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United States Department of Agriculture

Agricultural Research Service

Title: Evasion of the Innate Response of Circulation DC Populations by Foot-and-Mouth Disease Virus

Authors
item Nfon, Charles - ORISE, ARS PIADC FELLOW
item Ferman Ii, Geoffrey
item Golde, William

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: April 30, 2007
Publication Date: May 18, 2007
Citation: Nfon, C.K., Ferman Ii, G.S., Golde, W.T. 2007. Evasion of the Innate Response of Circulation DC Populations by Foot-and-Mouth Disease Virus. 94th Annual Meeting of The American Association of Immunologists, Inc., P 21

Technical Abstract: The evolution among viruses of multiple mechanisms to evade the innate immune response, particularly the actions of interferons, has also been described for FMDV infected cells. However, mechanisms involving the response of cells of the innate immune system, especially uninfected cells, are not well understood. Here we report the analysis of IFN producing dendritic cell subsets of PBMC. When pigs were infected with two serotypes of FMDV, viremia developed and serum IFN alpha peaked at 2-3 days post-infection. IFN alpah in serum is no longer detectable 4 to 5 days post infection. The IFN alpha response to CpG of plasmacytoid dendtritic cells (pDC) was significantly diminished. In addition, monocyte derived dendritic cells (MoDC) of pigs produce IFN alpha in response to poly I:C but not CpG. During FMDV infection, the MoDC response to poly I:C stimulation is blocked with similar kinetics to pDC. Analysis shows no infection of PBMC taken from these infected animals. We propose that this virus has evolved a mechanism to shut down the IFN alpha response of DC in the periphery. The virus induces a rapid IFN response from dendritic cells which is then blocked by anti-inflammatory signals from viral infected cells. This skews the balance of the host/pathogen interaction in favor of lateral viral spread during acute infection. We are currently evaluating potential mechanisms by which the virus blocks cytokine responses in non-infected cells.

Last Modified: 12/18/2014
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