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Review
. 2020 Sep;44(9):1792-1797.
doi: 10.1002/cbin.11403. Epub 2020 Jun 3.

Lymphopenia in COVID-19: Therapeutic opportunities

Nazanin Fathi  1   2 , Nima Rezaei  1   2   3
Affiliations
Review

Lymphopenia in COVID-19: Therapeutic opportunities

Nazanin Fathi et al. Cell Biol Int. 2020 Sep.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is uncontrollably spread all over the world. The host immune responses strongly try to confront it with all the potential cells and cytokines. With chronically condition of SARS-CoV-2, natural killer cells and T cells become exhausted and decreasing their count leads to lymphopenia. Inability to eradicate the infected organ makes hyperinitiation of the immune system, which releases the excessive inflammatory cytokines to compensate the exhausted one as well as the low lymphocytes counts; it consequently leads to the cytokine storm syndrome. These mechanisms and the potential therapeutic targeting are discussed in this paper.

Keywords: COVID-19; apoptosis; coronavirus; cytokine storm syndrome; inflammation; lymphopenia.

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Conflict of interest statement

The authors declare that there are no conflict of interests.

Figures

Figure 1
Figure 1
Hyperproinflammatory cytokines produce by activated macrophages, neutrophils and monocytes, dendritic cells, endothelial and epithelial by virus that induce granulopoiesis and reduce lymphopoiesis in the bone marrow. The increased number of monocytes and granulocytes produce more and more inflammatory cytokines and this detrimental positive feedback make intensify this condition (Created using BioRender: https://biorender.com/)
See this image and copyright information in PMC

References

    1. Barathan, M. , Gopal, K. , Mohamed, R. , Ellegård, R. , Saeidi, A. , Vadivelu, J. , … Zandi, K. (2015). Chronic hepatitis C virus infection triggers spontaneous differential expression of biosignatures associated with T cell exhaustion and apoptosis signaling in peripheral blood mononucleocytes. Apoptosis, 20(4), 466–480. 10.1007/s10495-014-1084-y - DOI - PubMed
    1. Barathan, M. , Mohamed, R. , Yong, Y. K. , Kannan, M. , Vadivelu, J. , Saeidi, A. , … Esaki ShankarShankar, E. M. (2018). Viral persistence and chronicity in hepatitis C virus infection: role of T‐cell apoptosis, senescence and exhaustion. Cells, 7(10), 165. 10.3390/cells7100165 - DOI - PMC - PubMed
    1. Bengsch, B. , Martin, B. , & Thimme, R. (2014). Restoration of HBV‐specific CD8+ T cell function by PD‐1 blockade in inactive carrier patients is linked to T cell differentiation. Journal of Hepatology, 61(6), 1212–1219. 10.1016/j.jhep.2014.07.005 - DOI - PubMed
    1. Bozza, F. A. , Cruz, O. G. , Zagne, S. M. , Azeredo, E. L. , Nogueira, R. M. , Assis, E. F. , … Kubelka, C. F. (2008). Multiplex cytokine profile from dengue patients: MIP‐1beta and IFN‐gamma as predictive factors for severity. BMC Infectious Diseases, 8(1), 86. 10.1186/1471-2334-8-86 - DOI - PMC - PubMed
    1. Bucks, C. M. , Norton, J. A. , Boesteanu, A. C. , Mueller, Y. M. , & Katsikis, P. D. (2009). Chronic antigen stimulation alone is sufficient to drive CD8+ T cell exhaustion. The Journal of Immunology, 182(11), 6697–6708. 10.4049/jimmunol.0800997 - DOI - PMC - PubMed

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