Journal
VIRUS RESEARCH
Volume 138, Issue 1-2, Pages 89-96Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.virusres.2008.08.009
Keywords
Classical swine fever virus; Virulence; Pathogenesis; Swine macrophages; Gene expression; Host cells
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Funding
- National Research Initiative Competitive Grants Program (NRI) at the Cooperative State Research, Education and Extension Service (CSREES), US Department of Agriculture [2006-01614]
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Experimental exposure of swine to highly virulent classical swine fever virus (CSFV) strain Brescia causes an invariably fatal disease of all infected animals by 8-14 days post-infection. Host mechanisms involved in this severe outcome of infection have not been clearly established. To understand these mechanisms, we analyzed the response of primary cultured swine macrophages, a CSFV primary target cell, to infection with Brescia strain. Steady state levels of mRNA accumulation were assessed for 58 genes involved in modulation of the host immune response, at 24 and 48 h post-infection (hpi), by means of quantitative reverse transcription real-time PCR analysis (qrt-PCR). Eighteen genes showed altered expression upon infection with CSFV strain Brescia including: cytokines (IL-1 alpha, IL-1 beta, IL-6, and IL-12p35): cytokine receptors (IL-2R alpha, IL-12R beta, and TGF-beta IIIR); chemokines (IL-8, AMCF-1, AMCF-2, MCP-2. and RANTES); interferons (INF alpha and INF beta); and toll-like receptors (TLR3, TLR5, TLR9, and TLR10). Although these genes are associated with mechanisms of innate immune response and antiviral activity, their altered expression does not curtail CSFV Brescia growth kinetics and virus yield in swine macrophages. Data gathered here suggests that the observed gene expression profile might explain immunological and pathological changes associated with virulent CSFV infections. (C) 2008 Elsevier B.V. All rights reserved.
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