Abstract
IntroductionCoronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, resulting in a range of clinical manifestations and outcomes. Laboratory and immunological alterations have been considered as potential markers of disease severity and clinical evolution. Type I interferons (IFN-I), mainly represented by IFN-α and β, are a group of cytokines with an important function in antiviral responses and have played a complex role in COVID-19. Some studies have demonstrated that IFN-I levels and interferon response is elevated in mild cases, while other studies have noted this in severe cases. The involvement of IFN-I on the pathogenesis and outcomes of SARS-CoV-2 infection remains unclear. In this study, we summarize the available evidence of the association of plasma protein levels of type I IFN with the severity of COVID-19.MethodsThe PRISMA checklist guided the reporting of the data. A systematic search of the MEDLINE (PubMed), EMBASE, and Web of Science databases was performed up to March of 2021, looking for articles that evaluated plasma protein levels of IFN-I in mild, severe, or critical COVID-19 patients. Comparative meta-analyses with random effects were performed to compare the standardized mean differences in plasma protein levels of IFN-I of mild versus severe and mild versus critical patients. Meta-regressions were performed to test the moderating role of age, sex, time that the IFN-I was measured, and limit of detection of the assay used in the difference between the means.ResultsThere was no significant difference in plasma levels of IFN-α when comparing between mild and severe patients (SMD = -0.236, 95% CI -0.645 to 0.173, p = 0.258, I2 = 82.11), nor when comparing between patients mild and critical (SMD = 0.203, 95% CI -0.363 to 0.770, p = 0.481, I2 = 64.06). However, there was a significant difference between healthy individuals and patients with mild disease (SMD = 0.447, 95% CI 0.085 to 0.810, p = 0.016, I2 = 62.89).ConclusionsPeripheral IFN-α cannot be used as a severity marker as it does not determine the clinical status presented by COVID-19 patients.
Highlights
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, resulting in a range of clinical manifestations and outcomes
There was no significant difference in plasma levels of IFN-a when comparing between mild and severe patients (SMD = -0.236, 95% confidence interval (95% CI) -0.645 to 0.173, p = 0.258, I2 = 82.11), nor when comparing between patients mild and critical (SMD = 0.203, 95% CI -0.363 to 0.770, p = 0.481, I2 = 64.06)
Peripheral IFN-a cannot be used as a severity marker as it does not determine the clinical status presented by COVID-19 patients
Summary
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, resulting in a range of clinical manifestations and outcomes. COVID-19 causes distinct clinical manifestations among affected individuals, ranging from asymptomatic cases to cases with mild, moderate, severe, or critical symptoms, where they might progress to an acute respiratory distress syndrome (SARS) or even to dysfunction of multiple organs, complications that lead to death [6, 7]. The risk of developing a more aggressive disease condition is influenced by age and the presence of comorbidities, such as diabetes, hypertension, obesity, and cardiovascular diseases [2, 8] Markers, such as the increase in C-reactive protein (CRP), Ddimer, and prothrombin time, are important to predict the outcome of the disease [9, 10]. Interferons present conflicting results [14]
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