{"id":29474,"date":"2020-06-29T07:35:00","date_gmt":"2020-06-29T05:35:00","guid":{"rendered":"https:\/\/www.embl.org\/news\/?p=29474"},"modified":"2024-03-22T13:21:31","modified_gmt":"2024-03-22T12:21:31","slug":"existing-drugs-can-prevent-sars-cov-2-from-highjacking-cells","status":"publish","type":"post","link":"https:\/\/www.embl.org\/news\/science\/existing-drugs-can-prevent-sars-cov-2-from-highjacking-cells\/","title":{"rendered":"Existing drugs can prevent SARS-CoV-2 from hijacking cells"},"content":{"rendered":"\n

An international team of researchers has analysed how SARS-CoV-2, the virus that causes COVID-19, hijacks the proteins in its target cells. The research, published in the journal Cell<\/em>, shows how the virus shifts the cell\u2019s activity to promote its own replication and to infect nearby cells. The scientists also identified seven clinically approved drugs that could disrupt these mechanisms, and recommend that these drugs are immediately tested in clinical trials.<\/p>\n\n\n\n

The collaboration included researchers at EMBL\u2019s European Bioinformatics Institute (EMBL-EBI)<\/a>, the Quantitative Biosciences Institute\u2019s Coronavirus Research Group in the School of Pharmacy at University of California San Francisco (UCSF), the Howard Hughes Medical Institute, the Institut Pasteur, and the Excellence Cluster CIBSS of the University of Freiburg.<\/p>\n\n\n\n

Viruses are unable to replicate and spread on their own: they need an organism \u2013 their host \u2013 to carry, replicate, and transmit them to further hosts. To facilitate this process, viruses need to take control of their host cell\u2019s machinery and manipulate it to produce new viral particles. Sometimes, this hijacking interferes with the activity of the host\u2019s enzymes and other proteins.<\/p>\n\n\n\n

Once a protein is produced, enzymes can change its activity by making chemical modifications to its structure. For example, phosphorylation \u2013 the addition of a phosphoryl group to a protein by a type of enzyme called a kinase \u2013 plays a pivotal role in the regulation of many cell processes, including cell-to-cell communication, cell growth, and cell death. By altering phosphorylation patterns in the host\u2019s proteins, a virus can potentially promote its own transmission to other cells and, eventually, other hosts.<\/p>\n\n\n\n

The scientists used mass spectrometry, a tool to analyse the properties of a sample by measuring the mass of its molecules and molecular fragments, to evaluate all host and viral proteins that showed changes in phosphorylation after SARS-CoV-2 infection. They found that 12% of the host proteins that interact with the virus were modified. The researchers also identified the kinases that are most likely to regulate these modifications. Kinases are potential targets for drugs to stop the activity of the virus and treat COVID-19.<\/p>\n\n\n\n

The extraordinary behaviour of infected cells<\/h3>\n\n\n\n

\u201cThe virus prevents human cells from dividing, maintaining them at a particular point in the cell cycle. This provides the virus with a relatively stable and adequate environment to keep replicating,\u201d explains Pedro Beltrao, Group Leader at EMBL-EBI<\/a>.<\/p>\n\n\n\n

SARS-CoV-2 not only impacts cell division, but also cell shape. One of the key findings from the study is that infected cells exhibit long, branched, arm-like extensions, or filopodia. These structures may help the virus reach nearby cells in the body and advance the infection, but further study is warranted.<\/p>\n\n\n\n

\u201cThe distinct visualisation of the extensive branching of the filopodia once again elucidates how understanding the biology of virus\u2013host interaction can illuminate possible points of intervention in the disease,\u201d says Nevan Krogan, Director of the Quantitative Biosciences Institute at UCSF and Senior Investigator at Gladstone Institutes.<\/p>\n\n\n\n

Old drugs, new treatments<\/h3>\n\n\n\n

\u201cKinases possess certain structural features that make them good drug targets. Drugs have already been developed to target some of the kinases we identified, so we urge clinical researchers to test the antiviral effects of these drugs in their trials,\u201d says Beltrao.<\/p>\n\n\n\n

In some patients, COVID-19 causes an overreaction of the immune system, leading to inflammation. An ideal treatment would relieve these exaggerated inflammatory symptoms while stopping the replication of the virus. Existing drugs targeting the activity of kinases may be the solution to both problems.<\/p>\n\n\n\n

The researchers identified dozens of drugs approved by the Food and Drug Administration (FDA) or ongoing clinical trials that target the kinases of interest. Seven of these compounds, primarily anticancer and inflammatory disease compounds, demonstrated potent antiviral activity in laboratory experiments.<\/p>\n\n\n\n

\u201cOur data-driven approach for drug discovery has identified a new set of drugs that have great potential to fight COVID-19, either by themselves or in combination with other drugs, and we are excited to see if they will help end this pandemic,\u201d says Krogan.<\/p>\n\n\n\n

\u201cWe expect to build upon this work by testing many other kinase inhibitors while identifying both the underlying pathways and additional potential therapeutics that may intervene in COVID-19 effectively,\u201d says Kevan Shokat, Professor in the Department of Cellular and Molecular Pharmacology at UCSF.<\/p>\n\n\n\n

Funding<\/h4>\n\n\n\n

This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell <\/em>paper.<\/p>\n\n\n\n\n

Source article<\/h3>\n

BOUHADDOU, M., et al. (2020). The Global Phosphorylation Landscape of SARS-CoV-2 Infection. Cell<\/em>, published online 28 June, DOI: 10.1016\/j.cell.2020.06.034<\/a><\/p>\n<\/div>\n\n\n\n\n

Related links<\/h3>\n

Research in the Beltrao Group<\/a>
Silencing the SARS-CoV-2 receptor with epigenetic modifications<\/a>
Understanding how SARS-CoV-2 behaves in the gut<\/a>
Investigating the structure and mechanisms of coronavirus biomolecules<\/a>
Quantitative Bioscience Institute Coronavirus Research Group<\/a><\/p>\n<\/div>\n\n\n

\n\n\n\n

Bestehende Medikamente k\u00f6nnen SARS-CoV-2 daran hindern, Zellen zu kapern<\/strong><\/h2>\n\n\n\n

Forscher untersuchen, wie das neue Coronavirus menschliche Proteine umprogrammiert, um sich selbst zu vermehren, und identifizieren mehrere antivirale Medikamente, die f\u00fcr klinische Studien bereit sind<\/strong><\/h3>\n\n\n\n
\"SARS-CoV-2
SARS-CoV-2 Viren auf einer Zelle mit Filopodien. Bildnachweis: Elizabeth Fischer, Microscopy Unit NIH\/NIAID<\/figcaption><\/figure>\n\n\n\n

Ein internationales Forscherteam hat analysiert wie SARS-CoV-2, das Virus das COVID-19 verursacht, Proteine in seinen Wirtszellen kapert. Die Studie, im Journal Cell <\/em>ver\u00f6ffentlicht, zeigt, wie das Virus die Funktionen der Zelle ver\u00e4ndert, um seine eigene Vermehrung zu f\u00f6rdern und angrenzende Zellen zu infizieren. Die Wissenschaftler haben auch sieben Medikamente identifiziert \u2013 einige bereits zugelassen \u2013 die diese Mechanismen unterbrechen k\u00f6nnten und empfehlen, dass diese Medikamente sofort in klinischen Studien getestet werden.<\/p>\n\n\n\n

Das Projekt war eine Zusammenarbeit bestehend aus Forschern von EMBLs Europ\u00e4ischem Institut f\u00fcr Bioinformatik<\/a> (EMBL-EBI), der Coronavirus-Forschungsgruppe des Instituts f\u00fcr Quantitative Biowissenschaften an der School of Pharmacy der University of California San Francisco (UCSF), dem Howard Hughes Medical Institute, dem Institut Pasteur und dem Exzellenzcluster CIBSS der Universit\u00e4t Freiburg. <\/p>\n\n\n\n

Viren k\u00f6nnen sich nicht alleine vermehren und verbreiten. Sie brauchen einen Organismus \u2013 ihren Wirt \u2013 der sie tr\u00e4gt, vermehrt und an neue Wirte weitergibt. Um diesen Vorgang zu erm\u00f6glichen, m\u00fcssen Viren die Kontrolle \u00fcber die Maschinerie ihrer Wirtszellen \u00fcbernehmen und diese manipulieren, um neue Virenpartikel zu produzieren. Manchmal st\u00f6rt diese \u00dcbernahme die Aktivit\u00e4t der Enzyme und anderer Proteine der Wirtszelle. <\/p>\n\n\n\n

Wenn ein Protein produziert wurde, k\u00f6nnen Enzyme seine Aktivit\u00e4t ver\u00e4ndern, indem sie chemische Ver\u00e4nderungen an seiner Struktur vornehmen. So spielt beispielsweise Phosphorylierung \u2013 das Anf\u00fcgen einer Phosphorylgruppe zu einem Protein durch eine Art von Enzym namens Kinase \u2013 eine wichtige Rolle in der Regulierung von vielen Vorg\u00e4ngen in der Zelle. Dazu geh\u00f6rt die Kommunikation zwischen Zellen, Zellwachstum und Zelltod. Indem er Phosphorylierungsmuster in den Proteinen der Wirtszelle ver\u00e4ndert, kann das Virus m\u00f6glicherweise seine \u00dcbertragung auf andere Zellen und schlie\u00dflich auch auf andere Wirte f\u00f6rdern.<\/p>\n\n\n\n

Die Wissenschaftler verwendeten Massenspektrometrie \u2013 eine Technologie, die die Eigenschaften einer Probe analysiert, indem sie die Masse ihrer Molek\u00fcle und Molek\u00fclfragmente misst \u2013 um alle Wirts- und Virenproteine zu untersuchen, die nach einer SARS-CoV-2 Infektion Ver\u00e4nderungen in ihrer Phosphorylierung zeigten. Sie stellten fest, dass 12% der Wirtsproteine, die mit dem Virus interagieren, ver\u00e4ndert waren. Die Forscher identifizierten auch die Kinasen, die diese Modifizierungen am wahrscheinlichsten regulieren. Kinasen sind potenzielle Ziele f\u00fcr Medikamente, um die Aktivit\u00e4t des Virus zu stoppen und COVID-19 zu behandeln. <\/p>\n\n\n\n

Das au\u00dfergew\u00f6hnliche Verhalten von infizierten Zellen <\/strong><\/h3>\n\n\n\n

\u201cDas Virus verhindert die Teilung menschlicher Zellen und h\u00e4lt sie an einem bestimmten Punkt im Zellzyklus fest. Dadurch erh\u00e4lt das Virus eine relativ stabile und angemessene Umgebung, um sich weiter zu vermehren,\u201d erkl\u00e4rt Pedro Beltrao, Gruppenleiter am EMBL-EBI<\/a>.<\/p>\n\n\n\n

SARS-CoV-2 beeinflusst nicht nur die Zellteilung, sondern auch die Zellform. Eines der wichtigsten Ergebnisse der Studie ist, dass infizierte Zellen Filopodien aufweisen: lange, verzweigte, arm\u00e4hnliche Verl\u00e4ngerungen. Diese Strukturen k\u00f6nnten dem Virus dabei helfen, nahe Zellen zu erreichen und sich weiter zu verbreiten \u2013 dies bedarf jedoch weiterer Studien. <\/p>\n\n\n\n

\u201cDie ausgepr\u00e4gte Visualisierung der ausgedehnten Verzweigung von Filopodien verdeutlicht einmal mehr, wie das Verst\u00e4ndnis der Biologie hinter Virus\u2013Wirt Interaktionen m\u00f6gliche Eingriffspunkte gegen die Krankheit aufzeigen kann\u201d, sagt Nevan Krogan, Direktor des Instituts f\u00fcr Quantitative Biowissenschaften an der UCSF und Senior Investigator an den Gladstone Institutes. <\/p>\n\n\n\n

Alte Medikamente, neue Therapien<\/strong><\/h3>\n\n\n\n

\u201cKinasen besitzen bestimmte strukturelle Merkmale die sie zu guten Zielen f\u00fcr Medikamente machen. Es wurden bereits Medikamente entwickelt, die gegen manche der von uns gefundenen Kinasen gerichtet sind. Deswegen appellieren wir an klinische Forscher, die antiviralen Effekte dieser Medikamente in ihren Studien zu testen\u201d, sagt Beltrao. <\/p>\n\n\n\n

In manchen Patienten verursacht COVID-19 eine \u00dcberreaktion des Immunsystems, was zu einer Entz\u00fcndung f\u00fchrt. Eine ideale Therapie w\u00fcrde diese Entz\u00fcndungssymptome lindern, w\u00e4hrend sie gleichzeitig die Vermehrung des Virus stoppt. Bereits existierende Medikamente, die die Aktivit\u00e4t der Kinasen unterbrechen, k\u00f6nnten eine L\u00f6sung f\u00fcr beide Probleme sein. <\/p>\n\n\n\n

Die Forscher haben Dutzende Medikamente bestimmt, die von der Food and Drug Administration (FDA) zugelassen sind, sowie laufende klinische Studien, welche die in Frage kommenden Kinasen zum Ziel haben. Sieben dieser Verbindungen \u2013 in erster Linie krebs- und entz\u00fcndungshemmende Medikamente \u2013 zeigten in Laborexperimenten starke antivirale Eigenschaften. <\/p>\n\n\n\n

\u201cUnser datenbasierter Ansatz zur Entdeckung von Medikamenten hat einen neuen Satz Medikamente bestimmt, die ein gro\u00dfes Potential zur Bek\u00e4mpfung von COVID-19 haben \u2013 entweder alleine oder in Kombination mit anderen Mitteln. Wir sind gespannt zu sehen, ob sie dabei helfen werden diese Pandemie zu beenden\u201d, sagt Krogan. <\/p>\n\n\n\n

\u201cWir wollen auf dieser Arbeit aufbauen, indem wir viele weitere Kinasehemmer testen und dabei sowohl die zugrunde liegenden Mechanismen als auch zus\u00e4tzliche potenzielle Therapieans\u00e4tze identifizieren, die wirksam in COVID-19 eingreifen k\u00f6nnten \u201d, sagt Kevan Shokat, Professor in der Abteilung f\u00fcr Zellul\u00e4re und Molekulare Pharmakologie an der UCSF.<\/p>\n\n\n\n

Funding<\/h4>\n\n\n\n

This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell <\/em>paper.<\/p>\n\n\n\n\n

Quellenartikel<\/h3>\n

BOUHADDOU, M., et al. (2020). The Global Phosphorylation Landscape of SARS-CoV-2 Infection. Cell<\/em>, Online Publikation am 28.06., DOI: 10.1016\/j.cell.2020.06.034<\/a><\/p>\n<\/div>\n\n\n\n\n

Links<\/h3>\n

Forschung der Beltrao Gruppe<\/a>
Silencing the SARS-CoV-2 receptor with epigenetic modifications<\/a>
Understanding how SARS-CoV-2 behaves in the gut<\/a>
Investigating the structure and mechanisms of coronavirus biomolecules<\/a>
Quantitative Bioscience Institute Coronavirus Research Group<\/a><\/p>\n<\/div>\n\n\n

\n\n\n\n

Comment certains m\u00e9dicaments peuvent emp\u00eacher le virus SARS-CoV-2 de manipuler ses cellules h\u00f4tes<\/strong><\/h2>\n\n\n\n

Des chercheurs ont d\u00e9couvert comment le coronavirus manipulent les prot\u00e9ines humaines pour sa propre r\u00e9plication, et ont identifi\u00e9  plusieurs m\u00e9dicaments antiviraux pr\u00eats pour des essais cliniques<\/strong><\/h3>\n\n\n\n
\"SARS-CoV-2
Des particules virales de SARS-CoV-2 sur une cellule avec des filopodes. Cr\u00e9dit: Elizabeth Fischer, Microscopy Unit NIH\/NIAID<\/figcaption><\/figure>\n\n\n\n

Une \u00e9quipe internationale de chercheurs a analys\u00e9 la fa\u00e7on dont le SARS-CoV-2, virus responsable du Covid-19, modifie les prot\u00e9ines de ses cellules h\u00f4tes. L\u2019\u00e9tude publi\u00e9e dans la revue Cell<\/em> montre comment le virus d\u00e9tourne l\u2019activit\u00e9 des cellules pour assurer sa propre r\u00e9plication et infecter les cellules voisines. Les scientifiques ont \u00e9galement identifi\u00e9 sept m\u00e9dicaments qui pourraient entraver ces m\u00e9canismes, et ils pr\u00e9conisent que ces m\u00e9dicaments soient imm\u00e9diatement test\u00e9s dans des essais cliniques.<\/p>\n\n\n\n

Cette collaboration comprend des scientifiques de l\u2019Institut Europ\u00e9en de Bioinformatique du Laboratoire Europ\u00e9en de Biologie Mol\u00e9culaire<\/a> (EMBL-EBI), du groupe de recherche sur le coronavirus de l\u2019Institut de Biosciences Quantitatives de l\u2019Universit\u00e9 de Californie \u00e0 San Francisco (UCSF), de l\u2019Institut M\u00e9dical Howard Hughes, de l\u2019Institut Pasteur, et de l\u2019Universit\u00e9 de Freiburg. <\/p>\n\n\n\n

Les virus sont incapables de se r\u00e9pliquer et de se propager seuls : ils ont besoin d\u2019un organisme \u2013 leur h\u00f4te \u2013 pour les transporter, les r\u00e9pliquer et les transmettre \u00e0 d\u2019autres h\u00f4tes. Pour encourager ce processus, les virus doivent prendre le contr\u00f4le de la machinerie cellulaire de leur h\u00f4te et la manipuler pour qu\u2019elle produise de nouvelles particules virales. Il arrive que ce d\u00e9tournement interf\u00e8re avec l\u2019activit\u00e9 des enzymes et autre prot\u00e9ines de l\u2019h\u00f4te. <\/p>\n\n\n\n

Apr\u00e8s qu\u2019une prot\u00e9ine est produite, des enzymes peuvent affecter son activit\u00e9 en apportant des modifications chimiques \u00e0 sa structure. Par exemple, la phosphorylation \u2013 l\u2019addition d\u2019un groupe phosphoryl \u00e0 la prot\u00e9ine par un type d\u2019enzymes appel\u00e9es kinases \u2013 joue un r\u00f4le majeur pour la r\u00e9gulation de nombreux processus cellulaires, y compris la croissance et la mort d\u2019une cellule ainsi que sa communication avec les cellules voisines. En alt\u00e9rant la phosphorylation des prot\u00e9ines de son h\u00f4te, un virus peut potentiellement assurer sa propre transmission \u00e0 d\u2019autres cellules, voire d\u2019autres h\u00f4tes.<\/p>\n\n\n\n

Les scientifiques ont utilis\u00e9 la spectrom\u00e9trie de masse, un outil permettant d\u2019analyser les propri\u00e9t\u00e9s d\u2019un \u00e9chantillon en mesurant la masse de ses mol\u00e9cules et fragments mol\u00e9culaires, pour d\u00e9terminer quelles prot\u00e9ines virales et quelles prot\u00e9ines de l\u2019h\u00f4te subissent un changement de phosphorylation apr\u00e8s une infection de SARS-CoV-2. Ils ont trouv\u00e9 que 12% des prot\u00e9ines de l\u2019h\u00f4te qui interagissent avec le virus \u00e9taient modifi\u00e9es. Les chercheurs ont \u00e9galement identifi\u00e9 les kinases les plus susceptibles de r\u00e9guler ces modifications. Les kinases sont des cibles m\u00e9dicamenteuses potentielles pour arr\u00eater l\u2019activit\u00e9 du virus, et pour traiter le Covid-19.<\/p>\n\n\n\n

Les caract\u00e9ristiques extraordinaires des cellules infect\u00e9es<\/strong><\/h3>\n\n\n\n

\u201cLe virus emp\u00eache les cellules humaines de se diviser, et les maintient dans un \u00e9tat interm\u00e9diaire du cycle cellulaire. Ceci procure un environnement stable au virus, id\u00e9al pour sa r\u00e9plication<\/em>\u201d, explique Pedro Beltrao, chef de groupe \u00e0 l\u2019EMBL-EBI<\/a>.<\/p>\n\n\n\n

Le SARS-CoV-2 a un impact sur la division cellulaire, mais aussi sur la forme des cellules infect\u00e9es. L\u2019une des d\u00e9couvertes cl\u00e9s de cette \u00e9tude est que les cellules infect\u00e9es portent de longs filopodes, des extensions filamenteuses et ramifi\u00e9es. Ces structures pourraient aider le virus \u00e0 atteindre des cellules avoisinantes dans le corps humain et faire progresser l\u2019infection, cependant des recherches suppl\u00e9mentaires seront n\u00e9cessaire pour valider cette hypoth\u00e8se.<\/p>\n\n\n\n

\u201cL\u2019embranchement consid\u00e9rable des filopodes d\u00e9montre encore une fois comment la compr\u00e9hension de la biologie des interactions virus-h\u00f4te peut mettre en lumi\u00e8re de potentiels points faibles de la maladie<\/em>\u201d, dit Nevan Krogan, Directeur de l\u2019Institut de Biosciences Quantitatives \u00e0 l\u2019UCSF et Chercheur Senior aux Instituts Gladstone.<\/p>\n\n\n\n

Vieux m\u00e9dicaments, nouveaux traitements<\/strong><\/h3>\n\n\n\n

\u201cLes kinases poss\u00e8dent certaines caract\u00e9ristiques structurales qui font d\u2019elles de bonnes cibles m\u00e9dicamenteuses. Certains m\u00e9dicaments ont d\u00e9j\u00e0 \u00e9t\u00e9 d\u00e9velopp\u00e9s pour cibler certaines des kinases que nous avons identifi\u00e9es. Nous encourageons donc d\u2019autres chercheurs \u00e0 tester les effets antiviraux de ces m\u00e9dicaments dans des essais cliniques<\/em>\u201d, dit Beltrao.<\/p>\n\n\n\n

Chez certains patients, le Covid-19 provoque une r\u00e9action excessive du syst\u00e8me immunitaire menant \u00e0 une inflammation. Un traitement optimal soulagerait ces sympt\u00f4mes inflammatoires tout en bloquant la r\u00e9plication du virus. Des m\u00e9dicaments existants ciblant l\u2019activit\u00e9 de certaines kinases pourraient permettre de r\u00e9soudre ces deux probl\u00e8mes.<\/p>\n\n\n\n

Les scientifiques ont identifi\u00e9 des dizaines de m\u00e9dicaments qui ciblent les kinases d\u2019int\u00e9r\u00eat et sont approuv\u00e9s par l\u2019agence am\u00e9ricaine des produits alimentaires et m\u00e9dicamenteux (Food and Drug Administration, FDA)  ou en cours  d\u2019essais cliniques. Sept de ces compos\u00e9s, principalement anti-cancer ou anti-inflammatoires, d\u00e9montrent des propri\u00e9t\u00e9s antivirales en laboratoire.<\/p>\n\n\n\n

\u201cNotre approche pour la d\u00e9couverte de m\u00e9dicaments a identifi\u00e9 un nouvel assortiment de m\u00e9dicaments qui offrent un grand potentiel pour combattre le Covid-19, soit individuellement ou en combinaison avec d\u2019autres m\u00e9dicaments, et nous sommes impatients de voir s\u2019ils vont contribuer \u00e0 mettre  fin \u00e0 la pand\u00e9mie<\/em>\u201d, dit Krogan.\u201cNous esp\u00e9rons consolider nos d\u00e9couvertes en testant de nombreux autres inhibiteurs de kinases, tout en identifiant les m\u00e9canismes mol\u00e9culaires de ces interactions et d’autres approches th\u00e9rapeutiques qui pourraient combattre efficacement le Covid-19<\/em>\u201d, dit Kevan Shokat, Professeur au d\u00e9partement de pharmacologie cellulaire et mol\u00e9culaire de l’UCSF.<\/p>\n\n\n\n

Funding<\/h4>\n\n\n\n

This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell <\/em>paper.<\/p>\n\n\n\n\n

Article source<\/h3>\n

BOUHADDOU, M., et al. (2020). The Global Phosphorylation Landscape of SARS-CoV-2 Infection. Cell<\/em>, Publi\u00e9 en ligne 28 juin, DOI: 10.1016\/j.cell.2020.06.034<\/a><\/p>\n<\/div>\n\n\n\n\n

Liens<\/h3>\n

La recherche du groupe de Pedro Beltrao<\/a>
Silencing the SARS-CoV-2 receptor with epigenetic modifications<\/a>
Understanding how SARS-CoV-2 behaves in the gut<\/a>
Investigating the structure and mechanisms of coronavirus biomolecules<\/a>
Quantitative Bioscience Institute Coronavirus Research Group<\/a><\/p>\n<\/div>\n\n\n

\n\n\n\n

Alcuni farmaci esistenti possono impedire l\u2019infezione da SARS-CoV-2<\/strong><\/h2>\n\n\n\n

I ricercatori hanno studiato come il nuovo coronavirus riprogramma la funzione delle proteine umane per potersi replicare, e hanno identificato diversi farmaci antivirali pronti per i test clinici<\/strong><\/h3>\n\n\n\n
\"SARS-CoV-2
The SARS-CoV-2 virus on a cell with long filopodia. Credit: Elizabeth Fischer, Microscopy Unit NIH\/NIAID<\/figcaption><\/figure>\n\n\n\n

Un team internazionale di ricercatori ha analizzato come SARS-CoV-2, il virus che causa COVID-19, dirotta il funzionamento delle proteine nelle sue cellule bersaglio. La ricerca, pubblicata sulla rivista Cell<\/em>, mostra come il virus modifica il funzionamento cellulare per potersi replicare ed infettare le cellule vicine. Gli scienziati hanno inoltre identificato sette farmaci, approvati per uso clinico, che potrebbero intercettare questi meccanismi, e ne raccomandano l\u2019immediato utilizzo per test clinici.<\/p>\n\n\n\n

La collaborazione ha coinvolto i ricercatori dell’Istituto Europeo di Bioinformatica dell’EMBL<\/a> (EMBL-EBI), il gruppo di ricerca Quantitative Biosciences Institute\u2019s Coronavirus Research Group della School of pharmacy dell’Universit\u00e0 di California a San Francisco (UCSF), l’Howard Hughes Medical Institute, l’Institut Pasteur e l’Universit\u00e0 di Friburgo.<\/p>\n\n\n\n

I virus non sono in grado di replicarsi e diffondersi da soli: hanno bisogno di un organismo – il loro ospite \u2013 che li trasporti, consenta loro di replicarsi e di trasmettersi ad altri ospiti. Per facilitare questo processo, i virus devono controllare il funzionamento della cellula ospite e manipolarlo per produrre nuove particelle virali. A volte, questo \u201cdirottamento\u201d interferisce con l’attivit\u00e0 degli enzimi dell’ospite e di altre proteine.<\/p>\n\n\n\n

Quando una proteina viene prodotta, gli enzimi possono modificare la sua attivit\u00e0 apportando modifiche chimiche alla sua struttura. Per esempio, la fosforilazione – l’aggiunta di un gruppo fosforilico a una proteina da parte di un tipo di enzima chiamato chinasi – gioca un ruolo fondamentale nella regolazione di molti processi cellulari, tra cui la comunicazione da cellula a cellula, la crescita e la morte cellulare. Alterando lo stato di fosforilazione delle proteine dell’ospite, un virus pu\u00f2 potenzialmente promuovere la propria trasmissione ad altre cellule ed eventualmente ad altri ospiti.<\/p>\n\n\n\n

Gli scienziati hanno utilizzato la spettrometria di massa, una tecnica che analizza le propriet\u00e0 di un campione misurando la massa delle sue molecole e dei suoi frammenti molecolari, per analizzare tutte le proteine dell’ospite e quelle virali che mostrano cambiamenti nella fosforilazione dopo l’infezione da SARS-CoV-2. L\u2019analisi ha rivelato che il 12% delle proteine dell’ospite che interagiscono con il virus vengono modificate. I ricercatori hanno anche identificato le chinasi che pi\u00f9 probabilmente regolano queste modifiche. Le chinasi sono potenziali bersagli farmacologici per fermare l’attivit\u00e0 del virus.<\/p>\n\n\n\n

Lo straordinario comportamento delle cellule infette<\/strong><\/h3>\n\n\n\n

“Il virus impedisce alle cellule umane di dividersi arrestandole in un punto preciso del ciclo cellulare. Questo fornisce al virus un ambiente relativamente stabile e adeguato per continuare a replicarsi”, spiega Pedro Beltrao, Group Leader di EMBL-EBI<\/a>.<\/p>\n\n\n\n

SARS-CoV-2 non solo ha un impatto sulla divisione cellulare, ma anche sulla forma delle cellule. Uno dei risultati chiave dello studio \u00e8 che le cellule infette presentano estensioni lunghe, ramificate, simili a braccia o filopodi<\/em>. Queste strutture possono aiutare il virus a raggiungere le cellule vicine nel corpo e a far progredire l’infezione, ma su questo aspetto saranno necessari ulteriori studi.<\/p>\n\n\n\n

“La visualizzazione dell’estesa ramificazione dei filopodi, ancora una volta, chiarisce come la comprensione della biologia dell’interazione virus-ospite possa fare luce su potenziali strategie terapeutiche nei confronti della malattia”, dice Nevan Krogan, direttore del Quantitative Biosciences Institute presso l’UCSF e Ricercatore Senior<\/em> presso i Gladstone Institutes<\/em>.<\/p>\n\n\n\n

Vecchi farmaci, nuovi trattamenti<\/strong><\/h3>\n\n\n\n

“Le chinasi possiedono alcune caratteristiche strutturali che le rendono bersagli farmacologici ideali. Sono gi\u00e0 stati sviluppati alcuni farmaci per colpire alcune delle chinasi che abbiamo identificato, quindi invitiamo i ricercatori clinici a testare gli effetti antivirali di questi farmaci nei loro studi”, dice Beltrao.<\/p>\n\n\n\n

In alcuni pazienti, COVID-19 provoca una reazione eccessiva del sistema immunitario, che porta all’infiammazione. Un trattamento ottimale dovrebbe quindi alleviare questi sintomi infiammatori eccessivi, arrestando la replicazione virale. I farmaci esistenti che interferiscono con l’attivit\u00e0 delle chinasi coinvolte potrebbero dunque essere la soluzione ad entrambi i problemi.<\/p>\n\n\n\n

I ricercatori hanno identificato decine di farmaci, gi\u00e0 approvati dalla Food and Drug Administration (FDA) o in corso di valutazione clinica, che prendono di mira le chinasi di interesse. Sette di questi composti, principalmente antitumorali e infiammatori, hanno mostrato una potente attivit\u00e0 antivirale nei test di laboratorio.<\/p>\n\n\n\n

“Il nostro approccio mirato alla scoperta di nuovi farmaci sulla base dei dati disponibili ad oggi, ha identificato una nuova serie di farmaci che hanno un grande potenziale per combattere il COVID-19, da soli o in combinazione con altri farmaci, e non vediamo l\u2019ora di sapere se saranno d’aiuto” dichiara Krogan.<\/p>\n\n\n\n

“Contiamo di proseguire in questa direzione testando molti altri inibitori delle chinasi, identificando al tempo stesso sia i meccanismi del loro funzionamento  che le potenziali terapie aggiuntive che possono intervenire efficacemente nel trattamento del COVID-19”, dice Kevan Shokat, professore del Dipartimento di Farmacologia Cellulare e Molecolare dell’UCSF.<\/p>\n\n\n\n

Funding<\/h4>\n\n\n\n

This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell <\/em>paper.<\/p>\n\n\n\n\n

Fonti<\/h3>\n

BOUHADDOU, M., et al. (2020). The Global Phosphorylation Landscape of SARS-CoV-2 Infection. Cell<\/em>, published online 28 June, DOI: 10.1016\/j.cell.2020.06.034<\/a><\/p>\n<\/div>\n\n\n\n\n

Related links<\/h3>\n

Research in the Beltrao Group<\/a>
Silencing the SARS-CoV-2 receptor with epigenetic modifications<\/a>
Understanding how SARS-CoV-2 behaves in the gut<\/a>
Investigating the structure and mechanisms of coronavirus biomolecules<\/a>
Quantitative Bioscience Institute Coronavirus Research Group<\/a><\/p>\n<\/div>\n\n\n

\n\n\n\n

Medicamentos existentes podr\u00edan prevenir que el SARS-CoV-2 infecte c\u00e9lulas<\/strong><\/h2>\n\n\n\n

Un grupo de cient\u00edficos eval\u00faa c\u00f3mo el nuevo coronavirus reorganiza prote\u00ednas humanas para replicarlas, e identifican varios f\u00e1rmacos antivirales listos para an\u00e1lisis cl\u00ednicos<\/strong><\/h3>\n\n\n\n
\"SARS-CoV-2
The SARS-CoV-2 virus on a cell with long filopodia. Credit: Elizabeth Fischer, Microscopy Unit NIH\/NIAID<\/figcaption><\/figure>\n\n\n\n

Un equipo de cient\u00edficos internacionales ha analizado c\u00f3mo el SARS-CoV-2, el virus que causa la enfermedad COVID-19, se apodera de las prote\u00ednas en las c\u00e9lulas objetivo. La investigaci\u00f3n, publicada en la revista cient\u00edfica Cell<\/em>, muestra c\u00f3mo el virus modifica la actividad celular para promover su r\u00e9plica y as\u00ed infectar c\u00e9lulas cercanas. Los investigadores tambi\u00e9n han identificado siete medicamentos ya aprobados que podr\u00edan perturbar dichos mecanismos, y recomiendan que se inicien los an\u00e1lisis cl\u00ednicos con esos medicamentos de inmediato. <\/p>\n\n\n\n

La colaboraci\u00f3n ha contado con investigadores del Instituto de Bioinform\u00e1tica Europeo<\/a> (EMBL-EBI), el grupo de investigaci\u00f3n en Coronavirus del Instituto de Biociencias Cuantitativas de la Universidad de California San Francisco (USCF), del Howard Hughes Medical Institute, del Instituto Pasteur y de la Universidad de Friburgo.<\/p>\n\n\n\n

Los virus no son capaces de reproducirse y propagarse independientemente: necesitan un organismo – el portador o hu\u00e9sped – para transportarse, replicarse y transmitirse a siguientes portadores. Para facilitar este proceso, los virus necesitan tomar el control del mecanismo celular de los portadores y manipularlo para producir nuevas part\u00edculas virales. A veces, esta toma de control interfiere en las enzimas y prote\u00ednas del hu\u00e9sped.   <\/p>\n\n\n\n

Cuando se produce una prote\u00edna, las enzimas pueden cambiar su actividad haciendo modificaciones qu\u00edmicas en su estructura. Por ejemplo, la fosforilaci\u00f3n – la adici\u00f3n de un grupo fosfato a una prote\u00edna a trav\u00e9s de una enzima llamada quinasa – juega un papel fundamental en la regulaci\u00f3n de varios procesos celulares, incluyendo la comunicaci\u00f3n entre c\u00e9lulas, el crecimiento celular y la muerte celular. Si se altera la fosforilaci\u00f3n en los patrones de las prote\u00ednas del portador, el virus puede, potencialmente, promover su propia transmisi\u00f3n a otras c\u00e9lulas y, con el tiempo, a otros portadores.   <\/p>\n\n\n\n

Los investigadores han usado la espectrometr\u00eda de masas, una herramienta para analizar las propiedades de una muestra midiendo la masa de sus mol\u00e9culas y de los fragmentos moleculares, para evaluar todas las prote\u00ednas del hu\u00e9sped y del virus que han mostrado cambios en la fosforilaci\u00f3n despu\u00e9s de una infecci\u00f3n de SARS-CoV-2. Los cient\u00edficos han visto que el 12% de las prote\u00ednas del portador que interactuaron con el virus hab\u00edan sido modificadas. Adem\u00e1s, los investigadores tambi\u00e9n han identificado las quinasas m\u00e1s propensas a regular esas modificaciones. Las quinasas son objetivos potenciales de los medicamentos para detener la actividad del virus y poder tratar la COVID-19. <\/p>\n\n\n\n

El comportamiento extraordinario de las c\u00e9lulas infectadas<\/strong><\/h3>\n\n\n\n

\u201cEl virus impide la divisi\u00f3n de c\u00e9lulas humanas y las mantiene en un punto concreto del ciclo celular. Esto proporciona al virus un entorno relativamente estable y adecuado para continuar replic\u00e1ndose\u201d, explica Pedro Beltrao, Investigador Principal del EMBL-EBI<\/a>.<\/p>\n\n\n\n

El SARS-CoV-2 no s\u00f3lo afecta a la divisi\u00f3n celular, sino que tambi\u00e9n influye en la forma celular. Uno de los descubrimientos clave de este estudio es que las c\u00e9lulas infectadas muestran largas extensiones ramificadas, o filopodios. Estas estructuras podr\u00edan ayudar al virus a alcanzar c\u00e9lulas cercanas y expandir la infecci\u00f3n, aunque se necesitar\u00eda un estudio m\u00e1s a fondo de esta cuesti\u00f3n.<\/p>\n\n\n\n

\u201cEsta visualizaci\u00f3n tan espec\u00edfica de las extensiones ramificadas de los filopodios dilucida la comprensi\u00f3n biol\u00f3gica entre la interacci\u00f3n virus-portador y ayuda a identificar posibles puntos de intervenci\u00f3n en la enfermedad\u201d, dice Nevan Krogan, Director del Instituto de Biociencias Cuantitativas de la UCSF e Investigador Senior del Gladstone Institutes. <\/p>\n\n\n\n

Medicamentos antiguos, tratamientos nuevos<\/strong><\/h3>\n\n\n\n

\u201cLas quinasas poseen ciertas caracter\u00edsticas estructurales que las hacen buenos objetivos para medicamentos. Algunos medicamentos ya fueron desarrollados para atacar algunas de las quinasas que hemos identificado. Por ese motivo instamos a los investigadores cl\u00ednicos a que prueben los efectos antivirales de esos medicamentos en sus ensayos\u201d, dice Beltrao. <\/p>\n\n\n\n

En algunos pacientes, la COVID-19 causa una reacci\u00f3n excesiva del sistema inmune, que conduce a inflamaci\u00f3n. Un tratamiento ideal deber\u00eda aliviar estos s\u00edntomas inflamatorios al mismo tiempo que detiene la reproducci\u00f3n del virus. Los f\u00e1rmacos existentes que interfieren con la actividad de las quinasas podr\u00edan ser la soluci\u00f3n a ambos problemas. <\/p>\n\n\n\n

Los investigadores han encontrado docenas de f\u00e1rmacos aprobados por la Food and Drug Administration (FDA) o ensayos cl\u00ednicos en curso que tienen c\u00f3mo objetivo las quinasas de inter\u00e9s. Siete de esos compuestos, principalmente compuestos anticancer\u00edgenos y antiinflamatorios, han demostrado una actividad antiviral potente en experimentos de laboratorio. <\/p>\n\n\n\n

\u201cNuestro enfoque basado en datos para el descubrimiento de f\u00e1rmacos ha identificado siete nuevos f\u00e1rmacos que tienen gran potencial para luchar contra la COVID-19, ya sea individualmente o en combinaci\u00f3n con otros medicamentos, y estamos entusiasmados por saber si podr\u00e1n ser de ayuda para acabar con esta pandemia\u201d, dice Krogan. <\/p>\n\n\n\n

\u201cEsperamos poder continuar trabajando en este estudio, probando otros inhibidores de quinasas al tiempo que identificamos su funcionamiento y otras terapias potenciales que podr\u00edan intervenir en la COVID-19 de manera eficaz\u201d, dice Kevan Shokat, Profesor del Departamento de Farmacolog\u00eda Celular y Molecular de la UCSF.<\/p>\n\n\n\n

Funding<\/h4>\n\n\n\n

This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell <\/em>paper.<\/p>\n\n\n\n\n

Source article<\/h3>\n

BOUHADDOU, M., et al. (2020). The Global Phosphorylation Landscape of SARS-CoV-2 Infection. Cell<\/em>, published online 28 June, DOI: 10.1016\/j.cell.2020.06.034<\/a><\/p>\n<\/div>\n\n\n\n\n

Related links<\/h3>\n

Research in the Beltrao Group<\/a>
Silencing the SARS-CoV-2 receptor with epigenetic modifications<\/a>
Understanding how SARS-CoV-2 behaves in the gut<\/a>
Investigating the structure and mechanisms of coronavirus biomolecules<\/a>
Quantitative Bioscience Institute Coronavirus Research Group<\/a><\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

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