Junín virus (JUNV), an arenavirus, is the causative agent of
Argentine hemorrhagic fever, an infectious human disease with 15-30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of
interferon and
cytokines are reported in AHF patients, which might be correlated to the severity of the disease. However the innate immune response to JUNV
infection has not been well evaluated. Previous studies have suggested that the virulent strain of JUNV does not induce IFN in human macrophages and monocytes, whereas the attenuated strain of JUNV was found to induce IFN response in murine macrophages via the TLR-2 signaling pathway. In this study, we investigated the interaction between JUNV and IFN pathway in human epithelial cells highly permissive to JUNV
infection. We have determined the expression pattern of
interferon-stimulated genes (ISGs) and IFN-β at both
mRNA and
protein levels during JUNV
infection. Our results clearly indicate that JUNV
infection activates the type I IFN response. STAT1 phosphorylation, a downstream marker of activation of IFN signaling pathway, was readily detected in JUNV infected IFN-competent cells. Our studies also demonstrated for the first time that RIG-I was required for IFN production during JUNV
infection. IFN activation was detected during
infection by either the virulent or
attenuated vaccine strain of JUNV. Curiously, both virus strains were relatively insensitive to human IFN treatment. Our studies collectively indicated that JUNV
infection could induce host type I IFN response and provided new insights into the interaction between JUNV and host innate immune system, which might be important in future studies on
vaccine development and
antiviral treatment.