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HGNC Genes

SARS-CoV-2 proteins

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    Longitudinal Analysis of Inflammatory Response to SARS-CoV-2 in the Upper Respiratory Tract Reveals an Association With Viral Load, Independent of Symptoms

    Authors: Arnaud Didierlaurent; Vu Diem-Lan; Paola Martinez Murillo; Fiona Pigny; Maria Vono; Benjamin Meyer; Christiane S Eberhardt; Sylvain Lemeille; Elodie Von Dach; Geraldine Blanchard-Rohner; Isabella Eckerle; Angela Huttner; Claire-Anne Siegrist; Laurent Kaiser

    doi:10.21203/rs.3.rs-203414/v1 Date: 2021-02-04 Source: ResearchSquare

    Background SARS-CoV-2 infection MESHD leads to high viral loads in the upper respiratory tract that may be determinant in virus dissemination. The extent of intranasal antiviral response in relation to symptoms is unknown. Understanding how local innate responses control virus is key in the development of therapeutic approaches. MethodsSARS-CoV-2-infected MESHD patients were enrolled in an observational study conducted at the Geneva University Hospitals, Switzerland, investigating virological and immunological characteristics. Nasal-wash and serum specimens from a subset of patients were collected to measure viral load and a cytokine panel at different time points after infection; cytokine levels were analyzed in relation to symptoms.ResultsSamples from 13 SARS-CoV-2-infected MESHD patients and six controls were analyzed. We found an increase in CXCL10 HGNC and IL-6 HGNC, whose levels remained elevated for up to 3 weeks after symptom onset. SARS-CoV-2 infection MESHD also induced CCL2 HGNC and GM-CSF HGNC, suggesting local recruitment and activation of myeloid cells. Local cytokine levels correlated with viral load but not with serum cytokine levels, nor with specific symptoms, including anosmia.ConclusionsThe nasal MESHD epithelium is an active site of cytokine response against SARS-CoV-2 that can last more than 2 weeks; in this cohort, anosmia MESHD was not associated with increases in any locally produced cytokines.

    Transcriptome Profiling of different types of human respiratory tract cells infected by SARS-CoV-2 Highlight an unique Role for Inflammatory and Interferon Response

    Authors: Luping Lei; Qiumei Cao; Yu Wang; Mario Hensen; Anu V. Chandran; Michelle L. Hill; J.L. Kiappes; Raymond A. Dwek; Dominic S. Alonzi; Weston B. Struwe; Nicole Zitzmann; Florian M Wurm; Xin Zheng; Jia Liu; Davey Smith; Daniela Weiskopf; Alessandro Sette; Shane Crotty; Jian Jin; Xian Chen; Andrew Pekosz; Sabra Klein; Irina Burd

    doi:10.1101/2020.11.15.383927 Date: 2020-11-16 Source: bioRxiv

    The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease MESHD ( COVID-19 MESHD) at the end of 2019 has caused a large global outbreak and now become a major public health issue. Lack of data underlying how the human host interacts with SARS-CoV-2 virus. In the current study, We performed Venn-analysis, Gene ontology (GO), KEGG pathway analysis and Protein-protein interaction analysis of whole transcriptome studies with the aim of clarifying the genes and pathways potentially altered during human respiratory tract cells infected with SARS-CoV-2. We selected four studies through a systematic search of the Gene Expression Omnibus (GEO) database or published article about SARS-CoV-2 infection MESHD in different types of respiratory tract cells. We found 36 overlapping upregulated genes among different types of cells after viral infection. Further functional enrichment analysis revealed these DEGs are most likely involved in biological processes related to inflammatory response and response to cytokine, cell component related to extracellular space and I-kappaB/NF-kappaB complex, molecular function related to protein binding and cytokine activity. KEGG pathways analysis highlighted altered conical and casual pathways related to TNF HGNC, NF-kappa B HGNC, Cytokine-cytokine receptor interaction and IL17 HGNC signaling pathways during SARS-CoV-2 infection MESHD with CXCL1 HGNC, CXCL2 HGNC, CXCL3 HGNC, CXCL8 HGNC, CXCL10 HGNC, IL32 HGNC, CX3CL1 HGNC, CCL20 HGNC, IRF1 HGNC, NFKB2 HGNC and NFKB1A up-regulated which may explain the inflammatory cytokine storms associated with severe cases of COVID-19 MESHD.

    CSF of SARS-CoV-2 patients with neurological syndromes reveals hints to understand pathophysiology

    Authors: Raphael Bernard-Valnet; Sylvain Perriot; Mathieu Canales; Beatrice Pizzarotti; Leonardo Caranzano; Mayte Castro-Jimenez; Jean-Benoit Epiney; Sergiu Vijiala; Paolo Salvioni Chiabotti; Angelica Anichini; Alexander Salerno; Katia Jaton; Julien Vaucher; Matthieu Perreau; Gilbert Greub; Giuseppe Pantaleo; Renaud Du Pasquier

    doi:10.1101/2020.11.01.20217497 Date: 2020-11-04 Source: medRxiv

    Objective: Coronavirus disease ( COVID-19 MESHD) has been associated with a large variety of neurological disorders MESHD. However the mechanisms underlying these neurological complications remain elusive. In this study we aimed at determining whether neurological symptoms were caused by SARS-CoV-2 direct infection of by pro-inflammatory mediators. Methods: We checked for SARS-CoV-2 RNA by RT-qPCR, SARS-CoV-2-specific antibodies and for 48 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluids (CSF) +/- sera of a cohort of 17 COVID-19 MESHD patients with neurological presentation and 55 neurological control patients (inflammatory [IND], non inflammatory [NIND], multiple sclerosis MESHD [ MS MESHD]). Results: We found SARS-CoV-2 RNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 MESHD patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (38%). An intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/16 patients. Of the four categories of tested patients, the CSF of IND exhibited the highest level of chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, CXCL10 HGNC, CXCL12 HGNC, and CXCL13 HGNC), followed by the CSF of MS MESHD patients ( CXCL12 HGNC, and CXCL13 HGNC). There was no significant difference between COVID-19 MESHD and NIND patients, even if some chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, andCXCL10) tended to be higher in the former. Interestingly, among COVD-19 patients, the CSF of those with a severe disease ( encephalitis MESHD/ encephalopathy MESHD) contained higher levels CXCL8 HGNC and CXCL10 HGNC than those with other neurological presentations. Interpretation: Our results do not show obvious SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD of the central nervous system, but point to a mild inflammatory reaction reflecting an astrocytic reaction. Methods: We checked for SARS-CoV-2 mRNA by qPCR, SARS-CoV-2-specific antibodies and for 49 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluid (CSF) +/- serum of a cohort of 17 COVID-19 MESHD patients with neurological presentation and 55 neurological controls (inflammatory, non inflammatory, multiple sclerosis MESHD). Results: We found SARS-CoV-2 mRNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 MESHD patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (37,5%), but an intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/17.As compared to SARS-CoV-2-negative NIND patients, the CSF of IND patients exhibited the highest level of chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, CXCL10 HGNC, CXCL12 HGNC, and CXCL13 HGNC), followed the CSF of MS MESHD patients ( CXCL12 HGNC, and CXCL13 HGNC). There was no difference between COVID-19 MESHD patients with neurological diseases MESHD compared to NIND even if some chemokines ( CCL4 HGNC, CCL5 HGNC, CXCL8 HGNC, andCXCL10) tended to be higher than NIND. Interestingly, among COVD-19 patients, the CSF of those with a severe disease ( encephalitis MESHD/ encephalopathy MESHD) contained higher levels CXCL8 HGNC and CXCL10 HGNC than those with other neurological presentations. Interpretation: Our results confirm the absence of obvious SARS-CoV-2 infection MESHD SARS-CoV-2 infection MESHD of the central nervous system and point to a mild inflammatory reaction reflecting an astrocytic reaction.

    A Meta-analysis of Comorbidities in COVID-19 MESHD: Which Diseases increase the Susceptibility of SARS-CoV-2 Infection MESHD?

    Authors: Srinivasan Ramachandran; Manoj Kumar Singh; Ahmed Mobeen; Amit Chandra; Sweta Joshi

    id:10.20944/preprints202009.0486.v1 Date: 2020-09-21 Source: Preprints.org

    Background: Comorbidities have been frequently reported in COVID-19 MESHD patients, which often lead to more severe outcomes. The underlying molecular mechanisms behind these clinical observations have not yet been explained. Herein, we investigated the disease-specific gene expression signatures that may induce susceptibility to SARS-CoV-2 infection MESHD. Methods: We studied 30 frequently occurring acute, chronic, or infectious diseases of recent times that have shown comorbidity in one or another respiratory disease MESHD(s) caused by pathogenic human infecting coronaviruses, especially SARS-CoV-2. We retrieved array-based gene expression data for each disease and control from relevant datasets. Subsequently, all the datasets were quantile normalized, and log-2 transformed data was used for analysis. Results The expression of ACE2 HGNC receptor and host proteases, namely FURIN HGNC and TMPRSS2 HGNC that are essential for cellular entry of SARS-CoV-2, was upregulated in all six studied subtypes of leukemia MESHD (hereafter, referred as leukemia MESHD). The expression of ACE2 HGNC was also increased in psoriasis MESHD, lung cancer MESHD, Non-alcoholic fatty liver disease MESHD ( NAFLD MESHD), breast cancer MESHD, and pulmonary arterial hypertension MESHD patients. The expression of FURIN HGNC was higher in psoriasis MESHD, NAFLD MESHD, lung cancer MESHD, and in type II diabetic liver MESHD, whereas it was lowered in breast cancer MESHD. Similarly, the expression of TMPRSS2 HGNC was increased during lung cancer MESHD and type II diabetes MESHD; it was decreased during psoriasis MESHD, NAFLD MESHD, lung cancer MESHD, breast cancer MESHD, and cervical cancer MESHD.Furthermore, a heightened expression of genes that are involved in immune response was observed in leukemia MESHD patients, as shown by the higher expression of IFNA2 HGNC, IFNA8 HGNC, IFNA10 HGNC, IFNA14 HGNC, IFNA16 HGNC, IFNA21 HGNC, IFNB1 HGNC, CXCL10 HGNC, and IL6 HGNC. The expression of JAK1 HGNC, STAT1 HGNC, IL6 HGNC, and CXCL10 HGNC was higher in NAFLD MESHD. Besides, JAK1 HGNC and STAT1 HGNC were upregulated in type II diabetic muscles MESHD. In addition, most of the upregulated genes in COVID-19 MESHD patients showed a similar trend in leukemia MESHD, NAFLD MESHD, and psoriasis MESHD. Furthermore, SARS-CoV-2, SARS-CoV MESHD and MERS CoV, were found to commonly alter two genes, namely, CARBONIC ANHYDRASE 11 and CLUSTERIN.Conclusions: The genes that may confer susceptibility to SARS-CoV-2 infection MESHD are mostly upregulated in leukemia MESHD patients; hence, leukemia MESHD patients are relatively more susceptible to develop COVID-19 MESHD, followed by other chronic disorders MESHD, such as, NAFLD MESHD, type II diabetes MESHD, psoriasis MESHD, and hypertension MESHD. This study identifies key genes that are altered in the studied diseases types, which may aid in the infection of SARS-CoV-2 MESHD and underlie COVID-19 MESHD associated comorbidities.

    Systematic review and meta-analysis identifies potential host therapeutic targets in COVID-19 MESHD.

    Authors: Nicholas Parkinson; Natasha Rodgers; Max Head Fourman; Bo Wang; Marie Zechner; Maaike Swets; Jonathan E Millar; Andy Law; Clark Russell; J Kenneth Baillie; Sara Clohisey

    doi:10.1101/2020.08.27.20182238 Date: 2020-09-01 Source: medRxiv

    An increasing body of literature describes the role of host factors in COVID-19 MESHD pathogenesis. There is a need to combine diverse, multi-omic data in order to evaluate and substantiate the most robust evidence and inform development of future therapies. We conducted a systematic review of experiments identifying host factors involved in human betacoronavirus infection (SARS-CoV-2, SARS-CoV MESHD, MERS-CoV, seasonal coronaviruses). Gene lists from these diverse sources were integrated using Meta-Analysis by Information Content (MAIC). This previously described algorithm uses data-driven gene list weightings to produce a comprehensive ranked list of implicated host genes. 5,418 genes implicated in human betacoronavirus infection MESHD were identified from 32 datasets. The top ranked gene was *PPIA*, encoding cyclophilin A. Pharmacological inhibition with cyclosporine in vitro exerts antiviral activity against several coronaviruses including SARS-CoV MESHD. Other highly-ranked genes included proposed prognostic factors (* CXCL10 HGNC*, *CD4*, * CD3E HGNC*) and investigational therapeutic targets (* IL1A HGNC*) for COVID-19 MESHD, but also previously overlooked genes with potential as therapeutic targets. Gene rankings also inform the interpretation of COVID-19 MESHD GWAS results, implicating * FYCO1 HGNC* over other nearby genes in a disease-associated locus on chromosome 3. Pathways enriched in gene rankings included T-cell receptor signalling, protein processing, and viral infections MESHD. We identified limited overlap of our gene list with host genes implicated in ARDS (innate immune and inflammation MESHD genes) and Influenza A virus infection MESHD (RNA-binding and ribosome-associated genes). We will continue to update this dynamic ranked list of host genes as the field develops, as a resource to inform and prioritise future studies. Updated results are available at https://baillielab.net/maic/ covid19 MESHD.

    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. 

    Bulk and single-cell gene expression profiling of SARS-CoV-2 infected human cell lines identifies molecular targets for therapeutic intervention

    Authors: Emanuel Wyler; Kirstin Mösbauer; Vedran Franke; Asija Diag; Lina Theresa Gottula; Roberto Arsie; Filippos Klironomos; David Koppstein; Salah Ayoub; Christopher Buccitelli; Anja Richter; Ivano Legnini; Andranik Ivanov; Tommaso Mari; Simone Del Giudice; Jan Patrick Papies; Marcel Alexander Müller; Daniela Niemeyer; Matthias Selbach; Altuna Akalin; Nikolaus Rajewsky; Christian Drosten; Markus Landthaler

    doi:10.1101/2020.05.05.079194 Date: 2020-05-05 Source: bioRxiv

    The coronavirus disease 2019 MESHD ( COVID-19 MESHD) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an ongoing global health threat with more than two million infected people since its emergence in late 2019. Detailed knowledge of the molecular biology of the infection is indispensable for understanding of the viral replication, host responses, and disease progression. We provide gene expression profiles of SARS-CoV and SARS-CoV-2 infections MESHD SARS-CoV-2 infection MESHDs in three human cell lines (H1299, Caco-2 and Calu-3 cells), using bulk and single-cell transcriptomics. Small RNA profiling showed strong expression of the immunity and inflammation MESHD-associated microRNA miRNA-155 HGNC upon infection with both viruses. SARS-CoV-2 elicited approximately two-fold higher stimulation of the interferon response compared to SARS-CoV in the permissive human epithelial cell line Calu-3, and induction of cytokines such as CXCL10 HGNC or IL6 HGNC. Single cell RNA sequencing data showed that canonical interferon stimulated genes such as IFIT2 HGNC or OAS2 HGNC were broadly induced, whereas interferon beta HGNC ( IFNB1 HGNC) and lambda (IFNL1-4) were expressed only in a subset of infected cells. In addition, temporal resolution of transcriptional responses suggested interferon regulatory factors (IRFs) activities precede that of nuclear factor-{kappa}B ( NF-{kappa}B HGNC). Lastly, we identified heat shock protein 90 ( HSP90 HGNC) as a protein relevant for the infection. Inhibition of the HSP90 HGNC charperone activity by Tanespimycin/17-N-allylamino-17-demethoxygeldanamycin (17-AAG) resulted in a reduction of viral replication, and of TNF HGNC and IL1B HGNC mRNA levels. In summary, our study established in vitro cell culture models to study SARS-CoV-2 infection MESHD and identified HSP90 HGNC protein as potential drug target for therapeutic intervention of SARS-CoV-2 infection MESHD.

    Could Unconventional Immunomodulatory Agents Help Alleviate COVID-19 MESHD Symptoms and Severity?

    Authors: Stephen Mamber; Steven Krakowka; Jeffrey Osborn; Lloyd Saberski; Ryan Rhodes; Albert Dahlberg; Kara Fitzgerald; Neal Wright; Sarah Beseme; John McMichael

    id:202004.0014/v2 Date: 2020-04-27 Source: Preprints.org

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS coronavirus 2 or SARS-CoV-2) is the cause of the respiratory infection MESHD known as COVID-19 MESHD. From an immunopathological standpoint, coronaviruses such as SARS-CoV-2 induce an increase in a variety of T-helper 1 ( Th1 HGNC) and inflammatory cytokines and chemokines including interleukins IL-1 HGNC, IL-6 HGNC, CCL2 HGNC protein and CXCL10 HGNC protein. In the absence of proven antiviral agents or an effective vaccine, substances with immunomodulatory activity may be able to inhibit inflammatory and Th1 HGNC cytokines and/or yield an anti-inflammatory and/or Th2 immune response to counteract COVID-19 MESHD symptoms and severity. This report briefly describes four unconventional but commercially accessible immunomodulatory agents that could be employed in clinical trials to evaluate their effectiveness at alleviating disease symptoms and severity: Low-dose oral interferon-alpha, microdose DNA, low-dose thimerosal and phytocannabinoids.

    An Update on SARS-COV-2/ COVID-19 MESHD with Particular Reference on Its Clinical Pathology, Pathogenesis, Immunopathology and Mitigation Strategies – A Review

    Authors: Kuldeep Dhama; Shailesh Kumar Patel; Mamta Pathak; Mohd. Iqbal Yatoo; Ruchi Tiwari; Yashpal Singh Malik; Rajendra Singh; Ranjit Sah; Ali A. Rabaan; D. Katterine Bonilla-Aldana; Alfonso J. Rodriguez-Morales

    id:10.20944/preprints202003.0348.v1 Date: 2020-03-23 Source: Preprints.org

    Coronavirus Disease 2019 MESHD ( COVID-19 MESHD), caused by a novel coronavirus named Severe Acute Respiratory Syndrome MESHD - Coronavirus-2 (SARS-CoV-2), emerged in early December 2019 in China and attained a pandemic situation worldwide by its rapid spread to nearly 167 countries with 287.239 confirmed cases and 11.921 human deaths with a case fatality rate (CFR) of around 4 per cent. Bats were considered as the reservoir host, and the search of a probable intermediate host is still going on. Animals have anticipated culprit of SARS-CoV-2 as of now. The disease is mainly manifested by pneumonia MESHD and related respiratory signs and symptoms, but the involvement of the gastrointestinal system and nervous system is also suggested. The severe form of the disease associated with death MESHD is mainly reported in older and immune-compromised patients with pre-existing disease history. Death MESHD in severe cases is attributed to respiratory failure MESHD associated with hyperinflammation. Cytokine storm syndrome associated with rampant inflammation MESHD in response to SARS-CoV-2 infection MESHD is considered as the leading killer of COVID-19 MESHD patients. COVID-19 MESHD patients were reported with higher levels of many pro-inflammatory cytokines and chemokines like IFN-g HGNC, IL-1b HGNC, IP-10 HGNC, and MCP-1 HGNC. Furthermore, severe cases of COVID-19 MESHD revealed higher levels of TNF-α HGNC, G-CSF HGNC, and MIP-1A HGNC. Blood profile of the COVID-19 MESHD patients exhibits lymphopenia MESHD, leucopenia, thrombocytopenia MESHD and RNAaemia along with increased levels of aspartate aminotransferase. SARS-CoV-2 infection MESHD in pregnant women does not lead to fetus mortalities unlike other zoonotic coronaviruses like SARS-CoV and MERS-CoV, with no evidence of intrauterine transmission to neonates. Rapid and confirmatory diagnostics have been developed, and high efforts are being made to develop effective vaccines and therapeutics. In the absence of any virus-specific therapeutic, internationally health care authorities are recommending adoption of effective prevention and control measures to counter and contain this pandemic virus. This paper is an overview of this virus and the disease with a particular focus on SARS-COV-2 / COVID-19 MESHD clinical pathology, pathogenesis and immunopathology along with a few recent research developments.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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