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The host immune responses to SARS-CoV-2 and therapeutic strategies in the treatment of COVID-19 cytokine storm

  • Received: 12 August 2021 Accepted: 01 November 2021 Published: 12 November 2021
  • The ravaging pandemic caused by SAR-CoV-2, a member of β-coronaviruses, marks the end of the year 2019. Despite being identified and classified at the earliest stage, the virus records worldwide soaring transmissibility, morbidity, and mortality. Global data have shown the infection with SARS-CoV-2 to be severe among at least 15% of the infected; the aged and those with premorbid conditions like cancer, cardiovascular, and respiratory diseases. The highest prevalence and mortality are seen in the Americas, with African countries least affected. Severe respiratory distress and multiorgan failure are the usual findings in severe cases. A hyperinflammatory, fulminant, hypercytokinemia that is often further complicated by hypercoagulopathy and multiorgan failure has been reported extensively among severely infected patients. Scientists describe hyper-activated immune response mediated by macrophages secreting copious amounts of interleukin (IL)-6 forming the epicenter of cytokine storm (CS), thereby perpetuating signaling cascade through JAK/Kinase pathway that yields a hypercytokinemia. Researchers globally are exploring JAK/kinase inhibitors, immunomodulatory (immunosuppressive) therapy, cytokines, and cytokine receptor blockers for CS management. In which interestingly some of these agents possess antiviral activity. Here, we reviewed published studies with their respective outcome. However, a lot needs to be done to address the CS of COVID-19 to avert its fatal outcome.

    Citation: Mansur Aliyu, Sayed-Hamidreza Mozhgani, Omid Kohandel Gargari, Mustapha Ahmed Yusuf, Ali Akbar Saboor-Yaraghi. The host immune responses to SARS-CoV-2 and therapeutic strategies in the treatment of COVID-19 cytokine storm[J]. AIMS Allergy and Immunology, 2021, 5(4): 240-258. doi: 10.3934/Allergy.2021018

    Related Papers:

  • The ravaging pandemic caused by SAR-CoV-2, a member of β-coronaviruses, marks the end of the year 2019. Despite being identified and classified at the earliest stage, the virus records worldwide soaring transmissibility, morbidity, and mortality. Global data have shown the infection with SARS-CoV-2 to be severe among at least 15% of the infected; the aged and those with premorbid conditions like cancer, cardiovascular, and respiratory diseases. The highest prevalence and mortality are seen in the Americas, with African countries least affected. Severe respiratory distress and multiorgan failure are the usual findings in severe cases. A hyperinflammatory, fulminant, hypercytokinemia that is often further complicated by hypercoagulopathy and multiorgan failure has been reported extensively among severely infected patients. Scientists describe hyper-activated immune response mediated by macrophages secreting copious amounts of interleukin (IL)-6 forming the epicenter of cytokine storm (CS), thereby perpetuating signaling cascade through JAK/Kinase pathway that yields a hypercytokinemia. Researchers globally are exploring JAK/kinase inhibitors, immunomodulatory (immunosuppressive) therapy, cytokines, and cytokine receptor blockers for CS management. In which interestingly some of these agents possess antiviral activity. Here, we reviewed published studies with their respective outcome. However, a lot needs to be done to address the CS of COVID-19 to avert its fatal outcome.


    Abbreviations

    CS

    cytokine storm

    COVID-19

    noble coronavirus pneumonia disease 2019

    SARS-CoV-2

    severe acute respiratory syndrome coronavirus 2

    ACE2

    angiotensin-converting enzyme receptor 2

    TMSPRS2

    transmembrane serine protease 2

    NAK

    numb-associated kinases

    JAK-STAT

    Janus kinase-signal transducer and activator of transcription

    NF-κβ

    nuclear factor-kappa beta

    IFN-γ

    interferon gamma

    TNF-α

    tumor necrosis factor alpha;

    NLRP3

    NLR (nod-like receptor) family pyrin domain containing 3

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    Conflict of interest



    All authors declare no conflicts of interest in this paper.

    Author contributions



    Conceptualization MA; literature search and review MA and AAS; drawing of Figures 1 and 2 MA, OKG and SHM; manuscript writing MA, MAY, AAS and SHM; supervision AAS; manuscript review and final version approval for submission MA, AAS, SHM, MAY and OKG.

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