Project description:Purpose: This goal of this study was to explore the host transcriptomic responses in African swine fever virus experimentally infected pigs using RNA-Sequencing. Methods: RNAs acquired from ten different organ tissue samples were sequenced. Sequencing reads were preprocessed, aligned with the reference genome, assembled and expressions were estimated through bioinformatics approaches. Result: Several uprugulated DEGs were identified. Conclusion: We found important candidate genes and pathways for further testing in African swine fever virus infection in pig.
Project description:Long noncoding RNAs (lncRNAs) participate in regulating many biological processes. However, their roles in African swine fever virus(ASFV) pathogenicity are largely unknown. Here, we analyzed the expression profile of lncRNAs and mRNAs in the ASFV-infected or uninfected PAMs by high-throughput sequencing
Project description:African swine fever virus (ASFV) is a large, icosahedral, double-stranded DNA virus in the Asfarviridae family and the causative agent of African swine fever (ASF). ASFV causes a hemorrhagic fever with high mortality rates in domestic and wild pigs. ASFV contains an open reading frame named EP152R, previous research has shown that EP152R is an essential gene for virusrescue in swine macrophages. However, the detailed functions of ASFV EP152R remain elusive. Herein, we demonstrate that EP152R, a membrane protein located in the endoplasmic reticulum (ER), induces ER stress and swelling, triggering the PERK/eIF2α pathway and broadly inhibiting host protein synthesis in vitro. Additionally, EP152R strongly promotes immune evasion, reduces cell proliferation, and alters cellular metabolism. These results suggest that ASFV EP152R plays a critical role in the intracellular environment, facilitating viral replication. Furthermore, virus-level experiments have shown that the knockdown of EP152R or PERK inhibitors efficiently affects viral replication by decreasing viral gene expression. In summary, these findings reveal a series of novel functions of ASFV EP152R and have important implications for understanding host-pathogen interactions.
