preVIEW: COVID-19

Corpus overview

Overview

MeSH Disease

COVID-19 (127)

Inflammation (32)

Severe Acute Respiratory Syndrome (27)

Necrosis (21)

Coronavirus Infections (17)


HGNC Genes

tumor necrosis factor (134)

interleukin 6 (81)

interleukin 10 (28)

C-X-C motif chemokine ligand 8 (25)

interferon gamma (25)


SARS-CoV-2 proteins

ProteinS (14)

NSP5 (4)

ProteinS1 (3)

ProteinN (2)

NSP2 (1)


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    Soluble angiotensin-converting enzyme 2 HGNC is transiently elevated in COVID-19 MESHD and correlates with specific inflammatory and endothelial markers

    Authors: Annika Lundstrom; Louise Ziegler; Sebastian Havervall; Ann-Sofie Rudberg; Fien Von Meijenfeldt; Ton Lisman; Nigel Mackman; Per Sanden; Charlotte Thalin

    doi:10.1101/2021.03.03.21252841 Date: 2021-03-05 Source: medRxiv

    RationaleAngiotensin-converting enzyme 2 ( ACE2 HGNC) is the main entry receptor of severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), but how SARS-CoV-2 interactions with ACE2 HGNC influences the renin-angiotensin system (RAS) in Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is unknown. ObjectiveTo measure circulating ACE2 HGNC and ACE HGNC levels in COVID-19 MESHD patients and investigate association with risk factors, outcome and inflammatory markers. Methods and resultsSoluble ACE2 HGNC (sACE2) and sACE concentrations were measured by ELISA in plasma samples from 114 hospital-treated COVID-19 MESHD patients and 10 healthy controls. Follow-up samples after four months were available for 58/114 patients. Von Willebrand MESHD Von Willebrand HGNC factor ( VWF HGNC), factor VIII ( fVIII HGNC), D-dimer, interleukin 6 ( IL-6 HGNC), tumor necrosis MESHD factor and plasminogen activator inhibitor 1 ( PAI-1 HGNC) had previously been determined. Levels of sACE2 were higher in COVID-19 MESHD patients than in healthy controls, median 5.0 (interquartile range 2.8-11.8) ng/ml versus 1.4 (1.1-1.6) ng/ml, p < 0.0001. sACE2 was higher in men than women, but were not affected by other risk factors for severe COVID-19 MESHD. sACE 2 decreased to 2.3 (1.6-3.9) ng/ml at follow-up, p < 0.0001, but remained higher than in healthy controls, p=0.012. Follow-up sACE2 levels were higher with increasing age, BMI, total number of comorbidities, for patients with diabetes MESHD and patients on RAS-inhibition. sACE was marginally lower during COVID-19 MESHD compared with at follow-up, 57 (45-70) ng/ml versus 72 (52-87) ng/ml, p=0.008. Levels of sACE2 and sACE did not differ depending on survival or disease severity (care level, respiratory support). sACE2 during COVID-19 MESHD correlated with VWF HGNC, fVIII HGNC and D-dimer, while sACE correlated with IL-6 HGNC, TNF HGNC and PAI-1 HGNC. ConclusionssACE2 was transiently elevated in COVID-19 MESHD, likely due to increased shedding from infected cells. sACE2 and sACE during COVID-19 MESHD differed distinctly in their correlations with markers of inflammation MESHD and endothelial dysfunction, suggesting release from different cell types and/or vascular beds.

    Targeting of the NLRP3 HGNC Inflammasome for early COVID-19 MESHD

    Authors: Carlo Marchetti; Kara Mould; Isak W. Tengesdal; William J. Janssen; Charles A. Dinarello

    doi:10.1101/2021.02.24.432734 Date: 2021-02-24 Source: bioRxiv

    Following entry and replication of Severe Acute Respiratory Syndrome-coronavirus MESHD 2 (SARS-CoV-2) into ACE2 expressing cells, the infected cells undergo lysis releasing more virus but also cell contents. In the lung, constitutive cytokines such as IL-1 HGNC are released together with other cell contents. A cascade of inflammatory cytokines ensues, including chemokines and IL-1{beta}, triggering both local as well as systemic inflammation MESHD. This cascade of inflammatory cytokines in patients with COVID-19 MESHD is termed Cytokine Release Syndrome ( CRS MESHD), and is associated with poor outcomes and death MESHD. Many studies reveal that blocking IL-1{beta HGNC} activities in COVID-19 MESHD patients reduces disease severity and deaths MESHD. Here we report highly significant circulating levels of IL-1{beta HGNC}, IL-1 Receptor antagonist HGNC, IL-6 HGNC, TNF HGNC, IL-10 HGNC and soluble urokinase plasminogen activator receptor HGNC in COVID-19 MESHD patients with mild or no symptoms. We also report that in circulating myeloid cells from the same patients, there is increased expression of the NOD-, LRR- and pyrin domain-containing 3 ( NLRP3 HGNC) early in the infection. We observed increased NLRP3 HGNC gene expression in myeloid cells correlated with IL-1{beta HGNC} gene expression and also with elevated circulating IL-1{beta HGNC} levels. We conclude that early in SARS-CoV-2 infection MESHD, NLRP3 HGNC activation takes place and initiates the CRS. Thus, NLRP3 HGNC is a target to reduce the organ damage of inflammatory cytokines of the CRS.

    Discovery of a AhR HGNC flavonoid agonist that counter-regulates ACE2 HGNC expression in rodent models of inflammation MESHD and attenuates ACE2 HGNC-SARS-CoV2 interaction in vitro

    Authors:

    doi:10.1101/2021.02.24.432203 Date: 2021-02-24 Source: bioRxiv

    The severe acute respiratory syndrome MESHD (SARS)-CoV-2, a newly emerged coronavirus first identified in 2019, is the pathogenetic agent od Corona Virus Induced Disease MESHD (COVID)19. The virus enters the human cells after binding to the angiotensin converting enzyme (ACE) 2 HGNC receptor in target tissues. ACE2 HGNC expression is induced in response to inflammation MESHD. The colon expression of ACE2 HGNC is upregulated in patients with inflammatory bowel disease MESHD ( IBD MESHD), highlighting a potential risk of intestinal inflammation MESHD in promoting viral entry in the human body. Because mechanisms that regulate ACE2 HGNC expression in the intestine are poorly understood and there is a need of anti-SARS-CoV2 therapies, we have settled to investigate whether natural flavonoids might regulate the expression of ACE2 HGNC in intestinal models of inflammation MESHD. The results of these studies demonstrated that pelargonidin, a natural flavonoid bind and activates the Aryl hydrocarbon Receptor HGNC ( AhR HGNC) in vitro and reverses intestinal inflammation MESHD caused by chronic exposure to high fat diet or to the intestinal braking-barrier agent DSS in a AhR HGNC-dependent manner. In these two models, development of colon inflammation MESHD associated with upregulation of ACE2 HGNC mRNA expression. Colon levels of ACE2 HGNC mRNA were directly correlated with TNF HGNC mRNA levels. In contrast to ACE2 HGNC the angiotensin 1-7 receptor MAS was downregulated in the inflamed tissues. Molecular docking studies suggested that pelargonidin binds a fatty acid binding pocket on the receptor binding domain of SARS-CoV2 Spike protein PROTEIN. In vitro studies demonstrated that pelargonidin significantly reduces the binding of SARS-CoV2 Spike protein PROTEIN to ACE2 HGNC and reduces the SARS-CoV2 replication in a concentration-dependent manner. In summary, we have provided evidence that a natural flavonoid might hold potential in reducing intestinal inflammation MESHD and ACE2 HGNC induction in the inflamed colon in a AhR HGNC-dependent manner.

    A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome MESHD in children (MIS-C) with severe myocarditis MESHD

    Authors: Camille de Cevins; Marine Luka; Nikaia Smith; Sonia Meynier; Aude Magerus; Francesco Carbone; Victor Garcia Paredes; Laura Barnabei; Maxime Batignes; Alexandre Boulle; Marie-Claude Stolzenberg; Brieuc P Perot; Bruno Charbit; Tinhinane Fali; Vithura Pirabarakan; Boris Sorin; Quentin Riller; Ghaith Abdessalem; Maxime Beretta; Ludivine Grzelak; Pedro Goncalves; Hugo Mouquet; Olivier Schwartz; Mohammed Zarhrate; Melanie Parisot; Christine Bole-Feysot; Cecile Masson; Nicolas Cagnard; Aurelien Corneau; Camille Bruneau; Shen-Ying Zhang; Jean-Laurent Casanova; Brigitte Bader Meunier; Julien Haroche; Isabelle Melki; Mathie Lorrot; Mehdi Oualha; Florence Moulin; Damien Bonnet; Zahra Belhadjer; Mariane Leruez; Slimane Allali; Christele Gras Leguen; Loic de Pontual; Alain Fischer; Darragh Duffy; Frederic Rieux-Laucat; Julie Toubiana; Mickael M Menager

    doi:10.1101/2021.02.23.432486 Date: 2021-02-23 Source: bioRxiv

    SARS-CoV-2 infection MESHD in children is generally milder than in adults, yet a proportion of cases result in hyperinflammatory conditions often including myocarditis MESHD. To better understand these cases, we applied a multi-parametric approach to the study of blood cells of 56 children hospitalized with suspicion of SARS-CoV-2 infection MESHD. The most severe forms of MIS-C ( multisystem inflammatory syndrome MESHD in children related to SARS-CoV-2), that resulted in myocarditis MESHD, were characterized by elevated levels of pro-angiogenesis cytokines and several chemokines. Single-cell transcriptomic analyses identified a unique monocyte/dendritic cell gene signature that correlated with the occurrence of severe myocarditis MESHD, characterized by sustained NF-kB activity, TNF-a HGNC signaling, associated with decreased gene expression of NF-kB inhibitors. We also found a weak response to type-I and type-II interferons, hyperinflammation and response to oxidative stress related to increased HIF-1a HGNC and VEGF HGNC signaling. These results provide potential for a better understanding of disease pathophysiology.

    A cannabinoid receptor agonist shows anti-inflammatory and survival properties in human SARS-CoV-2-infected iPSC-derived cardiomyocytes MESHD

    Authors: Luiz Guilherme H.S. Aragao; Julia T Oliveira; Jairo R Temerozo; Mayara A Mendes; Jose Alexandre Salerno; Carolina da S. G. Pedrosa; Teresa Puig-Pijuan; Carla Verissimo; Isis M Ornelas; Thayana Torquato; Gabriela Vitoria; Carolina Q. Sacramento; Natalia Fintelman-Rodrigues; Suelen da Silva Gomes Dias; Vinicius Cardoso Soares; Leticia R. Q. Souza; Karina Karmirian; Livia Goto-Silva; Diogo Biagi; Estela M. Cruvinel; Rafael Dariolli; Daniel R. Furtado; Patricia T. Bozza; Helena L. Borges; Thiago Moreno L. Souza; Marilia Zaluar P. Guimaraes; Stevens Rehen

    doi:10.1101/2021.02.20.431855 Date: 2021-02-21 Source: bioRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is caused by acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), which can infect several organs and lead to loss of vital organ function, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 MESHD is myocardial injury MESHD, caused both directly and indirectly by SARS-CoV-2, and which is associated with a high risk of mortality. One of the hallmarks of severe COVID-19 MESHD is the "cytokine storm", at which point the immune system malfunctions, leading to possible organ failure MESHD and death MESHD. Cannabinoids are known to have anti-inflammatory properties by negatively modulating the release of pro-inflammatory cytokines. Herein, we investigated the effects of the cannabinoid agonist WIN 55,212-2 (WIN) on SARS-CoV-2-infected MESHD human iPSC-derived cardiomyocytes (hiPSC-CMs). Although WIN did not modulate angiotensin-converting enzyme II, nor reduced SARS-CoV-2 infection MESHD and replication in hiPSC-CMs at the conditions tested, it had anti-inflammatory and protective effects by reducing the levels of interleukins 6, 8,18 and tumor necrosis factor-alpha HGNC tumor necrosis factor-alpha MESHD ( TNF HGNC-) and lactate dehydrogenase (LDH) activity in these cells without causing hypertrophic cardiac damage MESHD. These findings suggest that cannabinoids should be further investigated as an alternative therapeutic tool for the treatment of COVID-19 MESHD. HighlightsO_LIHuman iPSC-derived cardiomyocytes (hiPSC-CMs) express CB1 HGNC receptor. C_LIO_LIThe cannabinoid receptor agonist, WIN 55,212-2 (WIN), does not influence SARS-CoV-2 infection MESHD in hiPSC-CMs. C_LIO_LIWIN reduces inflammation MESHD and death MESHD in SARS-CoV-2-infected hiPSC-CMs MESHD. C_LI

    KLF2 HGNC is a therapeutic target for COVID-19 MESHD induced endothelial dysfunction MESHD

    Authors: Suowen Xu; Sihui Luo; Xueying Zheng; Jianping Weng

    doi:10.1101/2021.02.20.432085 Date: 2021-02-20 Source: bioRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is regarded as an endothelial disease ( endothelialitis MESHD) with its mechanism being incompletely understood. Emerging evidence has demonstrated that the endothelium represents the Achilles heel in COVID-19 MESHD patients and that endothelial dysfunction precipitates COVID-19 MESHD and accompanying multi-organ injuries. Thus, pharmacotherapies targeting endothelial dysfunction have potential to ameliorate COVID-19 MESHD and its cardiovascular complications. Primary human umbilical vein endothelial cells (HUVECs) and human pulmonary microvascular endothelial cells (HPMECs) were treated with serum from control subjects or COVID-19 MESHD patients. Downstream monocyte adhesion and associated gene/protein expression was evaluated in endothelial cells exposed to COVID-19 MESHD patient serum in the presence of KLF2 HGNC activator (Atorvastatin) or KLF2 HGNC overexpression by an adenoviral vector. Here, we demonstrate that the expression of KLF2 HGNC was significantly reduced and monocyte adhesion was increased in endothelial cells treated with COVID-19 MESHD patient serum due to elevated levels of pro-adhesive molecules, ICAM1 HGNC and VCAM1 HGNC. IL-1{beta HGNC} and TNF HGNC-, two cytokines observed in cytokine release syndrome in COVID-19 MESHD patients, decreased KLF2 HGNC gene expression. Next-generation RNA-sequencing data showed that atorvastatin treatment leads to a cardiovascular protective transcriptome associated with improved endothelial function (vasodilation, anti- inflammation MESHD, antioxidant status, anti- thrombosis MESHD/-coagulation, anti- fibrosis MESHD and reduced angiogenesis). Treatment of HPMECs with atorvastatin or KLF2 HGNC adenovirus ameliorate COVID-19 MESHD serum-induced increase in endothelial inflammation MESHD and monocyte adhesion by increasing KLF2 HGNC expression. Altogether, the present study demonstrates that genetic and pharmacological activation of KLF2 HGNC represses COVID-19 MESHD associated endothelial dysfunction, heralding a potentially new direction to treat endothelialitis MESHD accompanying COVID-19 MESHD. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=124 SRC="FIGDIR/small/432085v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@42bddforg.highwire.dtl.DTLVardef@1bf86e3org.highwire.dtl.DTLVardef@130de80org.highwire.dtl.DTLVardef@15fc5e9_HPS_FORMAT_FIGEXP M_FIG Endothelial dysfunction contributes to COVID-19 MESHD-associated multi-organ endothelialtis: potential role of KLF2 HGNC C_FIG

    Chyawanprash for the prevention of COVID-19 MESHD infection among healthcare workers: A Randomized Controlled Trial

    Authors: Arun Gupta; Amit Madan; Babita Yadav; Richa Singhal; Pallavi Suresh Mundada; Yogesh Kumar Pandey; Riju Agarwal; Rakesh Rana; Arunabh Tripathi; Bhagwan Sahay Sharma; BCS Rao; Bharti Gupta; Narayanam Srikanth; Kartar Singh Dhiman

    doi:10.1101/2021.02.17.21251899 Date: 2021-02-19 Source: medRxiv

    Background: Coronavirus disease 2019 MESHD ( Covid19 MESHD) occurs after exposure to severe acute respiratory syndrome coronavirus 2 MESHD (SARSCoV2). For persons who are at high risk of exposure, the standard of care is personal protection from getting infected. Whether Ayurvedic rasayana drug like Chyawanprash can prevent symptomatic infection in frontline health care workers is unknown. Objective: To evaluate the effect of the combination of Chyawanprash and Standard Preventive Regimen compared to the use of Standard Preventive Regimen alone on the proportion of RT-PCR confirmed COVID 19 infections among frontline healthcare workers (HCWs). Methods: An open label randomized controlled trial was conducted in the HCWs between 25 to 60 years age currently working in an environment with chance of direct exposure to COVID 19 cases. The interventions to be compared in this trial were Standard Preventive Regimen as per institutional guidelines and based on their roles (Group I) and Ayurvedic Intervention viz., Chyawanprash 12 g twice for 30 days from day of randomization plus Standard Preventive Regimen (Group II). The incidence of RT PCR confirmed COVID19 MESHD cases in both groups, was the primary outcome measure. Evaluation of the safety of the study drug (by any statistically significant change in various biochemical and hematological parameters and occurrence of any adverse drug reactions); incidence of any other infective diseases (bacterial / viral / fungal / etc.) like upper respiratory tract illness during the study period and any change in the immunoglobulins like IgG, IgM and IgE and inflammatory markers like TNF alpha HGNC, IL6 HGNC and IL10 HGNC were the secondary outcome measures. Results: Out of 193 participants who completed the study, no participant in both groups was COVID 19 positive at the end of one month. In post intervention follow up, 4 subjects in Group I and 2 subjects in Group II were COVID 19 positive. No adverse drug reaction or any serious adverse event was reported during the study. No clinically significant change in the safety parameters was observed before and after the study. Statistically significant rise in Serum IgG level was seen in Group II but other inflammatory and immune markers did not show statistically significant difference. Conclusion: Chyawanprash was well tolerated by all the participants in the intervention group but to prove its adaptogenic effect and efficacy as an add-on to the standard care in preventing the occurrence of COVID 19, clinical trial for longer duration with larger sample size is needed. Trial registration: Clinical Trials Registry of India vide CTRI/2020/05/025275 dated 20/05/2020 Date of IEC approval: 19.5.2020 Keywords: Adaptogen, Ayurveda, Health personnel, Prophylaxis, Rasayana, SARS CoV 2

    Immune characterization and profiles of SARS-CoV-2 infected MESHD patients

    Authors: Martine Policard; Sidharth Jain; Samantha Rego; Sivanesan Dakshanamurthy

    doi:10.1101/2021.02.17.431721 Date: 2021-02-18 Source: bioRxiv

    The spread of SARS-CoV-2 and the increasing mortality rates of COVID-19 MESHD create an urgent need for treatments, which are currently lacking. Although vaccines have been approved by the FDA for emergency use in the U.S., patients will continue to require pharmacologic intervention to reduce morbidity and mortality as vaccine availability remains limited. The rise of new variants makes the development of therapeutic strategies even more crucial to combat the current pandemic and future outbreaks. Evidence from several studies suggests the host immune response to SARS-CoV-2 infection MESHD plays a critical role in disease pathogenesis. Consequently, host immune factors are becoming more recognized as potential biomarkers and therapeutic targets for COVID-19 MESHD. To develop therapeutic strategies to combat current and future coronavirus outbreaks, understanding how the coronavirus hijacks the host immune system during and after the infection is crucial. In this study, we investigated immunological patterns or characteristics of the host immune response to SARS-CoV-2 infection MESHD that may contribute to the disease severity of COVID-19 MESHD patients. We analyzed large bulk RNASeq and single cell RNAseq data from COVID-19 MESHD patient samples to immunoprofile differentially expressed gene sets and analyzed pathways to identify human host protein targets. We observed an immunological profile of severe COVID-19 MESHD patients characterized by upregulated cytokines, interferon-induced proteins, and pronounced T cell lymphopenia MESHD, supporting findings by previous studies. We identified a number of host immune targets including PERK HGNC, PKR HGNC, TNF HGNC, NF-kB, and other key genes that modulate the significant pathways and genes identified in COVID-19 MESHD patients. Finally, we identified genes modulated by COVID-19 MESHD infection that are implicated in oncogenesis, including E2F7 HGNC and RB1 HGNC, suggesting a mechanism by which cancer MESHD may arise in patients infected with SARS-CoV2. Further clinical investigation of these targets may lead to bonafide therapeutic strategies to treat the current COVID-19 pandemic MESHD and protect against future outbreaks and viral escape variants.

    Tocilizumab-induced unexpected increase of several inflammatory cytokines in critically ill COVID-19 MESHD patients

    Authors: Fanny Ponthieux; Nicolas Dauby; Evelyne Maillart; Jean-François Fils; Julie Smet; Marc Claus; Tatiana Besse-Hammer; David De Bels; Francis Corazza; Carole Nagant

    doi:10.21203/rs.3.rs-234733/v1 Date: 2021-02-11 Source: ResearchSquare

    Early evidence during the COVID-19 pandemic MESHD indicated high levels of IL-6 HGNC in patients with severe COVID-19 MESHD. This led to the off-label use of tocilizumab (TCZ) during the first wave of the pandemic.We aimed to monitor IL-6 HGNC and several inflammatory cytokines in critically ill COVID-19 MESHD patients receiving off-label TCZ. Fifteen critically ill SARS-CoV-2 PCR confirmed cases were enrolled and serum samples were collected during 8 days, before and following administration of a single dose of TCZ. In parallel, a control group consisting of 8 non-treated COVID-19 MESHD patients not receiving TCZ was established. Serum profile of 12 cytokines (IL-1β, -2, -4, -6, -8, -10, -12, -13, -17, -18, TNF-α HGNC and INF-γ) and of  IL-6R HGNC were assessed in these two groups. Although the increased IL-6 HGNC concentrations after TCZ infusion were expected, we observed an unexpected increase in IL-1β, -2, -4, -10, -12p70, -18 and IL-6R HGNC levels in the treated patients with maximal values reached 2 to 4 days after TCZ. In contrast, no change in cytokine levels was observed in the control group. There was no significant difference in cytokine levels between survivors (TCZ/S) or non-survivors (TCZ/D). This observation suggests that some inflammatory pathways escape IL-6R HGNC blockade leading to an increase in several pro-inflammatory cytokines. Our findings could highlight an anti-inflammatory role of IL-6 HGNC and may explain why TCZ has failed to improve survival in critically ill COVID-19 MESHD patients when given alone.

    Exosomes from COVID-19 MESHD patients carry tenascin-C HGNC and fibrinogen-β in triggering inflammatory signals in distant organ cells

    Authors: Subhayan Sur; Mousumi B. Khatun; Robert Steele; Scott Isbell; Ranjit Ray; Ratna B Ray

    doi:10.1101/2021.02.08.430369 Date: 2021-02-09 Source: bioRxiv

    SARS-CoV-2 infection MESHD causes cytokine storm and overshoot immunity in humans; however, it remains to be determined whether genetic material of SARS-CoV-2 and/or virus induced soluble mediators from lung epithelial cells as natural host are carried out by macrophages or other vehicles at distant organs causing tissue damage. We speculated that exosomes as extracellular vesicles are secreted from SARS-CoV-2 infected MESHD cells may transport messages to other cells of distant organs leading to pathogenic consequences. For this, we took an unbiased proteomic approach for analyses of exosomes isolated from plasma of healthy volunteers and SARS-CoV-2 infected MESHD patients. Our results revealed that tenascin-C HGNC ( TNC HGNC) and fibrinogen-{beta} ( FGB HGNC) are highly abundant in exosomes from SARS-CoV-2 infected MESHD patient's plasma as compared to that of healthy normal controls. Since TNC HGNC and FGB HGNC stimulate pro-inflammatory cytokines via NF-kB pathway, we examined the status of TNF-a HGNC, IL-6 HGNC and CCL5 HGNC expression upon exposure of hepatocytes to exosomes from COVID-19 MESHD patients and observed significant increase when compared with that from healthy subjects. Together, our results demonstrated that soluble mediators, like TNC HGNC and FGB HGNC, are transported through plasma exosomes in SARS-CoV-2 infected MESHD patients and trigger pro-inflammatory cytokine expression in cells of distant organs in COVID-19 MESHD patients.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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