• Thromboinflammation: From Atherosclerosis to COVID-19 – “In this review, we chose to place neutrophils with their newfound ability for inflammasome assembly and NET production in the center of thromboinflammation. With NETs being equally involved in thrombosis, as well as perpetuating the immune response and tissue injury, they certainly are in the middle of it all. NETosis activates platelets, releases toxic histones110 and active enzymes, modifying thrombus stability. In a similar way, the assembly of the inflammasome paralleled by increased PAD4 activity leads to proinflammatory and prothrombotic cytokine release and activation of endothelium, thus further boosting leukocyte recruitment and inflammasome assembly in bystander cells.”
  • Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19 – “In this study, we examined the morphologic and molecular features of seven lungs obtained during autopsy from patients who died from SARS-CoV-2 infection. The lungs from these patients were compared with those obtained during autopsy from patients who had died from ARDS secondary to influenza A(H1N1) infection and from uninfected controls. The lungs from the patients with Covid-19 and the patients with influenza shared a common morphologic pattern of diffuse alveolar damage and infiltrating perivascular lymphocytes. There were three distinctive angiocentric features of Covid-19. The first feature was severe endothelial injury associated with intracellular SARS-CoV-2 virus and disrupted endothelial cell membranes. Second, the lungs from patients with Covid-19 had widespread vascular thrombosis with microangiopathy and occlusion of alveolar capillaries.12,19 Third, the lungs from patients with Covid-19 had significant new vessel growth through a mechanism of intussusceptive angiogenesis. Although our sample was small, the vascular features we identified are consistent with the presence of distinctive pulmonary vascular pathobiologic features in some cases of Covid-19.”
  • COVID-19 Severity Correlates with Weaker T-Cell Immunity, Hypercytokinemia, and Lung Epithelium Injury – “The key findings of this study are 1) the lung injury and inflammation effectors (syndecan-1 and IL-6) are associated with disease severity, and 2) CD8+ and CD4+ T cells play a major role in the recovery of patients with critical COVID-19 under the caveat that adequate amounts of nAbs must also be present.”
  • Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury – “Here we report the epidemiological, clinical, laboratory, and radiological characteristics, as well as potential biomarkers for predicting disease severity in 2019-nCoV-infected patients in Shenzhen, China.”