Abstract
Increased rates of indeterminate QuantiFERON-TB Gold Plus Assay (QFT-Plus) were demonstrated in patients hospitalized with Coronavirus Disease (COVID)-19. We aimed to define the prevalence and characteristics of hospitalized COVID-19 patients with indeterminate QFT-Plus. A retrospective study was performed including hospitalized COVID-19 patients, stratified in survivors and non-survivors, non-severe and severe according to the maximal oxygen supply required. Statistical analysis was performed using JASP ver0.14.1 and GraphPad Prism ver8.2.1. A total of 420 patients were included, median age: 65 years, males: 66.4%. The QFT-Plus was indeterminate in 22.1% of patients. Increased rate of indeterminate QFT-Plus was found in non-survivors (p = 0.013) and in severe COVID-19 patients (p < 0.001). Considering the Mitogen-Nil condition of the QFT-Plus, an impaired production of interferon-gamma (IFN-γ) was found in non-survivors (p < 0.001) and in severe COVID-19 patients (p < 0.001). A positive correlation between IFN-γ levels in the Mitogen-Nil condition and the absolute counts of CD3+ (p < 0.001), CD4+ (p < 0.001), and CD8+ (p < 0.001) T-lymphocytes was found. At the multivariable analysis, CD3+ T-cell absolute counts and CD4/CD8 ratio were confirmed as independent predictors of indeterminate results at the QFT-Plus. Our study confirmed the increased rate of indeterminate QFT-Plus in COVID-19 patients, mainly depending on the peripheral blood T-lymphocyte depletion found in the most severe cases.
Highlights
In December 2019, the first cases of pneumonia caused by a new coronavirus, namedSevere Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), was reported in Wuhan, province of Hubei, China, and quickly spread to the rest of the world, causing the Coronavirus Disease (COVID)-19 pandemic. [1,2,3]
424 patients hospitalized for COVID-19 in the Infectious
Four patients were excluded from the analysis because the QFT-Plus assay was performed more than 30 days after the first positive SARS-CoV-2 nasopharyngeal swab (NPhS); 420 patients were evaluated
Summary
In December 2019, the first cases of pneumonia caused by a new coronavirus, namedSevere Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), was reported in Wuhan, province of Hubei, China, and quickly spread to the rest of the world, causing the Coronavirus Disease (COVID)-19 pandemic. [1,2,3]. Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), was reported in Wuhan, province of Hubei, China, and quickly spread to the rest of the world, causing the Coronavirus Disease (COVID)-19 pandemic. The virus can cause a wide variety of clinical manifestations, from asymptomatic disease to severe pneumonia with respiratory failure, requiring mechanical ventilation. Despite several studies on pathophysiological processes, viral and host factors responsible for patient morbidity and mortality remain partially unknown [4]. SARS-CoV-2 pathogenesis is associated with the lung damage and the procoagulant state triggered by an exaggerated immune response characterized by the so-called “cytokine storm”; an increased mortality has been associated to a dysregulated host immune response [4,5,6,7,8,9,10,11]
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