A respiratory syncytial virus persistent-infected cell line system reveals the involvement of SOCS1 in the innate antiviral response

作者：Zheng, Junwen; Yang, Pu; Tang, Yan; Zhao, Dongchi^*

来源：VIROLOGICA SINICA, 2015, 30(3): 190-199.

DOI：10.1007/s12250-015-3597-0

• respiratory syncytial virus (RSV)
• suppressor of cytokine signaling 1 (SOCS1)
• interferon
• toll-like receptor 3 (TLR3)
• RSV-persistent cell line

HEp-2 cells persistently infected with respiratory syncytial virus (RSV) are a heterogeneous mixture of viral antigen-positive and -negative variants; however, the mechanism through which viral replication becomes latent remains unclear. In this study, we investigated the potential mechanism by which RSV escapes from innate immune surveillance. Persistent-infected RSV HEp-2 cells were isolated and cell clones were passaged. The RSV-persistent cells produced viruses at a lower titer, resisted wild-type RSV re-infection, and secreted high levels of interferon- (IFN-), macrophage inflammatory protein-1 alpha (Mip-1 alpha), interleukin-8 (IL-8), and Rantes. Toll-like receptor 3 (TLR3), retinoic acid inducible gene-I (RIG-I), and suppressor of cytokine signaling 1 (SOCS1) levels were upregulated in these cells. The silencing of TLR3 mRNA decreased the expression of SOCS1 protein and the secretion of cytokines. RSV-persistent cells are in an inflammatory state; upregulation of SOCS1 is related to the TLR3 signaling pathway, which could be associated with the mechanism of viral persistence.

• 出版日期2015-6
• 单位武汉大学