AI Article Synopsis
- PRV infection in pigs poses serious health risks and understanding how it interacts with its host is crucial for developing treatments.
- Researchers used CRISPR/Cas9 to create cells lacking the PARP11 gene and investigated its impact on PRV infection through various scientific methods.
- The study found that knocking out PARP11 enhanced PRV infection by increasing viral gene expression and activating certain cellular pathways, suggesting PARP11's role as a potential target for anti-PRV therapies.
Article Abstract
Introduction: PRV infection in swine can cause devastating disease and pose a potential threat to humans. Advancing the interplay between PRV and host is essential to elucidate the pathogenic mechanism of PRV and identify novel anti-PRV targets.
Methods: PARP11-KO PK-15 cells were firstly constructed by CRISPR/Cas9 technology. Next, the effect of PARP11-KO on PRV infection was determined by RT-qPCR, TCID50 assay, RNA-seq, and western blot.
Results And Discussion: In this study, we identified PARP11 as a host factor that can significantly affect PRV infection. Inhibition of PARP11 and knockout of PARP11 can significantly promoted PRV infection. Subsequently, we further found that PARP11 knockout upregulated the transcription of NXF1 and CRM1, resulting in enhanced transcription of viral genes. Furthermore, we also found that PARP11 knockout could activate the autophagy pathway and suppress the mTOR pathway during PRV infection. These findings could provide insight into the mechanism in which PARP11 participated during PRV infection and offer a potential target to develop anti-PRV therapies.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496260 | PMC |
| http://dx.doi.org/10.3389/fcimb.2024.1414827 | DOI Listing |
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