Abstract
Background: Monocytes are significant players in the detection of invading pathogens, particularly in pathogen defense. Bovine Viral Diarrhea Virus (BVDV) can cause a persistent infection and immune suppression if animals are infected with an non-cytopathic (ncp) biotype. However, its exact role in ncp BVDV-infected bovine monocytes remains poorly understood. To explore the immune suppression mechanisms of ncp BVDV, we used a transcriptomics approach to find genes with differential expression patterns in monocytes during infection with ncp BVDV over time. Results: Bovine monocytes were sampled at 2 and 24 h post-infection (hpi) to represent the early and late stages of an ncp biotype strain of bovine viral diarrhea virus infection. Compared with the non-infected cells, 9959 and 7977 differentially expressed gene (DEGs) were identified at 2 and 24 h hpi, respectively. These DEGs were associated with signal transduction, immune response, apoptotic process, cellular process , binding and cellular component. The differential expression profiles of select the type I interferon signaling pathway , interferon (IFN)-stimulated genes (ISGs), and genes involved in the innate immune response, including IRF7, DDX3X, TLR13, DDX58(RIG-I), MVAS, TLR9, TRAF6, IRF1, IFIT1, STAT1, ISG20, TRIM25, MX1,NLRX1, CYLD, SIKE1 and ZAP70 were confirmed by real-time quantitative PCR and consistent with the RNA-seq data. These results indicated that infection with ncp BVDV could activate type I interferon signaling pathway in bovine monocytes and induces weak ISGs responses, which extends our present understanding how the virus modulates the immune response and leads to better understanding behind the immunopathogenesis of ncp BVDV. Conclusion: Our transciptome anslysis provides useful initial data towards better understanding of the infection mechanisms used by ncp BVDV, while highlighting the potential molecular relationships occurring between the virus and the host’s immune response.
Bovine Viral Diarrhea Virus Strain- and Cell Type-Specific Inhibition of Type I Interferon Pathways
