Corpus overview


Overview

MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (723)

NSP5 (34)

ProteinN (30)

ProteinS1 (28)

ComplexRdRp (23)


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SARS-CoV-2 Proteins
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    In silico study of the spike protein PROTEIN from SARS-CoV-2 interaction with ACE2 HGNC: similarity with SARS-CoV, hot-spot analysis and effect of the receptor polymorphism

    Authors: Houcemeddine Othman; Zied Bouslama; Jean-Tristan Brandenburg; Jorge da Rocha; Yosr Hamdi; Kais Ghedira; Najet-Srairi Abid; Scott Hazelhurst

    doi:10.1101/2020.03.04.976027 Date: 2020-03-07 Source: bioRxiv

    The spread of COVID-19 MESHD caused by the SARS-CoV-2 outbreak has been growing since its first identification in December 2019. The publishing of the first SARS-CoV-2 genome made a valuable source of data to study the details about its phylogeny, evolution, and interaction with the host. Protein-protein binding assays have confirmed that Angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC) is more likely to be the cell receptor through which the virus invades the host cell. In the present work, we provide an insight into the interaction of the viral spike Receptor Binding Domain (RBD) from different coronavirus isolates with host ACE2 HGNC protein. By calculating the binding energy score between RBD and ACE2 HGNC, we highlighted the putative jump in the affinity from a progenitor form of SARS-CoV-2 to the current virus responsible for COVID-19 MESHD outbreak. Our result was consistent with previously reported phylogenetic analysis and corroborates the opinion that the interface segment of the spike protein PROTEIN RBD might be acquired by SARS-CoV-2 via a complex evolutionary process rather than a progressive accumulation of mutations. We also highlighted the relevance of Q493 and P499 amino acid residues of SARS-CoV-2 RBD for binding to human ACE2 HGNC and maintaining the stability of the interface. Moreover, we show from the structural analysis that it is unlikely for the interface residues to be the result of genetic engineering. Finally, we studied the impact of eight different variants located at the interaction surface of ACE2 HGNC, on the complex formation with SARS-CoV-2 RBD MESHD. We found that none of them is likely to disrupt the interaction with the viral RBD of SARS-CoV-2.

    Monoclonal antibodies for the S2 subunit of spike of SARS-CoV cross-react with the newly-emerged SARS-CoV-2

    Authors: Zhiqiang Zheng; Vanessa M. Monteil; Sebastian Maurer-Stroh; Chow Wenn Yew; Carol Leong; Suganya Cheyyatraivendran Arularasu; Vincent Tak Kwong Chow; Raymond Tzer Pin Lin; Ali Mirazimi; Wanjin Hong; Yee-Joo Tan

    doi:10.1101/2020.03.06.980037 Date: 2020-03-07 Source: bioRxiv

    The emergence of a novel coronavirus, SARS-CoV-2, at the end of 2019 has resulted in widespread human infections across the globe. While genetically distinct from SARS-CoV MESHD, the etiological agent that caused an outbreak of severe acute respiratory syndrome MESHD (SARS) in 2003, both coronaviruses exhibit receptor binding domain (RBD) conservation and utilize the same host cell receptor, angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC), for virus entry. Therefore, it will be important to test the cross-reactivity of antibodies that have been previously generated against the surface spike ( S) glycoprotein PROTEIN of SARS-CoV MESHD in order to aid research on the newly emerged SARS-CoV-2. Here, we show that an immunogenic domain in the S2 subunit of SARS-CoV S MESHD is highly conserved in multiple strains of SARS-CoV-2. Consistently, four murine monoclonal antibodies (mAbs) raised against this immunogenic SARS-CoV MESHD fragment were able to recognise the S protein PROTEIN of SARS-CoV-2 expressed in a mammalian cell line. Importantly, one of them (mAb 1A9) was demonstrated to detect S in SARS-CoV-2-infected MESHD cells. To our knowledge, this is the first study showing that mAbs targeting the S2 domain of SARS-CoV can cross-react with SARS-CoV-2 and this observation is consistent with the high sequence conservation in the S2 subunit. These cross-reactive mAbs may serve as tools useful for SARS-CoV-2 research as well as for the development of diagnostic assays for its associated coronavirus disease COVID-19 MESHD.

    Predicting the Angiotensin Converting Enzyme 2 HGNC ( ACE2 HGNC) Utilizing Capability as the Receptor of SARS-CoV-2

    Authors: Ye Qiu; Yuan-Bo Zhao; Qiong Wang; Jin-Yan Li; Zhi-JIan ZHou; Ce-Heng Liao; Xing-Yi Ge

    id:10.20944/preprints202003.0091.v1 Date: 2020-03-05 Source: Preprints.org

    SARS-CoV-2, the newly identified human coronavirus causing severe pneumonia epidemic MESHD, was probably originated from Chinese horseshoe bats. However, direct transmission of the virus from bats to humans is unlikely due to lack of direct contact, implying the existence of unknown intermediate hosts. Angiotensin converting enzyme 2 HGNC ( ACE2 HGNC) is the receptor of SARS-CoV-2, but only ACE2 HGNCs of certain species can be utilized by SARS-CoV-2. Here, we evaluated and ranked the receptor-utilizing capability of ACE2 HGNCs from various species by phylogenetic clustering and sequence alignment with the currently known ACE2 HGNCs utilized by SARS-CoV-2, predicting potential intermediate hosts of SARS-CoV-2.

    Susceptibility Analysis of COVID-19 MESHD in Smokers Based on ACE2

    Authors: Jin Wang; Qiulin Luo; Rui Chen; Tao Chen; Jianxiang Li

    id:10.20944/preprints202003.0078.v1 Date: 2020-03-05 Source: Preprints.org

    Background: Cigarette smoking (CS) is a global public health problem and a high-risk factor for various diseases. In December 2019, a novel coronavirus (HCoV-19) was identified in Wuhan, China. Because ACE2 HGNC has been identified as a receptor for HCoV-19, we hypothesize that CS affects the expression pattern of ACE2 HGNC in respiratory tract, causing differences in susceptibility to the virus. Methods: Three datasets (GSE994, GSE17913, and GSE18344), were downloaded from the Gene Expression Omnibus (GEO) database. Correlation and enrichment analysis were used to evaluate the function of ACE2 HGNC. Also, the different expression of ACE2 HGNC in different groups of three datasets were analyzed. Results: Genes associated with ACE2 HGNC were enriched in important biological processes such as viral processes and immune response. Elevated ACE2 HGNC were found in intrapulmonary airways (GSE994) and oral epithelial cells (GSE17913) of smokers but not those of non-smokers or former smokers. Significant dose- and time-dependent relationships between CS and ACE2 expression were observed in mouse lung tissues, and long periods without smoking were found to significantly reduce ACE2 expression. Conclusions: Both human and rat data confirmed that CS could induce increased ACE2 in the respiratory tract, indicating that smokers have a higher susceptibility to HCoV-19.

    Strong evolutionary convergence of receptor-binding protein spike PROTEIN between COVID-19 MESHD and SARS-related coronaviruses

    Authors: Yonghua Wu

    doi:10.1101/2020.03.04.975995 Date: 2020-03-04 Source: bioRxiv

    Coronavirus Disease 2019 MESHD ( COVID-19 MESHD) and severe acute respiratory syndrome MESHD (SARS)-related coronaviruses (e.g., 2019-nCoV and SARS-CoV MESHD) are phylogenetically distantly related, but both are capable of infecting human hosts via the same receptor, angiotensin-converting enzyme 2 HGNC, and cause similar clinical and pathological features, suggesting their phenotypic convergence. Yet, the molecular basis that underlies their phenotypic convergence remains unknown. Here, we used a recently developed molecular phyloecological approach to examine the molecular basis leading to their phenotypic convergence. Our genome-level analyses show that the spike protein PROTEIN, which is responsible for receptor binding, has undergone significant Darwinian selection along the branches related to 2019-nCoV and SARS-CoV MESHD. Further examination shows an unusually high proportion of evolutionary convergent amino acid sites in the receptor binding domain (RBD) of the spike protein PROTEIN between COVID-19 MESHD and SARS-related CoV clades, leading to the phylogenetic uniting of their RBD protein sequences. In addition to the spike protein PROTEIN, we also find the evolutionary convergence of its partner protein, ORF3a PROTEIN, suggesting their possible co-evolutionary convergence. Our results demonstrate a strong adaptive evolutionary convergence between COVID-19 MESHD and SARS-related CoV, possibly facilitating their adaptation to similar or identical receptors. Finally, it should be noted that many observed bat SARS-like CoVs that have an evolutionary convergent RBD sequence with 2019-nCoV and SARS-CoV MESHD may be pre-adapted to human host receptor ACE2 HGNC, and hence would be potential new coronavirus sources to infect humans in the future.

    Highly ACE2 HGNC Expression in Pancreas May Cause Pancreas Damage After SARS-CoV-2 Infection MESHD

    Authors: Furong Liu; Xin Long; Wenbin Zou; Minghao Fang; Wenjuan Wu; Wei Li; Bixiang Zhang; Wanguang Zhang; Xiaoping Chen; Zhanguo Zhang

    doi:10.1101/2020.02.28.20029181 Date: 2020-03-03 Source: medRxiv

    The ongoing outbreak of coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) started in the end of 2019 in China has triggered a global public health crisis. Previous studies have shown that SARS-CoV-2 infects MESHD cells by binding angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC), which is the same as SARS-CoV. The expression and distribution of ACE2 HGNC in the pancreas are unknown. At the same time, the injury of pancreas MESHD after SARS-CoV-2 infection MESHD has not been concerned. Here, we collected public datasets (bulk RNA-seq and single-cell RNA-seq) to indicate the expression and the distribution of ACE2 HGNC in pancreas (in both exocrine glands and islets). And further, clinical data including mild and severe patients with COVID-19 MESHD demonstrated there existed mild pancreatitis MESHD. In the 67 severe cases, 11 patients (16.41%) showed elevated levels of both amylase and lipase, and 5 patients (7.46%) showed imaging alterations. Only one patient (1.85%) showed elevated levels of both amylase and lipase in 54 mild cases, without imaging changes. Our study revealed the phenomenon and possible cause of mild pancreatic injury MESHD in patients with COVID-19 MESHD. This suggests that pancreatitis MESHD after SARS-CoV-2 infection MESHD should also be paid attention in clinical work.

    TWIRLS, an automated topic-wise inference method based on massive literature, suggests a possible mechanism via ACE2 HGNC for the pathological changes in the human host after coronavirus infection

    Authors: Xiaoyang Ji; Chunming Zhang; Yubo Zhai; Zhonghai Zhang; Chunli Zhang; Yiqing Xue; Guangming Tan; Gang Niu

    doi:10.1101/2020.02.27.967588 Date: 2020-03-02 Source: bioRxiv

    Faced with the current large-scale public health emergency, collecting, sorting, and analyzing biomedical information related to the "coronavirus" should be done as quickly as possible to gain a global perspective, which is a basic requirement for strengthening epidemic control capacity. However, for human researchers studying the viruses and the hosts, the vast amount of information available cannot be processed effectively and in a timely manner, particularly when the scientific understanding may be limited, which can further lower the information processing efficiency. We present TWIRLS, a method that can automatically acquire, organize, and classify information. Additionally, independent functional data sources can be added to build an inference system using a machine-based approach, which can provide relevant knowledge to help human researchers quickly establish subject cognition and to make more effective decisions. TWIRLS can automatically analyze more than three million words in more than 14,000 literature articles in only 4 hours. Combining with generalized gene interaction databases creates a data interface that can help researchers to further analyze the information. Using the TWIRLS system, we found that an important regulatory factor angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC) may be involved in the host pathological changes on binding to the coronavirus after infection. After triggering functional changes in ACE2 HGNC/AT2R, an imbalance in the steady-state cytokine regulatory axis involving the Renin-Angiotensin System and IP-10 HGNC leads to a cytokine storm.

    Predictions for the binding domain and potential new drug targets of 2019-nCoV

    Authors: Zehua Zeng; Luo Zhi; Hongwu Du

    doi:10.1101/2020.02.26.961938 Date: 2020-03-02 Source: bioRxiv

    An outbreak of new SARS-like viral in Wuhan, China has been named 2019-nCoV. The current state of the epidemic is increasingly serious, and there has been the urgent necessity to develop an effective new drug. In previous studies, it was found that the conformation change in CTD1 was the region where SARS-CoV MESHD bound to human ACE2 HGNC. Although there are mutations of the 2019-nCoV, the binding energy of ACE2 HGNC remains high. The surface glycoprotein of 2019-nCoV was coincident with the CTD1 region of the S-protein HGNC S-protein PROTEIN by comparing the I-TASSER prediction model with the actual SARS model, which suggests that 2019-nCoV may bind to the ACE2 HGNC receptor through conformational changes. Furthermore, site prediction on the surface glycoprotein of 2019-nCoV suggests some core amino acid area may be a novel drug target against 2019-nCoV.

    Activating organ’s immunizing power against COVID–19–learning from SARS

    Authors: Yi Wang; Chuanxin Xia

    doi:10.21203/rs.3.rs-16074/v1 Date: 2020-02-29 Source: ResearchSquare

    Background Coronaviruses cause respiratory diseases MESHD in many animals, including humans. Spike protein PROTEIN is an important component of coronavirus structure and the formation of ACE2 HGNC ( angiotensin converting enzyme 2 HGNC)–spike complex mediates virus entry to host cells. C–type lectin family are widely distribute on the surface of human cells and have been shown to activate the immune system. In this article, we first illustrate why we can “learn from SARS” with phylogenetic analysis. Then, we use SARS spike protein PROTEIN structure, to inferring our molecular docking experiment, revealing the potential capacity of C–type lectin to directly interact with spike protein PROTEIN obstructs the formation of spike– ACE2 HGNC complex. Considering the expression profile of C–type lectin family changing significantly during infection, we predict certain members of this kind of protein as potential therapeutic target and verify their assumed function by inferring an C–type lectin–dependent CD4/CD28 T cell survival molecular network with endogenous molecular network theory (EMT) and comparing the predicted expression trend corresponding to each molecular with experiment data. Methods Alignments are inferred by MAFFT V7 ( G–ins–i, Blosom). Maximum likelihood analyses and bootstrap test carried out by RAXML V8.2 ML+BP online platform. Protein structure is predicted by SWISSMODELLING online platform. Molecular docking experiment is carried out by Z–dock Version 3.0.2. C–type lectin–dependent CD4/CD28 T cell Network is inferred by EMT theory. Result Our molecular docking experiment revealing the potential capacity of C–type lectin to directly interact with spike protein PROTEIN obstructs the formation of spike– ACE2 HGNC complex. Based on the expression profile of C–type lectin family during infection, we predicting certain member of this kind of protein as potential therapeutic target such as Clec7a, Clec12a and Clec11a, corresponding immune cell types such as CD4/CD28 T cell simulated by EMT theory and verified by experiment data, antigen adjuvant with similar C–type lectin receptor–TDM and some immune–boosting drugs–radix sophorae, lactoferrin and Astragalus membranaceus, for future testing.  Conclusions C–type lectin and their corresponding immune cells predicted in this work may be the potential therapeutic targets for the disease caused by COVID–19. C–lectin with the capacity of directly interact with spike protein PROTEIN inhibiting the formation of ACE2 HGNC–spike complex may be the way they execute anti–virus function. The corresponding cell type such as CD4/CD28 T cell may participate and against virus while Clec7a, Clec12a and Clec11a presumed capacity for facilitating CD4/CD28 T cell survival during infection being verified by EMT combining with experiment data. Our prediction at least suggest the possibility of activating organ’s immunizing power to prevent from COVID–19 and the drugs we suggested are all need to be further tested.  Trial registration Retrospectively registered. Keywords C–type lectin, spike protein PROTEIN, coronavirus, COVID–19, TDM.

    Hypokalemia and Clinical Implications in Patients with Coronavirus Disease 2019 MESHD ( COVID-19 MESHD)

    Authors: dong chen Jr.; Xiaokuni Li; qifa song Sr.; Chenchan Hu Jr.; Feifei Su; Jianyi Dai

    doi:10.1101/2020.02.27.20028530 Date: 2020-02-29 Source: medRxiv

    BACKGROUND: SARS-CoV-2 has caused a series of COVID-19 MESHD globally. SARS-CoV-2 binds angiotensin I converting enzyme 2 HGNC ( ACE2 HGNC) of renin-angiotensin system (RAS) and causes prevalent hypokalemia MESHD METHODS: The patients with COVID-19 MESHD were classified into severe hypokalemia MESHD, hypokalemia MESHD, and normokalemia group. The study aimed to determine the relationship between hypokalemia MESHD and clinical features, the underlying causes and clinical implications of hypokalemia MESHD. RESULTS: By Feb 15, 2020, 175 patients with COVID-19 MESHD (92 women and 83 men; median age, 46 [IQR, 34-54] years) were admitted to hospital in Wenzhou, China, consisting 39 severe hypokalemia MESHD-, 69 hypokalemia MESHD-, and 67 normokalemia patients. Gastrointestinal symptoms were not associated with hypokalemia MESHD among 108 hypokalemia MESHD patients (P>0.05). Body temperature, CK, CK-MB, LDH, and CRP HGNC were significantly associated with the severity of hypokalemia MESHD (P<0.01). 93% of severe and critically ill MESHD patients had hypokalemia MESHD which was most common among elevated CK, CK-MB, LDH, and CRP HGNC. Urine K+ loss was the primary cause of hypokalemia MESHD. severe hypokalemia MESHD patients was given 3 g/day, adding up to an average of 34 (SD=4) g potassium during hospital stay. The exciting finding was that patients responded well to K+ supplements when they were inclined to recovery. CONCLUSIONS: Hypokalemia MESHD is prevailing in patients with COVID-19 MESHD. The correction of hypokalemia MESHD is challenging because of continuous renal K+ loss resulting from the degradation of ACE2 HGNC. The end of urine K+ loss indicates a good prognosis and may be a reliable, in-time, and sensitive biomarker directly reflecting the end of adverse effect on RAS system.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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