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Virologica Sinica, 30 (3) : 190-199, 2015
Research Article
A respiratory syncytial virus persistent-infected cell line system reveals the involvement of SOCS1 in the innate antiviral response
1. Department of Pediatrics, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan 430071,
China
2. Department of Anatomy, School of Medicine, Wuhan University, Donghu Road 185, Wuhan 430071, China
 Correspondence: zhao_wh2004@hotmail.com
(1198.69KB)  
Abstract
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-β (IFN-β), macrophage inflammatory protein-1α (Mip-1α), 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.
Received: 18 Apr 2015  Accepted: 12 Jun 2015  Published online: 19 Jun 2015
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