Submitted to: Archives of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 26, 2004
Publication Date: August 27, 2004
Citation: Miller, L.C., Laegreid, W.W., Bono, J.L., Chitko McKown, C.G., Fox, J.M. 2004. Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells. Archives of Virology. 149(12):2453-2463. Interpretive Summary: The pig respiratory virus, porcine reproductive and respiratory syndrome virus (PRRSV), causes highly significant losses to the swine industry worldwide. The ability of the virus to persist in its host shows that it has mechanisms to evade host immune response. The type I interferon system is an essential component of the host antiviral response, highlighted by the identification of sophisticated mechanisms that viruses have evolved to subvert the host interferon system. Cells infected with PRRSV fail to secrete type I interferon. We investigated gene expression of type I interferon in PRRSV-infected cells and found gene expression was unchanged in relation to mock-infected cells, whereas, in interferon-induced cells the type I interferon gene expression was increased in relation to mock-infected cells, which suggests that PRRSV infection is directly interfering with type I interferon gene activation.
Technical Abstract: Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I IFN (IFN-alpha, IFN-beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and IFN-beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and IFN-beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-infection with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.