Corpus overview


MeSH Disease

Human Phenotype


There are no transmission terms in the subcorpus


antibody (1)

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    SARS-CoV-2 and Covid-19 Immunopathogenesis

    Authors: Antonio Luiz Boechat; Beatriz Pessoa; Carlos Soares; Cecília Barroso; David Vila; Emanuelly Barbosa; Isabela Seffair; João Victor Melo; Julia Becil; Maria Polyanna Rebouças; Natascha Rodrigues; Pedro Henrique Freitas; Rebeka Rocha; Thaise Rodrigues; Vanessa Ferreira; Rosmery Ubiera; Maria Cristina Dos-Santos

    id:10.20944/preprints202008.0020.v1 Date: 2020-08-02 Source:

    The coronavirus disease MESHD 2019 (COVID-19) is now a global pandemic caused by the new severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2). Unlike other known coronaviruses, such as the Middle East respiratory syndrome MESHD coronavirus (MERS-CoV), SARS-CoV-2 reveals new clinical, immunological, and pathologic features. The lymphocyte depletion, macrophage and neutrophil hyperactivation, cytokine dysregulation, thrombophilia MESHD, delayed antiviral response, and immune exhaustion are key immunological findings linked to the clinical progression of this disease MESHD. Understanding and identifying the underlying immunological basis of COVID-19 is crucial to designing effective therapies. Here, we provide an overview of immunopathogenesis driven by SARS-CoV-2 after its interactions with the immune system.

    Prothrombotic antiphospholipid antibodies SERO in COVID-19

    Authors: Yu Zuo; Shanea K. Estes; Alex A. Gandhi; Srilakshmi Yalavarthi; Ramadan A. Ali; Hui Shi; Gautam Sule; Kelsey Gockman; Jacqueline A. Madison; Melanie Zuo; Wrenn Woodard; Sean P. Lezak; Njira L. Lugogo; Yogendra Kanthi; Jason S. Knight

    doi:10.1101/2020.06.15.20131607 Date: 2020-06-17 Source: medRxiv

    Patients with coronavirus disease MESHD 19 (COVID-19) are at high risk for thrombotic arterial and venous occlusions HP. At the same time, lung histopathology often reveals fibrin-based occlusion of small vessels in patients who succumb to the disease MESHD. Antiphospholipid syndrome MESHD (APS) is an acquired and potentially life-threatening thrombophilia MESHD in which patients develop pathogenic autoantibodies (aPL) targeting phospholipids and phospholipid-binding proteins. Small case series have recently detected aPL in patients with COVID-19. Here, we measured eight types of aPL (anticardiolipin IgG/IgM/IgA, anti-beta-2 glycoprotein I IgG/IgM/IgA, and anti- phosphatidylserine/prothrombin (PS/PT) IgG/IgM) in the sera of 172 patients hospitalized with COVID-19. We detected anticardiolipin IgM antibodies SERO in 23%, anti-PS/PT IgG in 24%, and anti-PS/PT IgM in 18%. Any aPL was present in 52% of patients using the manufacturer's threshold and in 30% using a more stringent cutoff (>40 units). Higher levels of aPL were associated with neutrophil hyperactivity HP (including the release of neutrophil extracellular traps/NETs), higher platelet count, more severe respiratory disease MESHD, and lower glomerular filtration rates. Similar to patients with known and longstanding APS, IgG fractions isolated from patients with COVID-19 promoted NET release from control neutrophils. Furthermore, injection of these COVID-19 IgG fractions into mice accelerated venous thrombosis MESHD venous thrombosis HP. Taken together, these studies suggest that a significant percentage of patients with COVID-19 become at least transiently positive for aPL and that these aPL are potentially pathogenic.

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MeSH Disease
Human Phenotype

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