Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (5)

NSP5 (2)

ProteinN (2)

ProteinS1 (2)

NSP3 (1)


SARS-CoV-2 Proteins
    displaying 41 - 50 records in total 73
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    Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C)

    Authors: Conor Gruber; Roosheel Patel; Rebecca Trachman; Lauren Lepow; Fatima Amanat; Florian Krammer; Karen M. Wilson; Kenan Onel; Daniel Geanon; Kevin Tuballes; Manishkumar Patel; Konstantinos Mouskas; Nicole Simons; Vanessa Barcessat; Diane Del Valle; Samantha Udondem; Gurpawan Kang; Sandeep Gangadharan; George Ofori-Amanfo; Adeeb Rahman; Seunghee Kim-Schulze; Alexander Charney; Sacha Gnjatic; Bruce Gelb; Miriam Merad; Dusan Bogunovic

    doi:10.1101/2020.07.04.20142752 Date: 2020-07-06 Source: medRxiv

    Initially, the global outbreak of COVID-19 MESHD caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spared children from severe disease. However, after the initial wave of infections, clusters of a novel hyperinflammatory disease MESHD have been reported in regions with ongoing SARS-CoV-2 MESHD epidemics. While the characteristic clinical features are becoming clear, the pathophysiology remains unknown. Herein, we report on the immune profiles of eight Multisystem Inflammatory Syndrome MESHD in Children ( MIS HGNC-C) cases. We document that all MIS HGNC-C patients had evidence of prior SARS-CoV-2 exposure, mounting an antibody response with normal isotype-switching and neutralization capability. We further profiled the secreted immune response by high-dimensional cytokine assays, which identified elevated signatures of inflammation MESHD ( IL-18 HGNC and IL-6 HGNC), lymphocytic and myeloid chemotaxis and activation ( CCL3 HGNC, CCL4 HGNC, and CDCP1 HGNC) and mucosal immune dysregulation ( IL-17A HGNC, CCL20 HGNC, CCL28 HGNC). Mass cytometry immunophenotyping of peripheral blood revealed reductions of mDC1 and non-classical monocytes, as well as both NK- and T- lymphocytes, suggesting extravasation to affected tissues. Markers of activated myeloid function were also evident, including upregulation of ICAM1 HGNC and FcR1 in neutrophil and non-classical monocytes, well-documented markers in autoinflammation MESHD and autoimmunity that indicate enhanced antigen presentation and Fc-mediated responses. Finally, to assess the role for autoimmunity secondary to infection, we profiled the auto-antigen reactivity of MIS HGNC-C plasma, which revealed both known disease-associated autoantibodies (anti-La) and novel candidates that recognize endothelial, gastrointestinal and immune-cell antigens. All patients were treated with anti- IL6R HGNC antibody or IVIG, which led to rapid disease resolution tracking with normalization of inflammatory markers.

    Increased Interleukin-6 HGNC and Macrophage Chemoattractant Protein-1 are associated with Respiratory Failure in COVID-19 MESHD 

    Authors: Marthe Jørgensen; Jan Cato Holter; Erik Egeland Christensen; Camilla Schjalm; Kristian Tonby; Søren Erik Pischke; Synne Jenum; Linda G Skeie; Sarah Nur; Andreas Lind; Hanne Opsand; Tone Burvald Enersen; Ragnhild Grøndahl; Anne Hermann; Susanne Dudman; Fredrik Müller; Thor Ueland; Tom Eirik Mollnes; Pål Aukrust; Lars Heggelund; Aleksander Rygh Holten; Anne Ma Dyrhol-Riise

    doi:10.21203/ Date: 2020-06-30 Source: ResearchSquare

    Background: In SARS-CoV-2 infection MESHD ARS-CoV-2 infection MESHDthere is an urgent need to identify patients that will progress to severe COVID-19 MESHD and may benefit from targeted treatment.Objectives: Analyze plasma cytokines in COVID-19 MESHD patients and investigate their association with r espiratory failure MESHD(R F) MESHD and treatment in Intensive Care Unit (ICU). Method: Hospitalized patients (n=34) with confirmed COVID-19 MESHD were recruited into a prospective cohort study. Clinical data and blood samples were collected at inclusion and after 2-5 and 7-10 days. R F MESHDwas defined as PaO2/FiO2 ratio (P/F) <40kPa. Plasma cytokines were analyzed by a Human Cytokine 27-plex assay. Measurements and Results:  COVID-19 MESHD patients with R F MESHDand/or treated in ICU showed overall increased systemic cytokine levels. Plasma I L-6, HGNC I L-8, HGNC G -CSF, HGNC M CP-1, HGNC M IP-1α HGNClevels were negatively correlated with P/F, whereas combinations of I L-6, HGNC I P-10, HGNC I L-1ra HGNCand M CP-1 HGNCshowed the best association with R F MESHDin ROC analysis (AUC 0.79-0.80, p<0.05). During hospitalization the decline was most significant for I P-10 HGNC(P<0.001). Conclusion: Elevated levels of pro-inflammatory cytokines were present in patients with severe COVID-19 MESHD. I L-6 HGNCand M CP-1 HGNCwere inversely correlated with P/F with the largest AUC in ROC analyses and should be further explored as biomarkers to identify patients at risk for severe R F MESHDand as targets for improved treatment strategies. 

    The in vitro antiviral activity of the anti-hepatitis C virus (HCV) drugs daclatasvir and sofosbuvir against SARS-CoV-2

    Authors: Carolina Q. Sacramento; Natalia Fintelman-Rodrigues; Jairo R. Temerozo; Suelen da Silva Gomes Dias; Andre C. Ferreira; Mayara Mattos; Camila R. R. Pao; Caroline S. de Freitas; Vinicius Cardoso Soares; Fernando A. Bozza; Dumith Chequer Bou-Habib; Patricia T. Bozza; Thiago Moreno L. Souza

    doi:10.1101/2020.06.15.153411 Date: 2020-06-16 Source: bioRxiv

    The infection by the Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes major public health concern and economic burden. Although clinically approved drugs have been repurposed to treat individuals with 2019 Coronavirus disease MESHD ( COVID-19 MESHD), the lack of safety studies and limited efficiency as well jeopardize clinical benefits. Daclatasvir and sofosbuvir (SFV) are clinically approved direct-acting antivirals (DAA) against hepatitis C virus MESHD ( HCV MESHD), with satisfactory safety profile. In the HCV MESHD replicative cycle, daclatasvir and SFV target the viral enzymes NS5A and NS5B, respectively. NS5A is endowed with pleotropic activities, which overlap with several proteins from SARS-CoV-2. HCV MESHD NS5B and SARS-CoV-2 nsp12 are RNA polymerases that share homology in the nucleotide uptake channel. These characteristics of the HCV MESHD and SARS-CoV-2 motivated us to further study the activity of daclatasvir and SFV against the new coronavirus. Daclatasvir consistently inhibited the production of infectious SARS-CoV-2 MESHD virus particles in Vero cells, in the hepatoma MESHD cell line HuH-7 HGNC and in type II pneumocytes (Calu-3), with potencies of 0.8, 0.6 and 1.1 M, respectively. Daclatasvir targeted early events during SARS-CoV-2 replication cycle and prevented the induction of IL-6 HGNC and TNF HGNC-, inflammatory mediators associated with the cytokine storm typical of SARS-CoV-2 infection MESHD. Sofosbuvir, although inactive in Vero cells, displayed EC50 values of 6.2 and 9.5 M in HuH-7 HGNC and Calu-3 cells, respectively. Our data point to additional antiviral candidates, in especial daclatasvir, among drugs overlooked for COVID-19 MESHD, that could immediately enter clinical trials.

    SARS-CoV-2 proteases cleave IRF3 HGNC and critical modulators of inflammatory pathways ( NLRP12 HGNC and TAB1): implications for disease presentation across species and the search for reservoir hosts.

    Authors: Mehdi Moustaqil; Emma Ollivier; Hsin-Ping Chiu; Paulina Rudolffi-Soto; Sarah Van Tol; Christian Stevens; Akshay Bhumkar; Dominic J.B. Hunter; Alexander N. Freiberg; David Jacques; Benhur Lee; Emma Sierecki; Yann Gambin

    doi:10.1101/2020.06.05.135699 Date: 2020-06-05 Source: bioRxiv

    The genome of SARS-CoV-2 ( SARS2 MESHD) encodes for two viral proteases ( NSP3 PROTEIN NSP3 HGNC/ papain-like protease PROTEIN and NSP5 HGNC NSP5 PROTEIN/ 3C-like protease or major protease) that are responsible for cleaving viral polyproteins for successful replication. NSP3 PROTEIN NSP3 HGNC and NSP5 HGNC NSP5 PROTEIN of SARS-CoV (SARS1) are known interferon antagonists. Here, we examined whether the protease function of SARS2 MESHD NSP3 HGNC NSP3 PROTEIN and NSP5 PROTEIN NSP5 HGNC target proteins involved in the host innate immune response. We designed a fluorescent based cleavage assay to rapidly screen the protease activity of NSP3 PROTEIN NSP3 HGNC and NSP5 PROTEIN NSP5 HGNC on a library of 71 human innate immune proteins (HIIPs), covering most pathways involved in human innate immunity. By expressing each of these HIIPs with a genetically encoded fluorophore in a cell-free system and titrating in the recombinant protease domain of NSP3 HGNC NSP3 PROTEIN or NSP5 PROTEIN NSP5 HGNC, we could readily detect cleavage of cognate HIIPs on SDS-page gels. We identified 3 proteins that were specifically and selectively cleaved by NSP3 PROTEIN NSP3 HGNC or NSP5 HGNC NSP5 PROTEIN: IRF-3 HGNC, and NLRP12 HGNC and TAB1, respectively. Direct cleavage of IRF3 HGNC by NSP3 HGNC NSP3 PROTEIN could explain the blunted Type- I IFN response seen during SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHDs while NSP5 PROTEIN NSP5 HGNC mediated cleavage of NLRP12 HGNC and TAB1 point to a molecular mechanism for enhanced production of IL-6 HGNC and inflammatory response observed in COVID-19 MESHD patients. Surprisingly, both NLRP12 HGNC and TAB1 have each two distinct cleavage sites. We demonstrate that in mice, the second cleavage site of NLRP12 is absent. We pushed this comparative alignment of IRF-3 and NLRP12 homologs and show that the lack or presence of cognate cleavage motifs in IRF-3 and NLRP12 could contribute to the presentation of disease in cats and tigers, for example. Our findings provide an explanatory framework for in-depth studies into the pathophysiology of COVID-19 MESHD and should facilitate the search or development of more effective animal models for severe COVID-19 MESHD. Finally, we discovered that one particular species of bats, Davids Myotis, possesses the five cleavage sites found in humans for NLRP12 HGNC, TAB1 and IRF3 HGNC. These bats are endemic from the Hubei province in China and we discuss its potential role as reservoir for the evolution of SARS1 and SASR2.

    Treatment with Arbidol and Moxifloxacin in Ordinary and Severe Adult Patients Infected with COVID-19 MESHD


    doi:10.1101/2020.05.30.20117598 Date: 2020-06-05 Source: medRxiv

    Background An outbreak of coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been widely spread. We aim to investigate the therapeutic effect of arbidol and moxifloxacin in patients infected with SARS-CoV-2. Methods We collected and analyzed data on 94 patients with COVID-19 MESHD including 27 severe patients at the Intensive Care Unit (ICU) and 74 ordinary patients at general isolation ward in Wuhan Xiehe Hospital, from February 15, 2020 to March 15, 2020. All patients were treated with arbidol (100mg each time, three times a day for 14 days) and moxifloxacin (0.4g each time, once a day for 7-14 days). Other data was also collected including demographic data, symptoms, laboratory findings, treatments and clinical outcomes. Results In basic characteristics, compared with the ordinary patients, the severe patients were older (median age was 63.0 years V.S 57.0 years, p=0.03), had higher proportion of hypertension MESHD (30% V.S 9%, p=0.03), higher possibility of getting fatigue and/or myalgia MESHD (26% V.S 6%, p=0.03), and had more obvious dyspnea MESHD symptom (26% V.S 3%, p=0.006). In regarding to laboratory results, we found the severe patients have higher white blood cell counts (p=0.003), neutrophil counts (p=0.007), higher levels of D-dimer (p<0.001), ALT (p<0.001) and AST HGNC (p=0.013) than the ordinary patients. After treatment of arbidol and moxifloxacin for one week, the rates of SARS-CoV-2 nucleic acid turning negative were 69.2% in the severe group and 77.8% in the ordinary group. A peculiar phenomenon was that IL-6 HGNC stands out among the cytokines in both groups, and higher in severe group than the ordinary one (p=0.011). After treating with arbidol and moxifloxacin for one week, IL-6 HGNC decreased significantly in severe group (p=0.023). Conclusion In summary, we proved the treatment of arbidol and moxifloxacin could be helpful in reducing viral load and inflammation MESHD during SARS-CoV2 infection MESHD, especially for negatively regulating fatal inflammation MESHD in severe COVID-19 MESHD patients. However, more evidence awaits further clinical verification.

    SARS-CoV2 drives JAK1 HGNC/2-dependent local and systemic complement hyper-activation

    Authors: Bingyu Yan; Tilo Freiwald; Daniel Chauss; Luopin Wang; Erin West; Jack Bibby; Matthew Olson; Shahram Kordasti; Didier Portilla; Arian Laurence; Michail S Lionakis; Claudia Kemper; Behdad Afzali; Majid Kazemian

    doi:10.21203/ Date: 2020-06-05 Source: ResearchSquare

    Patients with coronavirus disease 2019 MESHD ( COVID-19 MESHD) present with a range of devastating acute clinical manifestations affecting the lungs, liver, kidneys and gut. The best-characterized entry receptor for the disease-causing virus SARS-CoV2, angiotensin converting enzyme (ACE) 2 HGNC, is highly expressed in these tissues. However, the pathways that underlie the disease are still poorly understood. Here we show that the complement system is unexpectedly one of the intracellular pathways most highly induced by SARS-CoV2 infection MESHD in lung epithelial and liver cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Modelling the regulome of host genes induced by COVID-19 MESHD and the drugs that could normalize these genes both implicated the JAK1 HGNC/2- STAT1 HGNC signaling system downstream of type I interferon receptors, and NF-kB. Ruxolitinib, a JAK1/2 inhibitor and the top predicted pharmaceutical candidate, normalized interferon signature genes, IL-6 HGNC (the best characterized severity marker in COVID-19 MESHD) and all complement genes induced by SARS-CoV2, but did not affect NF-kB-regulated genes. We predict that combination therapy with JAK inhibitors and other agents with the potential to normalize NF-kB-signaling, such as anti-viral agents, may serve as an effective clinical strategy. 

    Clinical characteristics, outcomes and follow-up of COVID-19 MESHD infection in cancer patients

    Authors: Minghao Fang; Jianmin Ling; Yanqing Wu; Zhaohua Wang; Le Yang

    doi:10.21203/ Date: 2020-06-04 Source: ResearchSquare

    Purpose: The study is to describe the clinical characteristics, outcomes and follow-up  of cancer MESHD patients with COVID-19 MESHD. Methods: Clinical records, demographic data, signs and symptoms, laboratory results, cytokine profiles, chest CT scans, comorbidities, treatments, clinical outcomes, and RT-PCR of SARS-CoV-2 after discharge were retrospectively collected for fifty-six cancer MESHD patients with laboratory-confirmed COVID-19 MESHD pneumonia MESHD who were admitted to Tongji Hospital of Huazhong University of Science and Technology, Wuhan, China, from Feb 1 to Apr 1 HGNC, 2020. Evidence of cytokine profiles were assessed by testing for the IL1β HGNC, IL2R HGNC, IL6 HGNC, IL8 HGNC, IL10 HGNC, and TNF - α HGNC in the peripheral blood of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) infected cancer MESHD patients. Results: Of 2143 patients with COVID-19 MESHD, 56 cancer MESHD patients were included. The patients were divided into two groups, as cancer MESHD survivors, and cancer MESHD non-survivors. 12 (21%) patients with lymphopenia MESHD (0.5 [0.3-0.7]) had died during hospital stay. In non-survivors, IL2R HGNC, IL6 HGNC, and IL10 HGNC were higher. 3(6.8%) cancer MESHD survivors with COVID-19 MESHD had positive RT-PCR test results again shortly after discharge. Conclusion: The mortality rate of COVID-19 MESHD among cancer MESHD patients are considerable. Cancer non-survivors are characterized by more severe lymphopenia MESHD and a higher levels of cytokines. Recovered cancer MESHD survivors still may be virus carriers.

    An inflammatory cytokine signature helps predict COVID-19 MESHD severity and death

    Authors: Diane Marie Del Valle; Seunghee Kim-schulze; Huang Hsin-hui; Noam D Beckmann; Sharon Nirenberg; Bo Wang; Yonit Lavin; Talia Swartz; Deepu Madduri; Aryeh Stock; Thomas Marron; Hui Xie; Manish Kumar Patel; Oliver van Oekelen; Adeeb Rahman; Patricia Kovatch; Judith Aberg; Eric Schadt; Sundar Jagannath; Madhu Mazumdar; Alexander Charney; Adolfo Firpo-Betancourt; Damodara Rao Mendu; Jeffrey Jhang; David Reich; Keith Sigel; Carlos Cordon-Cardo; Marc Feldmann; Samir Parekh; Miriam Merad; Sacha Gnjatic

    doi:10.1101/2020.05.28.20115758 Date: 2020-05-30 Source: medRxiv

    The COVID-19 MESHD COVID-19 MESHD pandemic caused by infection with Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) has led to more than 100,000 deaths in the United States. Several studies have revealed that the hyper-inflammatory response induced by SARS-CoV-2 is a major cause of disease severity and death in infected MESHD patients. However, predictive biomarkers of pathogenic inflammation MESHD to help guide targetable immune pathways are critically lacking. We implemented a rapid multiplex cytokine assay to measure serum IL-6 HGNC, IL-8 HGNC, TNF HGNC-, and IL-1{beta HGNC} in hospitalized COVID-19 MESHD patients upon admission to the Mount Sinai Health System in New York. Patients (n=1484) were followed up to 41 days (median 8 days) and clinical information, laboratory test results and patient outcomes were collected. In 244 patients, cytokine measurements were repeated over time, and effect of drugs could be assessed. Kaplan-Meier methods were used to compare survival by cytokine strata, followed by Cox regression models to evaluate the independent predictive value of baseline cytokines. We found that high serum IL-6 HGNC, IL-8 HGNC, and TNF HGNC- levels at the time of hospitalization were strong and independent predictors of patient survival. Importantly, when adjusting for disease severity score, common laboratory inflammation markers, hypoxia MESHD and other vitals, demographics, and a range of comorbidities, IL-6 HGNC and TNF HGNC- serum levels remained independent and significant predictors of disease severity and death MESHD. We propose that serum IL-6 HGNC and TNF HGNC- levels should be considered in the management and treatment of COVID-19 MESHD patients to stratify prospective clinical trials, guide resource allocation and inform therapeutic options. We also propose that patients with high IL-6 HGNC and TNF HGNC- levels should be assessed for combinatorial blockade of pathogenic inflammation MESHD in this disease.

    Pathogenic Human Coronavirus Envelope Protein PROTEIN: A Clear Link to Immunopathology?

    Authors: Dewald Schoeman; Burtram C. Fielding

    id:202005.0414/v1 Date: 2020-05-25 Source:

    Since the severe acute respiratory syndrome MESHD (SARS) outbreak in 2003, human coronaviruses (hCoVs) have been identified as causative agents of severe acute respiratory tract infections MESHD. Two more hCoV outbreaks have since occurred, the most recent being SARS-CoV-2, the causative agent of coronavirus disease 2019 MESHD ( COVID-19 MESHD). The clinical presentation of SARS and MERS is remarkably similar to COVID-19 MESHD, with hyperinflammation causing a severe form of the disease in some patients. Previous studies show that the expression of the SARS-CoV E protein PROTEIN is associated with the hyperinflammatory response that could culminate in acute respiratory distress syndrome MESHD ( ARDS MESHD), a potentially fatal complication. This immune-mediated damage is largely caused by a cytokine storm, which is induced by significantly elevated levels of inflammatory cytokines interleukin (IL)-1beta HGNC and IL-6 HGNC, which are partly mediated by the expression of the SARS-CoV E protein PROTEIN. The interaction between the SARS-CoV E protein PROTEIN and the host protein, syntenin HGNC, as well as the viroporin function of SARS-CoV E, are linked to this cytokine dysregulation. This review aims to compare the clinical presentation of virulent hCoVs with a specific focus on the cause of the immunopathology. The review also proposes that inhibition of IL-1beta HGNC and IL-6 HGNC in severe cases can improve patient outcome.

    Pathophysiology of SARS-CoV-2: targeting of endothelial cells renders a complex disease with thrombotic microangiopathy and aberrant immune response. The Mount Sinai COVID-19 MESHD autopsy experience

    Authors: Clare Bryce; Zachary Grimes; Elisabet Pujadas; Sadhna Ahuja; Mary Beth Beasley; Randy Albrecht; Tahyna Hernandez; Aryeh Stock; Zhen Zhao; Mohamed Al Rasheed; Joyce Chen; Li Li; Diane Wang; Adriana Corben; Kenneth Haines; William Westra; Melissa Umphlett; Ronald E Gordon; Jason Reidy; Bruce Petersen; Fadi Salem; MariaIsabel Fiel; Siraj M El Jamal; Nadejda M Tsankova; Jane Houldsworth; Zarmeen Mussa; Wen-Chun Liu; Brandon Veremis; Emilia Sordillo; Melissa Gitman; Michael Nowak; Rachel Brody; Noam Harpaz; Miriam Merad; Sacha Gnjatic; Ryan Donnelly; Patricia Seigler; Calvin Keys; Jennifer Cameron; Isaiah Moultrie; Kae-Lynn Washington; Jacquelyn Treatman; Robert Sebra; Jeffrey Jhang; Adolfo Firpo; John Lednicky; Alberto Paniz-Mondolfi; Carlos Cordon-Cardo; Mary Fowkes

    doi:10.1101/2020.05.18.20099960 Date: 2020-05-22 Source: medRxiv

    BACKGROUND Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2) and its associated clinical syndrome COVID-19 MESHD are causing overwhelming morbidity and mortality around the globe, disproportionately affecting New York City. A comprehensive, integrative autopsy series that advances the mechanistic discussion surrounding this disease process is still lacking. METHODS Autopsies were performed at the Mount Sinai Hospital on 67 COVID-19 MESHD positive patients and data from the clinical records were obtained from the Mount Sinai Data Warehouse. The experimental design included a comprehensive microscopic examination carried out by a team of expert pathologists, along with transmission electron microscopy, immunohistochemistry, RNA in situ hybridization, as well as immunology and serology assays. RESULTS Laboratory results of our COVID-19 MESHD cohort show elevated inflammatory markers, abnormal coagulation values, and elevated cytokines IL-6 HGNC, IL-8 HGNC and TNF HGNC. Autopsies revealed large pulmonary emboli MESHD in four cases. We report microthrombi in multiple organ systems including the brain, as well as conspicuous hemophagocytosis MESHD and a secondary hemophagocytic lymphohistiocytosis-like syndrome MESHD in many of our patients. We provide electron microscopic, immunofluorescent and immunohistochemical evidence of the presence of the virus and the ACE2 HGNC receptor in our samples. CONCLUSIONS We report a comprehensive autopsy series of 67 COVID-19 MESHD positive patients revealing that this disease, so far conceptualized as a primarily respiratory viral illness MESHD, also causes endothelial dysfunction, a hypercoagulable state, and an imbalance of both the innate and adaptive immune responses. Novel findings reported here include an endothelial phenotype of ACE2 HGNC in selected organs, which correlates with clotting abnormalities and thrombotic microangiopathy MESHD, addressing the prominent coagulopathy and neuropsychiatric symptoms MESHD. Another original observation is that of macrophage activation syndrome MESHD, with hemophagocytosis MESHD and a hemophagocytic lymphohistiocytosis-like disorder MESHD, underlying the microangiopathy MESHD and excessive cytokine release. We discuss the involvement of critical regulatory pathways.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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