Aggressive immune response, due to overexpressed proinflammatory molecules, has been characterized in coronavirus disease 2019 (COVID‐19) patients. Some of those mediators have a dual and opposite role on immune systems at play behind dif- ferential disease severities. We investigated the expression of some cytokines and chemokines in COVID‐19 patients in Bangladesh. We diagnosed the patients by detecting severe acute respiratory syndrome coronavirus 2 RNA in nasal swab samples by the real‐time RT‐PCR method. Thirty adult patients were preselected based on their disease severities and grouped into mild, moderate, and severe cases. Nine healthy volunteers participated in this study as a control. Relative expression of nine cytokines/chemokine in total leukocytes was semi‐quantified in SYBRgreen‐ based real‐time quantitative reverse‐transcriptase polymerase chain reaction. We performed statistical tests on transformed log data using SPSS 24.0. At the onset of symptoms (Day 1), angiotensin‐converting enzyme 2 (ACE2) (p < 0.05) and inter- leukin (IL)‐6 (p > 0.05) were upregulated in all COVID‐19 groups, although the ex- pression levels did not significantly correlate with disease severities. However, expressions of IL‐6, monocyte chemotactic protein‐1, macrophage inflammatory protein‐1α, tumor necrosis factor‐α (TNF‐α), RANTES (regulated upon activation, normal T cell expressed and secreted), and ACE2, on Day 14, were positively cor- related with disease severities. Relative viral load at Day 1 showed no significant correlation with cytokine expression but had a significant positive correlation with RANTES and ACE2 expression on Day 14 (p < 0.05). Male patients had a higher level of IL‐6 than female patients on Day 1 (p < 0.05). All COVID‐19 patients showed upregulated cytokines and chemokines on Day 14 compared to Day 1 except TNF‐α. Female patients had a higher expression of ACE2 and IL‐12 on Day 14. Upregulated cytokines/chemokines at the convalescent stage, especially IL‐6, may help in tar- geting anticytokine therapy in post‐COVID‐19 patients' management.

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• Aggressive immune response, due to overexpressed proinflammatory molecules, has been characterized in coronavirus disease 2019 (COVID‐19) patients. Some of those mediators have a dual and opposite role on immune systems at play behind dif- ferential disease severities. We investigated the expression of some cytokines and chemokines in COVID‐19 patients in Bangladesh. We diagnosed the patients by detecting severe acute respiratory syndrome coronavirus 2 RNA in nasal swab samples by the real‐time RT‐PCR method. Thirty adult patients were preselected based on their disease severities and grouped into mild, moderate, and severe cases. Nine healthy volunteers participated in this study as a control. Relative expression of nine cytokines/chemokine in total leukocytes was semi‐quantified in SYBRgreen‐ based real‐time quantitative reverse‐transcriptase polymerase chain reaction. We performed statistical tests on transformed log data using SPSS 24.0. At the onset of symptoms (Day 1), angiotensin‐converting enzyme 2 (ACE2) (p < 0.05) and inter- leukin (IL)‐6 (p > 0.05) were upregulated in all COVID‐19 groups, although the ex- pression levels did not significantly correlate with disease severities. However, expressions of IL‐6, monocyte chemotactic protein‐1, macrophage inflammatory protein‐1α, tumor necrosis factor‐α (TNF‐α), RANTES (regulated upon activation, normal T cell expressed and secreted), and ACE2, on Day 14, were positively cor- related with disease severities. Relative viral load at Day 1 showed no significant correlation with cytokine expression but had a significant positive correlation with RANTES and ACE2 expression on Day 14 (p < 0.05). Male patients had a higher level of IL‐6 than female patients on Day 1 (p < 0.05). All COVID‐19 patients showed upregulated cytokines and chemokines on Day 14 compared to Day 1 except TNF‐α. Female patients had a higher expression of ACE2 and IL‐12 on Day 14. Upregulated cytokines/chemokines at the convalescent stage, especially IL‐6, may help in tar- geting anticytokine therapy in post‐COVID‐19 patients' management.