The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its associated coagulopathy are particularly worrisome in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), as these diseases carry an increased risk of thrombotic complications. Mathian et al recently reported the clinical course of COVID-19 in a series of 17 patients with SLE under chronic hydroxychloroquine therapy. 1 Of note, only one patient (6%) presented thrombosis despite the fact that four patients (24%) had a history of secondary APS, and five patients (29%) were receiving oral anticoagulants. Antiphospholipid (aPL) antibodies were not measured in these patients during active SARS-CoV-2 infection. 1 The American Society of Hematology recently stated that 'at the current time, there are only very limited data on aPL antibodies in COVID-19 and it is unclear if they represent an epiphenomenon or are actually involved in any haemostatic abnormalities seen in COVID-19 disease'. 2 Furthermore, almost all the available information refers to the lupus anticoagulant, with frequencies ranging from 45% to 87%. 3 4 This paucity of data led us to test a panel of aPL antibodies in blood specimens from 21 patients hospitalised in the intensive care unit between 12 and 19 April, due to severe or critical COVID-19, and received at our laboratory on 20 April to measure interleukin-6 levels. Anticardiolipin, anti-β 2 glycoprotein I, antiprothrombin, antiphosphatidylserine, antiphosphatidylinositol and antiannexin V antibodies were measured, each in IgM and IgG isotypes. Subsequently, demographic and clinical data were obtained from electronic medical records. Sera collected before the SARS-CoV-2 pandemic from 12 healthy individuals, matched for age and sex, were tested as controls.Pertinent results are summarised in table 1. The median age of patients was 62 years; 43% were men; and a high number of comorbidities were observed (median Charlson Comorbidity Index of 3). A total of 19 patients (90%) had shortness of breath on admission, and 12 (57%) eventually required invasive mechanical ventilation during hospitalisation. Elevated levels of D-dimer, ferritin and C reactive protein were found at presentation.Of the 21 patients with COVID-19 studied, 12 had at least one circulating aPL antibody, whereas only 1 of the 12 controls yielded a positive result (57% vs 8%; Fisher's exact test, p=0.009). The most frequently detected aPL antibodies were antiannexin V IgM (19%), anticardiolipin IgM (14%), antiphosphatidylserine IgM (14%), anticardiolipin IgG (10%) and antiphosphatidylserine IgG (10%) antibodies. One patient had triple positivity (8%); three patients had double positivity (25%); and the remaining eight had a single positivity (67%). Age and number of comorbidities tended to be lower in patients with aPL antibodies. In contrast, levels of D-dimer, ferritin and C reactive protein were higher both on admission and throughout the hospital stay in these patients. Elevated levels of interleukin-6 (>40 pg/mL) wer...

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The kidnapping of the lipid metabolism of the host’s cells by severe acute respiratory syndrome (SARS-CoV-2) allows the virus to transform the cells into optimal machines for its assembly and replication. Here we evaluated changes in the fatty acid (FA) profile and the participation of the activity of the desaturases, in plasma of patients with severe pneumonia by SARS-CoV-2. We found that SARS-CoV-2 alters the FA metabolism in the cells of the host. Changes are characterized by variations in the desaturases that lead to a decrease in total fatty acid (TFA), phospholipids (PL) and non-esterified fatty acids (NEFAs). These alterations include a decrease in palmitic and stearic acids (p ≤ 0.009) which could be used for the formation of the viral membranes and for the reparation of the host’s own membrane. There is also an increase in oleic acid (OA; p = 0.001) which could modulate the inflammatory process, the cytokine release, apoptosis, necrosis, oxidative stress (OS). An increase in linoleic acid (LA) in TFA (p = 0.03) and a decreased in PL (p = 0.001) was also present. They result from damage of the internal mitochondrial membrane. The arachidonic acid (AA) percentage was elevated (p = 0.02) in the TFA and this can be participated in the inflammatory process. EPA was decreased (p = 0.001) and this may decrease of pro-resolving mediators with increase in the inflammatory process. The total of NEFAs (p = 0.03), PL (p = 0.001), cholesterol, HDL and LDL were decreased, and triglycerides were increased in plasma of the COVID-19 patients. Therefore, SARS-CoV-2 alters the FA metabolism, the changes are characterized by alterations in the desaturases that lead to variations in the TFA, PL, and NEFAs profiles. These changes may favor the replication of the virus but, at the same time, they are part of the defense system provided by the host cell metabolism in its eagerness to repair damage caused by the virus to cell membranes.

Background Chagas disease is considered important and presents intense inflammatory and fibrotic processes induced by the perpetuation of the parasite in the affected tissues and organs. Therefore, it is necessary to inquire about the host defense and attack mechanisms to have a more detailed knowledge about Chagas disease. MicroRNAs are found in blood, tissues and extracellular vesicles. These small regulators of gene expression are involved in physiological and pathological processes in both mammals and parasites. Several microRNAs have deregulated expression in chagasic heart disease, although little is known about their extracellular expression. Our main objective was to evaluate the involvement of miR-21, miR-146a and miR-155 in several samples from mice infected with the TcI Ninoa strain from the acute and indeterminate phases. We also explored a potential functional association of the selected microRNAs using STRING software. This software identified 23 pathways associated with Trypanosoma cruzi infection. In addition, eleven genes were identified through bioinformatics analysis, and we found that SMAD family member 5 was downregulated in both phases. This gene serves as a mediator in the TGF-β signaling pathway. Thus, forty female mice of the CD1 strain were distributed into 4 groups and the expression levels of miR-21, miR-146a and miR-155 were measured in samples of heart tissue, total plasma and plasma extracellular vesicles by quantitative real-time polymerase chain reaction. Results Overexpression of miR-21, miR-146a and miR-155 was observed in heart and plasma in both phases. Moreover, in extracellular vesicles miR-21 and miR-146a were also overexpressed in the acute phase, whereas in the indeterminate chronic phase we found only miR-146a up-regulated. Conclusions The expression of inflammatory microRNAs miR-21, miR-146a and miR-155 were up-regulated in each of the samples from acutely and chronically infected mice. The relevant finding was that miR-146a was up-regulated in each sample in both phases; therefore, this miRNA could be a possible candidate biomarker in Chagas disease.