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In Vitro Infection with Classical Swine Fever Virus Inhibits the Transcription of Immune Response Genes

Overview
Journal Virol J
Publisher Biomed Central
Specialty Microbiology
Date 2012 Aug 29
PMID 22925563
Citations 5
Authors
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Abstract

Background: Classical swine fever virus (CSFV) can evade the immune response and establish chronic infection under natural and experimental conditions. Some genes related to antigen processing and presentation and to cytokine regulation are known to be involved in this response, but the precise mechanism through which each gene responds to CSFV infection remains unclear.

Results: In this study, the amplification standard curve and corresponding linear regression equations for the genes SLA-2, TAP1, SLA-DR, Ii, CD40, CD80, CD86, IFN-α, and IFN-β were established successfully. Real-time RT-PCR was used to quantify the immune response gene transcription in PK-15 cells post CSFV infection. Results showed that: (1) immune response genes were generally down-regulated as a result of CSFV infection, and (2) the expression of SLA-2, SLA-DR, Ii and CD80 was significantly decreased (p < 0.001).

Conclusion: We conclude that in vitro infection with CSFV inhibits the transcription of host immune response genes. These findings may facilitate the development of effective strategies for controlling CSF.

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References
1.
Edwards S, Fukusho A, Lefevre P, Lipowski A, Pejsak Z, Roehe P . Classical swine fever: the global situation. Vet Microbiol. 2000; 73(2-3):103-19. DOI: 10.1016/s0378-1135(00)00138-3. View

2.
Choi C, Hwang K, Chae C . Classical swine fever virus induces tumor necrosis factor-alpha and lymphocyte apoptosis. Arch Virol. 2004; 149(5):875-89. DOI: 10.1007/s00705-003-0275-6. View

3.
Moennig V . The hog cholera virus. Comp Immunol Microbiol Infect Dis. 1992; 15(3):189-201. DOI: 10.1016/0147-9571(92)90092-6. View

4.
Cheville N, Mengeling W . The pathogenesis of chronic hog cholera (swine fever). Histologic, immunofluorescent, and electron microscopic studies. Lab Invest. 1969; 20(3):261-74. View

5.
Susa M, Konig M, Saalmuller A, Reddehase M, Thiel H . Pathogenesis of classical swine fever: B-lymphocyte deficiency caused by hog cholera virus. J Virol. 1992; 66(2):1171-5. PMC: 240821. DOI: 10.1128/JVI.66.2.1171-1175.1992. View