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ARS Home » Research » Publications at this Location » Publication #162640
Title: EARLY INNATE IMMUNE RESPONSE IN PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS-INFECTED MARC-145 CELLS

Author
item Miller, Laura
item Fox, James
item Bono, James - Jim
item Chitko-Mckown, Carol
item Laegreid, William

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/30/2004
Publication Date: 5/1/2004
Citation: Miller, L.C., Fox, J.M., Bono, J.L., Chitko Mckown, C.G., Laegreid, W.W. 2004. Early innate immune response in porcine reproductive and respiratory syndrome virus-infected marc-145 cells [abstract]. 7th Int. Symp. Positive Strand RNA Viruses. Paper No. P2-G1.

Interpretive Summary:

Technical Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) causes highly significant losses to the swine industry worldwide. PRRSV infection 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 innate immune response genes. We are currently focused on the early innate immune response genes, specifically type I IFN (IFN-alpha, IFN-beta) and IFN-beta transcriptional enhanceasome genes, and pro-apoptotic cellular factors. 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.