Data are shown as medians and interquartile range (IQR) or n and the percentage. P values were computed using χ² tests for categorical variables or two-sided Kruskal-Wallis tests for continuous variables. CD4, CD4 T cells; CD8, CD8 T cells; WBCs, white blood cells. a P value on clinical grade was based on comparison among symptomatic S2, S3 and convalescent S4 patients excluding S1. Clinical grade classification was infeasible for presymtomatic S1 patients who did not exhibit any clinical symptoms at the time of blood collection.

A highly specific and very sensitive serological SARS-CoV-2 antibody assay with overall accuracy at 97.3% was developed using CHO-expressed SARS-CoV-2 S1 protein for screening medical staff and others for SARS-CoV-2 infection. AbstractBackground: Thousands of medical staff had been infected with SARS-CoV-2 virus with hundreds of deaths reported. Such loss could be prevented if there is a serologic assay for SARS-CoV-2-specific antibodies for serological surveillance of its infection at the early stage of disease.Methods: Using CHO cell expressed full length SARS-CoV-2 S1 protein as capturing antigen, a COVID-19/SARS-CoV-2 S1 serology ELISA kit was developed and validated with negative samples collected prior to the outbreaks or during the outbreak, and positive samples from patients confirmed with COVID-19. Results:The specificity of the ELISA kit was 97.5%, as examined against total 412 normal human samples. The sensitivity was 97.1% by testing against 69 samples from hospitalized and/or recovered COVID-19 patients. The overall accuracy rate reached 97.3%. The assay was able to detect SARS-CoV-2 antibody on day one after the onset of COVID-19 disease. The average antibody levels increased during the hospitalization and after been discharged for two weeks. SARS-CoV-2 antibodies were detected in 28 out of 276 asymptomatic medical staff and one out of five nucleic acid test-negative "Close contacts" of COVID-19 patient. Conclusion:With the assays developed here, we can screen medical staff, in-coming patients, passengers and people who are in close contact with the confirmed patients to identify the "innocent viral spreaders", protect the medical staff and stop the further spreading of the virus.

Some gamma-ray bursts (GRBs) have a tera–electron volt (TeV) afterglow, but the early onset of this has not been observed. We report observations with the Large High Altitude Air Shower Observatory of the bright GRB 221009A, which serendipitously occurred within the instrument field of view. More than 64,000 photons >0.2 TeV were detected within the first 3000 seconds. The TeV flux began several minutes after the GRB trigger, then rose to a peak about 10 seconds later. This was followed by a decay phase, which became more rapid ~650 seconds after the peak. We interpret the emission using a model of a relativistic jet with half-opening angle ~0.8°. This is consistent with the core of a structured jet and could explain the high isotropic energy of this GRB.

Context: The coronavirus disease 2019 (COVID-19) is a highly contagious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coagulation dysfunction is a hallmark in patients with COVID-19. Fulminant thrombotic complications emerge as critical issues in patients with severe COVID-19. Objective: To present a review of the literature and discuss the mechanisms of COVID-19 underlying coagulation activation and the implications for anticoagulant and thrombolytic treatment in the management of COVID-19. Data Sources: We performed a systemic review of scientific papers on the topic of COVID-19, online available via the PubMed NCBI, medRxiv, and Preprints as of May 15, 2020. We also shared our experience on the management of thrombotic events in patients with COVID-19. Conclusions: COVID-19-associated coagulopathy ranges from mild laboratory alterations to disseminated intravascular coagulation (DIC) with a predominant phenotype of thrombotic/multiple organ failure. Characteristically, high D-dimer levels on admission and/or continuously increasing concentrations of D-dimer is associated with disease progression and poor overall survival. SARS-CoV-2 infection triggers the immune-hemostatic response. Drastic inflammatory responses including, but not limited to, cytokine storm, vasculopathy, and NETosis may contribute to an overwhelming activation of coagulation. Hypercoagulability and systemic thrombotic complications necessitate anticoagulant and thrombolytic interventions, which provide opportunities to prevent or reduce “excessive” thrombin generation, while preserving “adaptive” hemostasis and bring additional benefit via their anti-inflammatory effect in the setting of COVID-19.