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SARS-CoV-2 proteins

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    Single-cell immunophenotyping of the fetal immune response to maternal SARS-CoV-2 infection MESHD in late gestation

    Authors: Juan Matute; Benjamin Finander; David Pepin; Xinbin Ai; Neal Smith; Jonathan Li; Andrea Edlow; Alexandra Villani; Paul Lerou; Brian Kalish

    doi:10.21203/rs.3.rs-311000/v1 Date: 2021-03-09 Source: ResearchSquare

    During the COVID-19 pandemic MESHD, thousands of pregnant women have been infected with SARS-CoV-2. The implications of maternal SARS-CoV-2 infection MESHD on fetal and childhood well-being are unknown. We aimed to characterize the fetal immune response to maternal SARS-CoV-2 infection MESHD. We performed single-cell RNA sequencing and T-cell receptor (TCR) sequencing on cord blood mononuclear cells (CBMC) from newborns of mothers infected with SARS-CoV-2 in the third-trimester (cases) or without SARS-CoV-2 infection MESHD. We identified widespread gene expression changes in CBMC from cases, including upregulation of interferon-stimulated genes and Major Histocompatibility Complex genes in CD14 HGNC + monocytes; transcriptional changes suggestive of activation of plasmacytoid dendritic cells, and activation and exhaustion of NK cells and CD8 + T-cells. Lastly, we observed fetal TCR repertoire expansion in cases. As none of the infants were infected with SARS-CoV-2, our results suggest that SARS-CoV-2 maternal infection MESHD might modulate the fetal immune system in the absence of vertical transmission.

    The aging whole blood transcriptome reveals a potential role of FASLG HGNC in COVID-19 MESHD

    Authors: Luiz Gustavo Chuffa Sr.; Jeferson dos Santos Souza Sr.; Mariana Costa de Mello; Mario de Oliveira Neto Sr.; Robson Francisco Carvalho Sr.; Kevin S. Cashman; Richard P. Ramonell; Shuya Kyu; Ankur Singh Saini; Monica Cabrera-Mora; Andrew Derrico; David Alter; John D. Roback; Michael Horwath; Henry M. Wu; An-Kwok Ian Wong; Alexandra W. Dretler; Ria Gripaldo; Andrea N. Lane; Hao Wu; Saeyun Lee; Mindy Hernandez; Vanessa Engineer; John Varghese; Sang Le; Iñaki Sanz; John L. Daiss; Frances Eun-Hyung Lee

    doi:10.1101/2020.12.04.412494 Date: 2020-12-06 Source: bioRxiv

    The risk for severe illness from COVID-19 MESHD increases with age as older patients are at the highest risk. Although it is still unclear whether the virus is blood-transmitted, the viral RNA is detected in serum. Identifying how Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) interacts with specific blood components during aging is expected to guide proper therapies. Considering that all human coronavirus require host cellular molecules to promote infection, we investigated the aging whole blood transcriptome from the Genotype-Tissue Expression (GTEx) database to explore differentially expressed genes (DEGs) translated into proteins potentially interacting with viral proteins. From a total of 22 DEGs in aged blood, five genes ( FASLG HGNC, CTSW HGNC, CTSE HGNC, VCAM1 HGNC, and BAG3 HGNC) changed expression during aging. These age-related genes are involved in immune response, inflammation MESHD, cell component and cell adhesion, and platelet activation/aggregation. Both males and females older than 50 overexpress FASLG HGNC compared with younger adults (20-30 years old), possibly inducing a hyper-inflammatory cascade that activates specific immune cells. Furthermore, the expression of cathepsins ( CTSW HGNC and CTSE HGNC) and the anti-apoptotic co-chaperone molecule BAG3 HGNC was significantly increased throughout aging in both gender. By exploring publicly available Single-Cell RNA-Sequencing (scRNA-Seq) data on peripheral blood of SARS-CoV-2-infected MESHD patients, we found FASLG HGNC and CTSW HGNC expressed mainly in natural killer (NK) cells and CD8+ (cytotoxic) T lymphocytes whereas BAG3 HGNC was expressed in CD4+ T cells, naive T cells, and CD14 HGNC+ monocytes. The increased expression of FASLG HGNC in blood during aging may explain why older patients are more prone to severe acute viral infection complications MESHD. These results indicate FASLG HGNC as a prognostic candidate and potential therapeutic target for more aggressive clinical manifestation of COVID-19 MESHD.

    Induction of a regulatory myeloid program in bacterial sepsis and severe COVID-19 MESHD

    Authors: Miguel Reyes; Michael R. Filbin; Roby P. Bhattacharyya; Abraham Sonny; Arnav Mehta; Kianna Billman; Kyle R. Kays; - MGH COVID-19 Collection & Processing Team; Alexandra-Chloe Villani; Moshe Sade-Feldman; Marcia B. Goldberg; Paul C. Blainey; Nir Hacohen

    doi:10.1101/2020.09.02.280180 Date: 2020-09-02 Source: bioRxiv

    A recent estimate suggests that one in five deaths globally are associated with sepsis MESHD. To date, no targeted treatment is available for this syndrome, likely due to substantial patient heterogeneity and our lack of insight into sepsis MESHD immunopathology. These issues are highlighted by the current COVID-19 MESHD COVID-19 MESHD pandemic, wherein many clinical manifestations of severe SARS-CoV-2 infection parallel bacterial sepsis MESHD. We previously reported an expanded CD14 HGNC+ monocyte state, MS1, in patients with bacterial sepsis MESHD or non-infectious critical illness, and validated its expansion in sepsis MESHD across thousands of patients using public transcriptomic data. Despite its marked expansion in the circulation of bacterial sepsis MESHD patients, its relevance to viral sepsis MESHD and association with disease outcomes have not been examined. In addition, the ontogeny and function of this monocyte state remain poorly characterized. Using public transcriptomic data, we show that the expression of the MS1 program is associated with sepsis mortality MESHD and is up-regulated in monocytes from patients with severe COVID-19 MESHD. We found that blood plasma from bacterial sepsis MESHD or COVID-19 MESHD patients with severe disease induces emergency myelopoiesis and expression of the MS1 program, which are dependent on the cytokines IL-6 HGNC and IL-10 HGNC. Finally, we demonstrate that MS1 cells are broadly immunosuppressive, similar to monocytic myeloid-derived suppressor cells (MDSCs), and have decreased responsiveness to stimulation. Our findings highlight the utility of regulatory myeloid cells in sepsis MESHD prognosis, and the role of systemic cytokines in inducing emergency myelopoiesis during severe bacterial and SARS-CoV-2 infections MESHD.

    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.

    SARS-CoV-2 Spike PROTEIN protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity

    Authors: Ganna Petruk; Manoj Puthia; Jitka Petrlova; Ann-Charlotte Strömdahl; Sven Kjellström; Artur Schmidtchen

    doi:10.1101/2020.06.29.175844 Date: 2020-06-29 Source: bioRxiv

    ABSTRACTThere is a well-known and established link between high lipopolysaccharide ( LPS HGNC) levels in blood and the metabolic syndrome MESHD ( MS MESHD). MS MESHD is a risk factor for developing severe COVID-19 MESHD and acute respiratory distress syndrome MESHD ( ARDS MESHD). Here we define an interaction between SARS-CoV-2 Spike PROTEIN SARS-CoV-2 Spike MESHD ( S) protein PROTEIN and LPS HGNC and its link to aggravated inflammation MESHD in vitro and in vivo. Electrophoresis under native conditions demonstrated that SARS-CoV-2 S MESHD S protein PROTEIN binds to Escherichia coli LPS HGNC, forming high molecular weight aggregates. Microscale thermophoresis analysis further defined the interaction, having a KD of ~47 nM, similar to the observed affinity between LPS HGNC and the human receptor CD14 HGNC. Moreover, S protein PROTEIN, when combined with low levels of LPS HGNC, boosted nuclear factor-kappa B (NF-κB) and cytokine responses in monocytic THP-1 cells and human blood, respectively. In an experimental model of localized inflammation MESHD, employing NF-κB reporter mice and in vivo bioimaging, S protein PROTEIN in conjunction with LPS significantly increased the inflammatory response when compared with S protein PROTEIN and LPS alone. Apart from providing information on LPS HGNC as a ligand for S protein PROTEIN, our results are of relevance for studies on comorbidities involving bacterial endotoxins, such as the MS MESHD, or co-existing acute and chronic infections MESHD in COVID-19 MESHD patients.Competing Interest StatementA.S is a founder and shareholder of in2cure AB, a company developing therapies based on host defense peptides. A patent application related to the present work, with A.S. and G.P. listed as inventors, has been filed.AbbreviationsARDSacute respiratory distress syndromeCOVID-19coronavirus disease 2019MSmetabolic syndromeLBPLPS MESHD COVID-19 MESHD coronavirus disease 2019 MESHDMSmetabolic syndromeLBPLPS-binding proteinLPSlipopolysaccharideNF-κBnuclear factor-kappa BSARS-CoV-2 Spike proteinS PROTEIN proteinTLR4Toll-like receptor 4View Full Text

    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
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