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  • Title: RSV replication is attenuated by counteracting expression of the suppressor of cytokine signaling (SOCS) molecules.
    Author: Hashimoto K, Ishibashi K, Ishioka K, Zhao D, Sato M, Ohara S, Abe Y, Kawasaki Y, Sato Y, Yokota S, Fujii N, Peebles RS, Hosoya M, Suzutani T.
    Journal: Virology; 2009 Sep 01; 391(2):162-70. PubMed ID: 19595407.
    Abstract:
    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 SOCS1, 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.
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