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. 2020 May 2;12(9):7639-7651.
doi: 10.18632/aging.103101. Epub 2020 May 2.

Immune environment modulation in pneumonia patients caused by coronavirus: SARS-CoV, MERS-CoV and SARS-CoV-2

Zhixian Yao  1 , Zhong Zheng  1 , Ke Wu  1 , Zheng Junhua  1
Affiliations

Immune environment modulation in pneumonia patients caused by coronavirus: SARS-CoV, MERS-CoV and SARS-CoV-2

Zhixian Yao et al. Aging (Albany NY). .

Abstract

Currently, we are on a global pandemic of Coronavirus disease-2019 (COVID-19) which causes fever, dry cough, fatigue and acute respiratory distress syndrome (ARDS) that may ultimately lead to the death of the infected. Current researches on COVID-19 continue to highlight the necessity for further understanding the virus-host synergies. In this study, we have highlighted the key cytokines induced by coronavirus infections. We have demonstrated that genes coding interleukins (Il-1α, Il-1β, Il-6, Il-10), chemokine (Ccl2, Ccl3, Ccl5, Ccl10), and interferon (Ifn-α2, Ifn-β1, Ifn2) upsurge significantly which in line with the elevated infiltration of T cells, NK cells and monocytes in SARS-Cov treated group at 24 hours. Also, interleukins (IL-6, IL-23α, IL-10, IL-7, IL-1α, IL-1β) and interferon (IFN-α2, IFN2, IFN-γ) have increased dramatically in MERS-Cov at 24 hours. A similar cytokine profile showed the cytokine storm served a critical role in the infection process. Subsequent investigation of 463 patients with COVID-19 disease revealed the decreased amount of total lymphocytes, CD3+, CD4+, and CD8+ T lymphocytes in the severe type patients which indicated COVID-19 can impose hard blows on human lymphocyte resulting in lethal pneumonia. Thus, taking control of changes in immune factors could be critical in the treatment of COVID-19.

Keywords: COVID-19; SARS-Cov-2; cytokine storm.

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Conflict of interest statement

CONFLICTS OF INTEREST: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
The pathogenic mechanisms of the three pneumonias. (A) SARS-CoV; (B) MERS-CoV; (C) SARS-CoV-2.
Figure 2
Figure 2
The pneumonia related interleukin cytokines variation trend after SARS-CoV treatment 12h, 24h and 48h respectively. (A) IL-1α; (B) IL-1β; (C) IL-6; (D) IL-7; (E) IL-10; (F) IL-23α.
Figure 3
Figure 3
The interferon variation trend after SARS-CoV treatment 12h, 24h and 48h respectively. (A) IFN-α2; (B) IFN-β1; (C) IFN-2.
Figure 4
Figure 4
The variation trend of chemokines after SARS-CoV treatment 12h, 24h and 48h respectively. (A) Ccl2; (B) Ccl3; (C) Ccl5; (D) Cxcl3; (E) Cxcl5; (F) Cxcl10.
Figure 5
Figure 5
The interleukin cytokines and interferon variation trend after MERS-CoV treatment in 24 hours. (A) IL-6; (B) IL-23α; (C) IL-10; (D) IL-7; (E) IL-1α; (F) IL-1β; (G) IFN-α2; (H) IFN-2; (I) IFN-γ. (Mock: Control group; icMERS: MERS-CoV treated group).
Figure 6
Figure 6
Cytokine variation in young and aged mice after MERS-CoV treated for 12 and 24 hours. (A) IL-1α; (B) IL-1β; (C) IL-6; (D) IL-7; (E) IL-10; (F) IL-23α.
Figure 7
Figure 7
The quantification of immune cell in SARS-CoV infected different age groups mice for 12 and 24 hours based on ssGSEA method. (A) IL-1α; (B) IL-1β; (C) IL-6; (D) IL-7; (E) IL-10; (F) IL-23α.
Figure 8
Figure 8
The quantification of total lymphocytes, CD3+, CD4+ and CD8+ T lymphocytes from peripheral blood from COVID-19 patients by flow cytometry. (A–D) Count variation between common and severe type disease. (E–H) Count variation between different age groups.
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