CRISPR/Cas9-generated CD46-knockout spermatogonial stem cells reveal mechanisms of BVDV-induced reproductive dysfunction in male livestock

Research Hypothesis
This study tests the hypothesis that BVDV directly impairs male reproductive function by infecting spermatogonial stem cells (SSCs), disrupting proliferation/self-renewal pathways, and inducing novel cell death mechanisms (e.g., ferroptosis). We further hypothesize that CD46 serves as a key receptor facilitating BVDV entry into SSCs.

Data Overview
This dataset comprises experimental results from in vitro BVDV infection of bovine and caprine SSCs, including:
Viral replication kinetics (qPCR, TCID₅₀ assays)
Gene/protein expression (RNA-seq/qRT-PCR data; Western blots for PCNA, CCND1, CDK2, Lin28A, OCT4, SOX2)
Ferroptosis markers (Lipid ROS assays, iron quantification, GPX4 expression)
Cell viability/proliferation (CCK-8)
Significance Statement
This dataset provides the first evidence that BVDV directly targets SSCs, causing ferroptosis and transcriptional dysregulation of fertility genes. CD46 editing data validate a strategy for generating BVDV-resistant livestock. Data reuse can accelerate antiviral therapy development and precision breeding programs.