Interferon type I response in porcine reproductive and respiratory syndrome virus-infected U.S. Meat Animal Research Center-145 cells

Authors

L. C. Miller, Roman L. Hruska U.S. Meat Animal Research Center (U.S. Meat Animal Research Center), ARS, USDA
W. W. Laegried, Roman L. Hruska U.S. Meat Animal Research Center (U.S. Meat Animal Research Center), ARS, USDA
J. L. Bono, Roman L. Hruska U.S. Meat Animal Research CenterFollow
C. G. Chitko-McKown, Roman L. Hruska U.S. Meat Animal Research Center (U.S. Meat Animal Research Center), ARS, USDAFollow
J. M. Fox, Roman L. Hruska U.S. Meat Animal Research Center (U.S. Meat Animal Research Center), ARS, USDA

Date of this Version

2004

Document Type

Article

Citation

Arch Virol (2004) 149: 2453–2463, DOI 10.1007/s00705-004-0377-9

Comments

U.S. Government Work

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 interferons (IFN-α and -β) and IFN-β transcriptional enhanceasome genes. In U.S. Meat Animal Research Center-145 cells, both IFN- α and -β transcript abundance were unaffected by PRRSV infection. However, stimulation of U.S. Meat Animal Research Center-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-α and -β as well as IFN-β 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-exposure 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-β gene transcription.