Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Lower respiratory tract myeloid cells harbor SARS-CoV-2 and display an inflammatory phenotype

    Authors: William Bain; Hernan F. Penaloza; Mark S. Ladinsky; Rick van der Geest; Mara Sullivan; Mark Ross; Georgios D Kitsios; Barbara Methe; Bryan J. McVerry; Alison Morris; Alan M. Watson; Simon C. Watkins; Claudette M. St. Croix; Donna B. Stolz; Pamela J. Bjorkman; Janet S. Lee

    doi:10.1101/2020.08.11.20171967 Date: 2020-08-14 Source: medRxiv

    SARS-CoV-2 pneumonia MESHD may induce an aberrant immune response with brisk recruitment of myeloid cells into the lower respiratory tract, which may contribute to morbidity and mortality. We describe endotracheal aspirate samples from seven patients with SARS-CoV-2 pneumonia MESHD requiring mechanical ventilation. We note SARS-CoV-2 virions within lower respiratory tract myeloid cells shown by electron tomography, immunofluorescence confocal imaging, and immuno-electron microscopy. Endotracheal aspirates are primarily composed of mononuclear and polymorphonuclear leukocytes. These myeloid cells that harbor virus are frequently positive for CD14 HGNC and/or CD16 HGNC and most display an inflammatory phenotype marked by expression of IL-6 HGNC and tissue factor HGNC mRNA transcript and protein expression.

    Symptomatic SARS-CoV-2 infection MESHDs display specific IgG Fc structures

    Authors: Saborni Chakraborty; Joseph Gonzalez; Karlie Edwards; Vamsee Mallajosyula; Anthony S. Buzzanco; Robert Sherwood; Cindy Buffone; Nimish Kathale; Susan Providenza; Markus M. Xie; Jason R. Andrews; Catherine A. Blish; Upinder Singh; Haley Dugan; Patrick C. Wilson; Tho D. Pham; Scott D. Boyd; Kari C. Nadeau; Benjamin Pinsky; Sheng Zhang; Matthew J. Memoli; Jeffery K. Taubenberger; Tasha Morales; Jeffrey M. Schapiro; Gene S. Tan; Prasanna Jagannathan; Taia T. Wang

    doi:10.1101/2020.05.15.20103341 Date: 2020-05-18 Source: medRxiv

    The ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has caused a public health crisis that is exacerbated by our poor understanding of correlates of immunity. SARS-CoV-2 infection MESHD can cause Coronavirus Disease 2019 MESHD ( COVID-19 MESHD), with a spectrum of symptoms ranging from asymptomatic carriage to life threatening pneumonia MESHD and cytokine dysregulation [1-3]. Although antibodies have been shown in a variety of in vitro assays to promote coronavirus infections MESHD through mechanisms requiring interactions between IgG antibodies and Fc gamma receptors (Fc{gamma}Rs), the relevance of these observations to coronavirus infections MESHD in humans is not known [4-7]. In light of ongoing clinical trials examining convalescent serum therapy for COVID-19 MESHD patients and expedited SARS-CoV-2 vaccine testing in humans, it is essential to clarify the role of antibodies in the pathogenesis of COVID-19 MESHD. Here we show that adults with PCR-diagnosed COVID-19 MESHD produce IgG antibodies with a specific Fc domain repertoire that is characterized by reduced fucosylation, a modification that enhances interactions with the activating Fc{gamma}R, Fc{gamma}RIIIa HGNC. Fc fucosylation was reduced when compared with SARS-CoV-2-seropositive children and relative to adults with symptomatic influenza virus infections MESHD. These results demonstrate an antibody correlate of symptomatic SARS-CoV-2 infections MESHD in adults and have implications for novel therapeutic strategies targeting Fc{gamma}RIIIa HGNC pathways.

    Aberrant pathogenic GM-CSF HGNC+ T cells and inflammatory CD14 HGNC+ CD16 HGNC+ monocytes in severe pulmonary syndrome patients of a new coronavirus

    Authors: Yonggang Zhou; Binqing Fu; Xiaohu Zheng; Dongsheng Wang; Changcheng Zhao; Yingjie Qi; Rui Sun; Zhigang Tian; Xiaoling Xu; Haiming Wei

    doi:10.1101/2020.02.12.945576 Date: 2020-02-20 Source: bioRxiv

    Pathogenic human coronavirus infections MESHD, such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) MESHD, cause high morbidity and mortality 1,2. Recently, a severe pneumonia-associated respiratory syndrome MESHD caused by a new coronavirus was reported at December 2019 (2019-nCoV) in the city Wuhan, Hubei province, China3-5, which was also named as pneumonia-associated respiratory syndrome MESHD (PARS)6. Up to 9th of February 2020, at least 37, 251 cases have been reported with 812 fatal cases according to the report from China CDC. However, the immune mechanism that potential orchestrated acute mortality from patients of 2019-nCoV is still unknown. Here we show that after the 2019-nCoV infection MESHD, CD4+T lymphocytes are rapidly activated to become pathogenic T helper (Th) 1 cells and generate GM-CSF HGNC etc. The cytokines environment induces inflammatory CD14 HGNC+ CD16 HGNC+ monocytes with high expression of IL-6 HGNC and accelerates the inflammation MESHD. These aberrant and excessive immune cells may enter the pulmonary circulation in huge numbers and play an immune damaging role to causing lung functional disability and quick mortality. Our results demonstrate that excessive non-effective host immune responses by pathogenic T cells and inflammatory monocytes may associate with severe lung pathology. Therefore, we suggest that monoclonal antibody that targets the GM-CSF HGNC or interleukin 6 receptor HGNC may potentially curb immunopathology caused by 2019-nCoV and consequently win more time for virus clearance.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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