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Volume 39 Issue 2
Feb.  2024
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Article Contents
PENG B Q, HU J Y, MAO Y N, et al. A Preliminary Study on Influenza Virus-induced Interferon Regulating Mechanism of SOCS3 [J]. Fujian Journal of Agricultural Sciences,2024,39(2):131−136 doi: 10.19303/j.issn.1008-0384.2024.02.002
Citation: PENG B Q, HU J Y, MAO Y N, et al. A Preliminary Study on Influenza Virus-induced Interferon Regulating Mechanism of SOCS3 [J]. Fujian Journal of Agricultural Sciences,2024,39(2):131−136 doi: 10.19303/j.issn.1008-0384.2024.02.002

A Preliminary Study on Influenza Virus-induced Interferon Regulating Mechanism of SOCS3

doi: 10.19303/j.issn.1008-0384.2024.02.002
  • Received Date: 2024-01-03
  • Rev Recd Date: 2024-01-29
  • Available Online: 2024-03-28
  • Publish Date: 2024-02-28
  •   Objective  Regulatory function of the suppressor of cytokine signaling 3 (SOCS3) in the interferon signaling pathway during an influenza virus infection on cells was studied.   Method  A549 cell lines were constructed with SOCS3 overexpression by a lentivirus infection and knockdown by siRNA technology. Along with control, they were infected with the influenza virus and sampled at times to assess the expressions and activation of crucial molecules within the interferon signaling pathway using RT-PCR and western blot analysis.   Result  Decreasing expressions of type I interferon IFN-β and type III interferons IL-28 and IL-29 were observed following the SOCS3 overexpression in cells. Conversely, the SOCS3 knockdown raised the expressions of IFN-β, IL-28, and IL-29. SOCS3 overexpression also suppressed the expressions of the interferon regulatory factor IRF7 as well as those of the pattern recognition receptors RIG-I, MDA5, and TLR3 responsible for detecting influenza virus RNA. The virus induced SOCS3 overexpression inhibited, but the knockdown enhanced, the STAT1 phosphorylation.   Conclusion  An influenza virus invasion on cells induced SOCS3 to recognize the receptors and regulate the mRNA expression inhibiting the type I and III interferon productions and STAT1 activation resulting in a blockage on the interferon signal transmission.
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  • [1]
    HUTCHINSON E C. Influenza virus [J]. Trends in Microbiology, 2018, 26(9): 809−810. doi: 10.1016/j.tim.2018.05.013
    [2]
    UYEKI T M, HUI D S, ZAMBON M, et al. Influenza [J]. Lancet, 2022, 400(10353): 693−706. doi: 10.1016/S0140-6736(22)00982-5
    [3]
    GORAYA M U, ZAIGHUM F, SAJJAD N, et al. Web of interferon stimulated antiviral factors to control the influenza A viruses replication [J]. Microbial Pathogenesis, 2020, 139: 103919. doi: 10.1016/j.micpath.2019.103919
    [4]
    WONG P T, GOFF P H, SUN R J, et al. Combined intranasal nanoemulsion and RIG-I activating RNA adjuvants enhance mucosal, humoral, and cellular immunity to influenza virus [J]. Molecular Pharmaceutics, 2021, 18(2): 679−698. doi: 10.1021/acs.molpharmaceut.0c00315
    [5]
    MA W, HUANG G, WANG Z, et al. IRF7: Role and regulation in immunity and autoimmunity [J]. Frontiers in Immunology, 2023, 14: 1236923. doi: 10.3389/fimmu.2023.1236923
    [6]
    YAO D D, BAO L L, LI F D, et al. H1N1 influenza virus dose dependent induction of dysregulated innate immune responses and STAT1/3 activation are associated with pulmonary immunopathological damage [J]. Virulence, 2022, 13(1): 1558−1572. doi: 10.1080/21505594.2022.2120951
    [7]
    HALLER O, KOCHS G. Mx genes: Host determinants controlling influenza virus infection and trans-species transmission [J]. Human Genetics, 2020, 139(6): 695−705.
    [8]
    周斌, 万少兵, 王瑛, 等. SOCS3通过调控JAK2/STAT3信号通路改善急性肺损伤 [J]. 山西医科大学学报, 2023, 54(6):778−784.

    ZHOU B, WAN S B, WANG Y, et al. SOCS3 improves acute lung injury by regulating JAK2/STAT3 signaling pathway [J]. Journal of Shanxi Medical University, 2023, 54(6): 778−784. (in Chinese)
    [9]
    SIMS N A. The JAK1/STAT3/SOCS3 axis in bone development, physiology, and pathology [J]. Experimental & Molecular Medicine, 2020, 52: 1185−1197.
    [10]
    LIU S S, YAN R X, CHEN B, et al. Influenza virus-induced robust expression of SOCS3 contributes to excessive production of IL-6 [J]. Frontiers in Immunology, 2019, 10: 1843. doi: 10.3389/fimmu.2019.01843
    [11]
    SUN Y P, JIANG J W, PO T E, et al. IFN-λ: A new spotlight in innate immunity against influenza virus infection [J]. Protein & Cell, 2018, 9(10): 832−837.
    [12]
    BIONDO C, LENTINI G, BENINATI C, et al. The dual role of innate immunity during influenza [J]. Biomedical Journal, 2019, 42(1): 8−18. doi: 10.1016/j.bj.2018.12.009
    [13]
    HUANG B Z, CHEN H P, ZHENG Y B. MiR-103/miR-107 inhibits enterovirus 71 replication and facilitates type I interferon response by regulating SOCS3/STAT3 pathway [J]. Biotechnology Letters, 2021, 43(7): 1357−1369. doi: 10.1007/s10529-021-03115-z
    [14]
    YAKASS M B, FRANCO D, QUAYE O. Suppressors of cytokine signaling and protein inhibitors of activated signal transducer and activator of transcriptions As therapeutic targets in flavivirus infections [J]. Journal of Interferon & Cytokine Research, 2020, 40(1): 1−18.
    [15]
    LI L, WU H Y, LI Q M, et al. SOCS3-deficient lung epithelial cells uptaking neutrophil-derived SOCS3 worsens lung influenza infection [J]. Molecular Immunology, 2020, 125: 51−62. doi: 10.1016/j.molimm.2020.06.022
    [16]
    YANG H, DONG Y R, BIAN Y, et al. The influenza virus PB2 protein evades antiviral innate immunity by inhibiting JAK1/STAT signalling [J]. Nature Communications, 2022, 13: 6288. doi: 10.1038/s41467-022-33909-2
    [17]
    ZHANG Y L, XU L L, ZHANG Z, et al. Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host [J]. Virologica Sinica, 2023, 38(5): 755−766. doi: 10.1016/j.virs.2023.08.007
    [18]
    WANG X W, JIA Y Q, REN J, et al. Newcastle disease virus nonstructural V protein upregulates SOCS3 expression to facilitate viral replication depending on the MEK/ERK pathway [J]. Frontiers in Cellular and Infection Microbiology, 2019, 9: 317. doi: 10.3389/fcimb.2019.00317
    [19]
    XIE J Y, WANG M S, CHENG A C, et al. DHAV-1 inhibits type I interferon signaling to assist viral adaption by increasing the expression of SOCS3 [J]. Frontiers in Immunology, 2019, 10: 731. doi: 10.3389/fimmu.2019.00731
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