RSV replication is attenuated by counteracting expression of the suppressor of cytokine signaling (SOCS) molecules
RSV replication is attenuated by counteracting expression of the suppressor of cytokine signaling (SOCS) molecules
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DOI：
10.1016/j.virol.2009.06.026
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发表时间：
2009-09-01
期刊：
影响因子：
3.7
通讯作者：
Suzutani, Tatsuo
中科院分区：
文献类型：
--
作者：
Hashimoto, Koichi;Ishibashi, Kei;Suzutani, Tatsuo
人RSV每年在婴儿和老年人中引起呼吸道疾病的流行。RSV拮抗IFN介导的抗病毒应答的机制包括抑制I型IFN mRNA转录和阻断JAK/STAT家族成员的信号转导。细胞因子信号转导抑制因子（SOCS）基因家族利用反馈环抑制细胞因子应答并阻断JAK/STAT信号通路的激活。为了评估SOCS分子破坏对RSV感染的先天免疫应答的潜力，检查了8个SOCS家族基因。RSV感染可上调HEp-2细胞中SOCS 1、SOCS 3和CIS mRNA的表达。此外，抑制SOCS 1、SOCS 3或CIS通过诱导STAT 1/2磷酸化激活I型IFN信号传导。这些结果表明，RSV感染通过诱导SOCS 1、SOCS 3或CIS在上皮细胞中表达而逃避先天性抗病毒应答。(C)2009 Elsevier Inc. All rights reserved.
Human RSV causes an annual epidemic of respiratory tract illness in infants and in elderly. Mechanisms by which RSV antagonizes IFN-mediated antiviral responses include inhibition of type I IFN mRNA transcription and blocking signal transduction of JAK/STAT family members. The suppressor of cytokines signaling (SOCS) gene family utilizes a feedback loop to inhibit cytokine responses and block the activation of the JAK/STAT signaling pathway. To evaluate the potential of SOCS molecules to subvert the innate immune response to RSV infection, eight SOCS family genes were examined. RSV infection up-regulated SOCS1, SOCS3, and CIS mRNA expression in HEp-2 cells, Suppression of SOCS 1, SOCS3 and CIS by short interfering ribonucleic acid (siRNA) inhibited viral replication. Furthermore, inhibition of SOCS1, SOCS3, or CIS activated type I IFN signaling by inducing STAT1/2 phosphorylation. These results suggest that RSV infection escapes the innate antiviral response by inducing SOCS1, SOCS3 or CIS expression in epithelial cells. (C) 2009 Elsevier Inc. All rights reserved.