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HGNC Genes

SARS-CoV-2 proteins

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SARS-CoV-2 Proteins
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    Exaggerated cytokine production in human peripheral blood mononuclear cells by recombinant SARS-CoV-2 spike PROTEIN glycoprotein S1 and its inhibition by dexamethasone

    Authors: Olumayokun A Olajide; Victoria U Iwuanyanwu; Izabela Lepiarz-Raba; Alaa A Al-Hindawi

    doi:10.1101/2021.02.03.429536 Date: 2021-02-03 Source: bioRxiv

    An understanding of the pathological inflammatory mechanisms involved in SARS CoV-2 virus infection MESHD is necessary in order to discover new molecular pharmacological targets for SARS-CoV-2 spike PROTEIN glycoprotein. In this study, the effects of a recombinant SARS CoV-2 spike PROTEIN glycoprotein S1 was investigated in human peripheral blood mononuclear cells (PBMCs). Stimulation with spike glycoprotein S1 PROTEIN (100 ng/mL) resulted in significant elevation in the production of TNF HGNC, IL-6 HGNC, IL-1{beta HGNC} and IL-8 HGNC. However, pre-treatment with dexamethasone (100 nM) caused a significant reduction in the release of these cytokines. Further experiments revealed that S1 stimulation of PBMCs increased phosphorylation of NF-{kappa}B HGNC p65 HGNC and I{kappa}B, while increasing I{kappa}B degradation. DNA binding of NF-{kappa}B HGNC p65 HGNC was also significantly increased following stimulation with S1. Treatment of PBMCs with dexamethasone (100 nM) or BAY11-7082 (1 M) resulted in inhibition of S1-induced NF-{kappa}B HGNC activation. Activation of p38 HGNC MAPK by S1 was blocked in the presence of dexamethasone and SKF 86002. CRID3, but not dexamethasone pre-treatment produced significant inhibition of S1-induced activation of NLRP3 HGNC/ caspase 1 HGNC. Further experiments revealed that S1-induced increase in the production of TNF HGNC, IL-6 HGNC, IL-1{beta HGNC} and IL-8 HGNC was reduced in the presence of BAY11-7082 and SKF 86002, while CRID3 pre-treatment resulted in the reduction of IL-1{beta HGNC} production. These results suggest that SARS-CoV-2 spike PROTEIN glycoprotein S1 stimulate PBMCs to release pro inflammatory cytokines through mechanisms involving activation of NF-{kappa}B HGNC, p38 MAPK and NLRP3 HGNC inflammasome. It is proposed that clinical benefits of dexamethasone in COVID-19 MESHD is possibly due to its anti-inflammatory activity in reducing SARS-CoV-2 cytokine storm.

    Network of “drug-target-SARS-CoV-2 Related Genes” Through Integrated Analysis of Pharmacology and Geo Database

    Authors: Jin ping Hou; Yong heng Wang; Yu meng Chen; Yi hao Chen; Xiao Zhu; Rui si Qin; Tingting Chen

    doi:10.21203/rs.3.rs-117894/v1 Date: 2020-11-28 Source: ResearchSquare

    BackgroundCoronavirus Disease MESHD Coronavirus Disease 2019 MESHD ( COVID-19 MESHD) respiratory disease MESHD rapidly caused a global pandemic and social and economic disruption. The combination of Traditional Chinese medicine (TCM) and Conventional Western medicine (CWM) is more effective for COVID-19 MESHD treatment. Moreover, TCM and CWM are important data source for developing new drug targets and promote strategies treat SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHDs. However, many studies have analyzed the therapeutic mechanism of CWM or TCM alone for COVID-19 MESHD, it is still unclear the interaction mechanism between TCM and CWM on COVID-19 MESHD.MethodsThis paper integrates network pharmacology and GEO database to mine and identify COVID-19 MESHD molecular therapeutic targets, providing potential targets and new ideas for COVID-19 MESHD gene therapy and new drug development. It includes: 1) using TCMSP, TTD, PubChem and CTD databases to analyze drug interactions and associated phenotypes for SARS-CoV-2, to correlate drug and disease interaction mechanisms to screen key drug targets; 2) using GEO database to correlate differential genes and drug targets to screen potential antiviral gene therapy targets, to construct regulatory network and key points of SARS-CoV-2 therapeutic drugs; 3) using computer simulation of molecular docking to screen virus-related proteins for new drugs. ResultsIntegrated analysis of network pharmacology discovered that baicalein, estrone and quercetin are the pivotal active ingredients in TCM and CWM. Combining drug target genes in pharmacology database and virus induced genes in GEO database, the result showed the core hub genes related to COVID-19 MESHD: STAT1 HGNC, IL1B HGNC, IL6 HGNC, IL8 HGNC, PTGS2 HGNC and NFKBIA HGNC, and these genes were significantly downregulated in A549 and NHBE cells by SARS-CoV-2 infection MESHD. Moreover, chemical interaction and molecular docking analysis of hub genes showed that folic acid might as be potential therapeutic drug for COVID-19 MESHD treatment, and SARS-CoV-2 nucleocapsid phosphoprotein was a potential drug target. The network of “drug-target-SARS-CoV-2 related genes” provide noval potential compounds and targets for further studies of SARS-CoV-2.ConclusionsIntegrated analysis of network pharmacology and big data mining provided noval potential compounds and targets for further studies of SARS-CoV-2. Our research implied folic acid and SARS-CoV-2 N as therapeutic target in TCM and CWM. Our research also suggests that targeting SARS-CoV-2 N MESHD N protein PROTEIN is likely to be a common mechanism of TCM and CWM. On the one hand, the identification of pivotal genes provides a target for COVID-19 MESHD molecular therapy, on the other hand, it provides ideas for the analysis of interaction mechanism between virus and host.

    Early initiation of Extracorporeal Blood Purification using the AN69ST (oXiris®) hemofilter as a treatment modality for COVID - 19 patients: a single-centre case series

    Authors: Petar Ugurov; Dijana Popevski; Tanja Gramosli; Dashurie Neziri; Dragica Vuckova; Emil Stoicovski; Lidija Veljanovska-Kiridjievska; Katerina Ignevska; Sanja Mehandziska; Elena Ambarkova; Rodney Alexander Rosalia; Zan Mitrev

    doi:10.21203/rs.3.rs-44717/v1 Date: 2020-07-17 Source: ResearchSquare

    Introduction: Our understanding of the COVID-19 MESHD disease has been steadily evolving since the original outbreak in December 2019. Advanced disease is characterised by a hyperinflammatory state, systemic coagulopathies MESHD and multiorgan involvement, in particular respiratory distress. We here describe our initial experience with treating of COVID-19 MESHD patients based on early initiation of extracorporeal blood purification, systemic heparinisation and respiratory support.Methods: 15 patients were included; 2 were females. We monitored real-time several biochemical, immunological and coagulation biomarkers associated with disease severity following admission to our dedicated COVID-19 MESHD intensive care unit. To guide personalised treatment, we monitored among others levels of IL-6 HGNC, IL-8 HGNC, TNF-α HGNC, C-Reactive Protein HGNC ( CRP HGNC), Neutrophil-to-Lymphocyte ratios, Thrombocyte counts, D-Dimers, Fibrinogen HGNC, and Activation Clotting time (ACT).Treatment consisted of individualised respiratory support supplemented with 1 - 4 cycles of 24-hour Extracorporeal Organ Support (ECOS) and Blood Purification using the AN69ST (oXiris®) hemofilter. We administered heparin (300 U/kg) to counter suspected hypercoagulability MESHD (= elevated Fibrinogen HGNC or D-dimers) states to maintain ACT ≥ 180 seconds.Results: N = 10 presented with severe to critical disease MESHD (= dyspnoea MESHD, hypoxia MESHD, respiratory rate > 30/min, peripheral oxygen saturation < 90%, or > 50% lung involvement on X-ray imaging). A single case was admitted with a critical condition (= respiratory failure MESHD). One patient died after 5 days of hospitalisation after developing Acute Respiratory Syndrome MESHD. 8 Patients have been discharged - average ICU length-of-stay was 9.9 ± 2.4 days. Clinical improvement was associated with normalisation (increase) of thrombocytes, white blood cells, stable levels of IL-6 HGNC (< 50 ng/mL) and a decrease of CRP HGNC and Fibrinogen HGNC. Conclusion: Means to monitor COVID-19 MESHD disease severity during hospitalisation are crucial to control disease progression and prevent hyperinflammation and irreversible multiorgan failure. We present here a real-time monitoring system accounting for biochemical, immunological, coagulation parameters and radiological imaging. The combination of systemic heparin anticoagulation regimens and blood purification may prevent hyperinflammation, thromboembolism MESHD during hospitalisation and thus support clinical recovery. 

    Immunophenotyping of Circulating Leukocytes Reveal Non-specific Activation of Innate and Adaptive Immune Systems in Multi-System Inflammatory Syndrome of Childhood Temporally Associated with SARS-Cov-2 Infection MESHD: Descriptive Cohort Study

    Authors: Michael J. Carter; Matthew Fish; Aislinn Jennings; Katie J. Doores; Paul Wellman; Jeffrey Seow; Sam Acors; Emma Timms; Julia Kenny; Stuart Neil; Michael H. Malim; Shane M. Tibby; Manu Shankar-Hari

    id:10.20944/preprints202007.0252.v1 Date: 2020-07-12 Source: Preprints.org

    We describe the innate and adaptive immune system trajectory in Multi-system inflammatory syndrome MESHD of childhood (MIS-C), at acute(within 72 hours of hospitalization), resolution (at clinical improvement) and convalescent phase. In our cohort, in the acute phase, 68% of the children were SARS-CoV-2 seropositive, with hypercytokinenemia (high interleukin(IL)-1beta HGNC, IL-6 HGNC, IL-8 HGNC, IL-10 HGNC, IL-17 HGNC, interferon gamma HGNC), procoagulant state, myocardial dysfunction MESHD, activated neutrophils and monocytes; differential T and B cell subset lymphopenia MESHD; activated chemokine receptor type-7 positive and gamma-delta T cell subsets; antigen presenting cells had reduced HLA-DR expression; and B-cell class-switch responses occurred with illness resolution. MIS-C is an immunopathogenic illness associated with SARS-CoV-2 infections MESHD in children.

    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/rs.3.rs-39162/v1 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. 

    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/rs.3.rs-33276/v1 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.

    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.

    Type I and Type III IFN Restrict SARS-CoV-2 Infection MESHD of Human Airway Epithelial Cultures

    Authors: Abigail Vanderheiden; Philipp Ralfs; Tatiana Chirkova; Amit A Upadhyay; Matthew G Zimmerman; Shamika Bedoya; Hadj Aoued; Gregory K Tharp; Kathryn Pellegrini; Anice C Lowen; Vineet D. Menachery; Larry J Anderson; Arash Grakoui; Steven E. Bosinger; Mehul S Suthar

    doi:10.1101/2020.05.19.105437 Date: 2020-05-20 Source: bioRxiv

    The newly emerged human coronavirus, SARS-CoV-2, has caused a pandemic of respiratory illness MESHD. The innate immune response is critical for protection against Coronaviruses. However, little is known about the interplay between the innate immune system and SARS-CoV-2. Here, we modeled SARS-CoV-2 infection MESHD using primary human airway epithelial (pHAE) cultures, which are maintained in an air-liquid interface. We found that SARS-CoV-2 infects MESHD and replicates in pHAE cultures and is directionally released on the apical, but not basolateral surface. Transcriptional profiling studies found that infected pHAE cultures had a molecular signature dominated by pro-inflammatory cytokines and chemokine induction, including IL-6 HGNC, TNF HGNC, CXCL8 HGNC. We also identified NF-{kappa}B HGNC and ATF4 HGNC transcription factors as key drivers of this pro-inflammatory cytokine response. Surprisingly, we observed a complete lack of a type I or III IFN induction during SARS-CoV-2 infection MESHD. Pre-treatment or post-treatment with type I and III IFNs dramatically reduced virus replication in pHAE cultures and this corresponded with an upregulation of antiviral effector genes. Our findings demonstrate that SARS-CoV-2 induces a strong pro-inflammatory cytokine response yet blocks the production of type I and III IFNs. Further, SARS-CoV-2 is sensitive to the effects of type I and III IFNs, demonstrating their potential utility as therapeutic options to treat COVID-19 MESHD patients. IMPORTANCEThe current pandemic of respiratory illness, COVID-19 MESHD, is caused by a recently emerged coronavirus named SARS-CoV-2. This virus infects airway and lung cells causing fever, dry cough, and shortness of breath. Severe cases of COVID-19 MESHD can result in lung damage, low blood oxygen levels, and even death. As there are currently no vaccines or antivirals approved for use in humans, studies of the mechanisms of SARS-CoV-2 infection MESHD are urgently needed. SARS-CoV-2 infection MESHD of primary human airway epithelial cultures induces a strong pro-inflammatory cytokine response yet blocks the production of type I and III IFNs. Further, SARS-CoV-2 is sensitive to the effects of type I and III IFNs, demonstrating their potential utility as therapeutic options to treat COVID-19 MESHD patients.

    Virus-host interactome and proteomic survey of PMBCs from COVID-19 MESHD patients reveal potential virulence factors influencing SARS-CoV-2 pathogenesis

    Authors: Qiming Liang; Jingjiao Li; Mingquan Guo; Xiaoxu Tian; Chengrong Liu; Xin Wang; Xing Yang; Ping Wu; Zixuan Xiao; Yafei Qu; Yue Yin; Joyce Fu; Zhaoqin Zhu; Zhenshan Liu; Chao Peng; Tongyu Zhu

    doi:10.1101/2020.03.31.019216 Date: 2020-04-02 Source: bioRxiv

    The ongoing coronavirus disease MESHD ( COVID-19 MESHD) pandemic caused by Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2) is a global public health concern due to relatively easy person-to-person transmission and the current lack of effective antiviral therapy. However, the exact molecular mechanisms of SARS-CoV-2 pathogenesis remain largely unknown. We exploited an integrated proteomics approach to systematically investigate intra-viral and virus-host interactomes for the identification of unrealized SARS-CoV-2 host targets and participation of cellular proteins in the response to viral infection using peripheral blood mononuclear cells (PBMCs) isolated from COVID-19 MESHD patients. Using this approach, we elucidated 251 host proteins targeted by SARS-CoV-2 and more than 200 host proteins that are significantly perturbed in COVID-19 MESHD derived PBMCs. From the interactome, we further identified that non-structural protein nsp9 and nsp10 interact with NKRF HGNC, a NF-[Kcy]B repressor, and may precipitate the strong IL-8 HGNC/ IL-6 HGNC mediated chemotaxis of neutrophils and overexuberant host inflammatory response observed in COVID-19 MESHD patients. Our integrative study not only presents a systematic examination of SARS-CoV-2-induced perturbation of host targets and cellular networks to reflect disease etiology, but also reveals insights into the mechanisms by which SARS-CoV-2 triggers cytokine storms and represents a powerful resource in the quest for therapeutic intervention.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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