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Electronic Journal of General Medicine ; 17(6), 2020.
Article in English | ProQuest Central | ID: covidwho-2111442
J Med Virol ; 94(8): 3642-3652, 2022 08.
Article in English | MEDLINE | ID: covidwho-1777593


Interleukin-38 (IL-38) has recently been considered as a cytokine with anti-inflammatory properties in viral respiratory infections, particularly coronavirus disease 19 (COVID-19), but the evidence has not been well elucidated. Therefore, a case-control study was conducted to determine IL-38 serum levels in 148 patients with COVID-19 (45 moderate, 55 severe, and 48 critical) and 113 controls. Results demonstrated that IL-38 levels did not show significant differences between patients and controls (68.7 [interquartile range: 62.7-75.6] vs. 67.7 [58.0-82.6] pg/ml; probability = 0.457). Similarly, patients stratified by disease severity, age group, gender, or chronic disease showed no significant differences between IL-38 levels in each stratum. Whereas, overweight/obese patients had a significantly lower median of IL-38 compared to normal-weight patients. Further, IL-38 showed significantly higher levels in the age group ≥50 years of patients with critical illness than in the age group <50 years. Female patients with severe disease also showed significantly elevated levels of IL-38 compared to male patients. In conclusion, the study indicated that serum IL-38 levels were not affected by COVID-19 infection, but the distribution of patients according to disease severity, age, gender, and body mass index may better reveal the role of IL-38 in disease pathogenesis.

COVID-19 , Case-Control Studies , Cytokines , Female , Humans , Interleukin-6 , Interleukin-8 , Interleukins , Male , Middle Aged , Severity of Illness Index
Medeni Med J ; 35(2): 151-160, 2020.
Article in English | MEDLINE | ID: covidwho-690169


A shocking third species emerged from a family of coronaviruses (CoV) in late 2019 following viruses causing SARS (Severe Acute Respiratory Syndrome-CoV) in 2003 and MERS (Middle East Respiratory Syndrome-CoV) in 2012; it's a novel coronavirus now called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; formerly called 2019-nCoV). First emerging in China, it has spread rapidly across the globe, giving rise to significant social and economic costs and imposing severe strain on healthcare systems. Since many attempts to control viral spread has been futile, the only old practice of containment including city lockdown and social distancing are working to some extent. Unfortunately, specific antiviral drugs and vaccines remain unavailable yet. Many factors are encountered to play essential roles in viral pathogenesis. These include a broad viral-host range with high receptor binding affinity to various human tissues, viral adaptation to humans, a high percentage of asymptomatic but infected carriers, prolonged incubation, and viral shedding periods. There are also a wide variety of pulmonary and extrapul-monary tissue damage mechanisms including direct cell injury or immune-mediated damages involving the immune cells, upregulation of proinflammatory cytokines, and antibody dependent enhancement that can result in multi-organ failure. In this article, we summarise some evidence on the various steps in SARS-CoV-2 pathogenesis and immune evasion strategies to assess their contribution to our understanding of unresolved problems related to SARS-CoV-2 prevention, control, and treatment protocols.