RESUMEN
Diverse psychological consequences of the COVID-19 pandemic have been reported for 6 months after infection. We conducted a prospective study to evaluate the psychological impact of COVID-19 infection in newly diagnosed cases that were followed up at 1, 6, and 9 months after infection. 137 people were recruited and divided into four groups based on the COVID-19 Treatment Guidelines. They were evaluated using the Pittsburgh Sleep Quality Index (PSQI), Post-traumatic stress disorder Checklist for DSM-5 (PCL-5), and Symptom Checklist 90 (SCL-90). We found that 9 months after infection, patients continued to report poor sleep (74.5%), PTSD (78.3%), somatization (17%), anxiety (17%), aggression (5.7%), phobic anxiety (4.7%), psychoticism (1.9%), paranoid (3.8%), and obsessive-compulsive (9.4%) symptoms, as well as depression and interpersonal sensitivity. The most significant risk factors for psychiatric complications were older age, level of education, smoking, hospitalization duration, hypertension, and critical severity. The negative mental health effects of COVID-19 persist after hospital discharge, and many patients continue to experience moderate-to-severe issues that may endure for 9 months. Notably, there was a progressive improvement in these symptoms over that time.
RESUMEN
Viral infections trigger inflammation by controlling ATP release. CD39 ectoenzymes hydrolyze ATP/ADP to AMP, which is converted by CD73 into anti-inflammatory adenosine (ADO). ADO is an anti-inflammatory and immunosuppressant molecule which can enhance viral persistence and severity. The CD39-CD73-adenosine axis contributes to the immunosuppressive T-reg microenvironment and may affect COVID-19 disease progression. Here, we investigated the link between CD39 expression, mostly on T-regs, and levels of CD73, adenosine, and adenosine receptors with COVID-19 severity and progression. Our study included 73 hospitalized COVID-19 patients, of which 33 were moderately affected and 40 suffered from severe infection. A flow cytometric analysis was used to analyze the frequency of T-regulatory cells (T-regs), CD39+ T-regs, and CD39+CD4+ T-cells. Plasma concentrations of adenosine, IL-10, and TGF-ß were quantified via an ELISA. An RT-qPCR was used to analyze the gene expression of CD73 and adenosine receptors (A1, A2A, A2B, and A3). T-reg cells were higher in COVID-19 patients compared to healthy controls (7.4 ± 0.79 vs. 2.4 ± 0.28; p < 0.0001). Patients also had a higher frequency of the CD39+ T-reg subset. In addition, patients who suffered from a severe form of the disease had higher CD39+ T-regs compared with moderately infected patients. CD39+CD4+ T cells were increased in patients compared to the control group. An analysis of serum adenosine levels showed a marked decrease in their levels in patients, particularly those suffering from severe illness. However, this was paralleled with a marked decline in the expression levels of CD73. IL-10 and TGF-ß levels were higher in COVID-19; in addition, their values were also higher in the severe group. In conclusion, there are distinct immunological alterations in CD39+ lymphocyte subsets and a dysregulation in the adenosine signaling pathway in COVID-19 patients which may contribute to immune dysfunction and disease progression. Understanding these immunological alterations in the different immune cell subsets and adenosine signaling provides valuable insights into the pathogenesis of the disease and may contribute to the development of novel therapeutic approaches targeting specific immune mechanisms.