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HGNC Genes

SARS-CoV-2 proteins

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    Comprehensive evaluation of ACE2 HGNC expression in female ovary by single-cell RNA-seq analysis

    Authors: Siming Kong; Zhiqiang Yan; Peng Yuan; Xixi Liu; Yidong Chen; Ming Yang; Wei Chen; Shi Song; Jie Yan; Liying Yan; Jie Qiao

    doi:10.1101/2021.02.23.432460 Date: 2021-02-23 Source: bioRxiv

    Pneumonia induced by severe acute respiratory coronavirus MESHD 2 (SARS-CoV-2) via ACE2 HGNC receptor may affect many organ systems like lung, heart and kidney. An autopsy report revealed positive SARS-Cov-2 detection results in ovary MESHD, however, the developmental-stage-specific and cell-type-specific risk in fetal primordial germ cells (PGCs) and adult women ovary remained unclear. In this study, we used single-cell RNA-sequencing (scRNA-seq) datasets spanning several developmental stages of ovary MESHD including PGCs and cumulus-oocyte complex (COC) to investigate the potential risk of SARS-CoV-2 infection MESHD. We found that PGCs and COC exhibited high ACE2 HGNC expression. More importantly, the ratio of ACE2 HGNC-positive cells was sharply up-regulated in primary stage and ACE2 HGNC was expressed in all oocytes and cumulus cells in preovulatory stage, suggesting the possible risk of SARS-CoV-2 infection MESHD in follicular development. CatB HGNC/L, not TMPRSS2 HGNC, was identified to prime for SARS-CoV-2 entry MESHD in follicle. Our findings provided insights into the potential risk of SARS-CoV-2 infection MESHD during folliculogenesis in adulthood and the possible risk in fetal PGCs.

    Genomics-guided identification of potential modulators of SARS-CoV-2 entry proteases, TMPRSS2 HGNC and Cathepsins B/L

    Authors: Kartikay Prasad; Vijay Kumar

    doi:10.21203/rs.3.rs-138273/v1 Date: 2020-12-30 Source: ResearchSquare

    The entry of SARS-CoV-2 into host cells requires the activation of its spike protein PROTEIN by host cell proteases. The serine protease HGNC, transmembrane serine protease 2 ( TMPRSS2 HGNC) and cysteine proteases, cathepsins B, L ( CTSB HGNC/L) activate spike protein PROTEIN and enabling SARS-CoV-2 entry to the host cell through two completely different and independent pathways. Given that the uncertainty of how SARS-CoV-2 infects MESHD and kills, the need for a deep understanding of SARS-CoV-2 biology is imperative. Herein, we performed genomic-guided meta-analysis to identify upstream regulatory elements altering the expression of TMPRSS2 HGNC and CTSB HGNC/L genes. Further, drugs and medicinal compounds were identified based on their effects on gene expression signatures of the modulators of TMPRSS2 HGNC and CTSB HGNC/L genes. Using this strategy, estradiol and retinoic acid have been identified as putative SARS-CoV-2 alleviation agents. Further, we analysed drug-gene and gene-gene interaction network using 332 human targets of SARS-CoV-2 proteins. The network results indicate that out of 332 human proteins, estradiol interacts with 135 (41%) and retinoic acid interacts with 40 (12%) proteins. Interestingly, a combination of both estradiol and retinoic acid interacts with 153 (46%) of human proteins acting as SARS-CoV-2 targets and affect the functions of nearly all of the SARS-CoV-2 viral proteins, indicating the therapeutic benefits of drug combination therapy. Finally, molecular docking analysis suggest that both the drugs binds to TMPRSS2 HGNC and CTSL HGNC with the nanomolar to low micromolar affinity. This study, for the first time, reports the molecules like estradiol and retinoic acid as candidate drugs against both the host proteases, TMPRSS2 HGNC and CTSB HGNC/L. We here thus suggest that these antiviral drugs alone or in combination can simultaneously target both the entry pathways and thus can be considered as a potential treatment option for COVID-19 MESHD.

    The human brain vasculature shows a distinct expression pattern of SARS-CoV-2 entry factors

    Authors: Moheb Ghobrial; Jason Charish; Shigeki Takada; Taufik Valiante; Philippe Monnier; Ivan Radovanovic; Gary Bader; Thomas Waelchli; John E. Bradley; Shihong Qiu; Guang Yang; Fen Zhou; Esther Zumaquero; Thomas S. Simpler; Betty Mousseau; John T. Killian Jr.; Brittany Dean; Qiao Shang; Jennifer L. Tipper; Christopher Risley; Kevin S. Harrod; Ray Feng; Young Lee; Bethlehem Shiberu; Vyjayanthi Krishnan; Isabelle Peguillet; Jianfeng Zhang; Todd Green; Troy D. Randall; Bertrand Georges; Frances E Lund; Scot Roberts; Akshay Pai; Mads Nielsen; Martin Sillesen

    doi:10.1101/2020.10.10.334664 Date: 2020-10-11 Source: bioRxiv

    A large number of hospitalized COVID-19 MESHD patients show neurological symptoms such as ischemic- and hemorrhagic stroke MESHD as well as encephalitis MESHD, and SARS-CoV-2 can directly infect endothelial cells leading to endotheliitis across multiple vascular beds. These findings suggest an involvement of the brain- and peripheral vasculature in COVID-19 MESHD, but the underlying molecular mechanisms remain obscure. To understand the potential mechanisms underlying SARS-CoV-2 tropism MESHD for brain vasculature, we constructed a molecular atlas of the expression patterns of SARS-CoV-2 viral entry-associated genes (receptors and proteases) and SARS-CoV-2 interaction partners in human (and mouse) adult and fetal brain as well as in multiple non-CNS tissues in single-cell RNA-sequencing data across various datasets. We observed a distinct expression pattern of the cathepsins B ( CTSB HGNC) and -L ( CTSL HGNC) - which are able to substitute for the ACE2 HGNC co-receptor TMPRSS2 HGNC - in the human vasculature with CTSB HGNC being mainly expressed in the brain vasculature and CTSL HGNC predominantly in the peripheral vasculature, and these observations were confirmed at the protein level in the Human Protein Atlas and using immunofluorescence stainings. This expression pattern of SARS-CoV-2 viralentry associated proteases and SARS-CoV-2 interaction partners was also present in endothelial cells and microglia in the fetal brain, suggesting a developmentally establishedSARS-CoV-2 entry machinery in the human vasculature. At both the adult and fetal stages, we detected a distinct pattern of SARS-CoV-2 entry associated genes' transcripts in brain vascular endothelial cells and microglia, providing a potential explanation for an inflammatory response in the brain endothelium upon SARS-CoV-2 infection MESHD. Moreover, CTSB HGNC was co-expressed in adult and fetal brain endothelial cells with genes and pathways involved in innate immunity and inflammation MESHD, angiogenesis, blood-brain-barrier permeability, vascular metabolism, and coagulation, providing a potential explanation for the role of brain endothelial cells in clinically observed (neuro)vascular symptoms in COVID-19 MESHD patients. Our study serves as a publicly available single-cell atlas of SARS-CoV-2 related entry factors and interaction partners in human and mouse brain endothelial- and perivascular cells, which can be employed for future studies in clinical samples of COVID-19 MESHD patients.

    Single-cell RNA Expression of SARS-CoV-2 Cell Entry Factors in Human Endometrium during Preconception

    Authors: Felipe Vilella Mitjana; Wanxin Wang; Inmaculada Moreno Gimeno; Stephen Quake; Carlos Simon; Jeff Green; Julia Schaletzky; Ahmet Yildiz; Louise Rowntree; Thi Nguyen; Katherine Kedzierska; Denise Doolan; Carola Vinuesa; Matthew Cook; Nicholas Coatsworth; Paul Myles; Florian Kurth; Leif Sander; Russell Gruen; Graham Mann; Amee George; Elizabeth Gardiner; Ian Cockburn; Bala Pesala; Debojyoti Chakraborty; Souvik Maiti

    doi:10.1101/2020.09.14.296806 Date: 2020-09-14 Source: bioRxiv

    We investigated potential SARS-CoV-2 tropism MESHD in human endometrium by single-cell RNA-sequencing of viral entry-associated genes in healthy women. Percentages of endometrial cells expressing ACE2 HGNC, TMPRSS2 HGNC, CTSB HGNC, or CTSL HGNC were <2%, 12%, 80%, and 80%, respectively, with 0.7% of cells expressing all four genes. Our findings imply low efficiency of SARS-CoV-2 infection MESHD in the endometrium before embryo implantation, providing information to assess preconception risk in asymptomatic carriers.

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MeSH Disease
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SARS-CoV-2 Proteins


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