HSV-2 infection induces TLRs and NF-κB-dependent cytokines in human cervical epithelial cells (133.41)

Abstract

Abstract Herpes Simplex Virus type 2 (HSV-2) is one of the most common sexually transmitted pathogen worldwide. The host immune response induced by viral infection is cell-type specific. Little is known about the innate immune response to this virus in its natural host cells. In this study, we established an in vitro HSV-2 infection model with human cervical epithelial (HCE) cells. The viral infection was sufficient to induce expression of Toll-like receptors (TLRs), and western blot and reporter assays suggest that HSV-2 infection leads to dramatic activation of the NF-κB signaling pathway. The two critical cytokines,IL-6 and IFN-beta,were also induced after HSV-2 infection and maintained high levels during the course of experiment. The presence of NF-κB inhibitor, Isohelenin significantly blocked the production of both IL-6 and IFN-beta in response to HSV-2. Thus, our data provide direct evidence that the activation of NF-κB is required for the production of both IL-6 and IFN-beta induced by HSV-2 in HCE cells. Taken together, our results suggest the potential contributions of TLRs and a critical role of NF-κB in the innate immune response to HSV-2 infection in its natural host cells. This work was supported by grants from the National Natural Science Foundation of China (No. 30500465,30810103052)