Research Square Platform LLC

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