Transcription of interferon stimulated genes in response to porcine rubulavirus infection in vitro

Brazilian Journal of Microbiology

María Del Rosario Flores-ocelotl²  Nora Hilda Rosas-murrieta¹  Verónica Vallejo-ruiz²  Julio Reyes-leyva²  Irma Herrera-camacho¹  Gerardo Santos-lópez² 

[1] ,Instituto Mexicano del Seguro Social Centro de Investigación Biomédica de Oriente Laboratorio de Biología Molecular y VirologíaPuebla,México

关键词: Porcine rubulavirus;    Interferon;    STAT;    LPMV;    Gene expression;   

DOI  :  10.1590/S1517-83822011000300041

来源: SciELO

【 摘 要 】

Porcine rubulavirus (PoRV) is an emerging virus causing meningo-encephalitis and reproductive failures in pigs. Little is known about the pathogenesis and immune evasion of this virus; therefore research on the mechanisms underlying tissue damage during infection is essential. To explore these mechanisms, the effect of PoRV on the transcription of interferon (IFN) pathway members was analyzed in vitro by semi-quantitative RT-PCR. Ten TCID50 of PoRV stimulated transcription of IFNα, IFNβ, STAT1, STAT2, p48 and OAS genes in neuroblastoma cells, whereas infection with 100 TCID50 did not stimulate transcription levels more than non-infected cells. When the cells were primed with IFNα, infection with 1 TCDI50 of PoRV sufficed to stimulate the transcription of the same genes, but 10 and 100 TCID50 did not modify the transcription level of those genes as compared with non-infected and primed controls. MxA gene transcription was observed only when the cells were primed with IFNα and stimulated with 10 TCID50, whereas 100 TCID50 of PoRV did not modify the MxA transcription level as compared to non-infected and primed cells. Our results show that PoRV replication at low titers stimulates the expression of IFN-responsive genes in neuroblastoma cells, and suggest that replication of PoRV at higher titers inhibits the transcription of several members of the IFN pathway. These findings may contribute to the understanding of the pathogenesis of PoRV.

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