An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks

Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and epigenet...

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Autores principales: Jenny Paola Alfaro-García, María Camila Granados-Alzate, Miguel Vicente-Manzanares, Juan Carlos Gallego-Gómez
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/cc05584a1b6043d4818ede378cc49fe1
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spelling oai:doaj.org-article:cc05584a1b6043d4818ede378cc49fe12021-11-25T17:08:12ZAn Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks10.3390/cells101128632073-4409https://doaj.org/article/cc05584a1b6043d4818ede378cc49fe12021-10-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2863https://doaj.org/toc/2073-4409Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and epigenetic changes that expand the tumorigenic program, including modifications to the ability of cancer cells to migrate. The best-characterized group of changes is collectively known as the epithelial–mesenchymal transition, or EMT. This is a complex phenomenon classically described using biochemistry, cell biology and genetics. However, these methods require enormous, often slow, efforts to identify and validate novel therapeutic targets. Systems biology can complement and accelerate discoveries in this field. One example of such an approach is Boolean networks, which make complex biological problems tractable by modeling data (“nodes”) connected by logical operators. Here, we focus on virus-induced cellular plasticity and cell reprogramming in mammals, and how Boolean networks could provide novel insights into the ability of some viruses to trigger uncontrolled cell proliferation and EMT, two key hallmarks of cancer.Jenny Paola Alfaro-GarcíaMaría Camila Granados-AlzateMiguel Vicente-ManzanaresJuan Carlos Gallego-GómezMDPI AGarticlecellular plasticityepithelial–mesenchymal transitionsystems biologyBooleanviral infectionBiology (General)QH301-705.5ENCells, Vol 10, Iss 2863, p 2863 (2021)
institution DOAJ
collection DOAJ
language EN
topic cellular plasticity
epithelial–mesenchymal transition
systems biology
Boolean
viral infection
Biology (General)
QH301-705.5
spellingShingle cellular plasticity
epithelial–mesenchymal transition
systems biology
Boolean
viral infection
Biology (General)
QH301-705.5
Jenny Paola Alfaro-García
María Camila Granados-Alzate
Miguel Vicente-Manzanares
Juan Carlos Gallego-Gómez
An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
description Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and epigenetic changes that expand the tumorigenic program, including modifications to the ability of cancer cells to migrate. The best-characterized group of changes is collectively known as the epithelial–mesenchymal transition, or EMT. This is a complex phenomenon classically described using biochemistry, cell biology and genetics. However, these methods require enormous, often slow, efforts to identify and validate novel therapeutic targets. Systems biology can complement and accelerate discoveries in this field. One example of such an approach is Boolean networks, which make complex biological problems tractable by modeling data (“nodes”) connected by logical operators. Here, we focus on virus-induced cellular plasticity and cell reprogramming in mammals, and how Boolean networks could provide novel insights into the ability of some viruses to trigger uncontrolled cell proliferation and EMT, two key hallmarks of cancer.
format article
author Jenny Paola Alfaro-García
María Camila Granados-Alzate
Miguel Vicente-Manzanares
Juan Carlos Gallego-Gómez
author_facet Jenny Paola Alfaro-García
María Camila Granados-Alzate
Miguel Vicente-Manzanares
Juan Carlos Gallego-Gómez
author_sort Jenny Paola Alfaro-García
title An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
title_short An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
title_full An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
title_fullStr An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
title_full_unstemmed An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks
title_sort integrated view of virus-triggered cellular plasticity using boolean networks
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/cc05584a1b6043d4818ede378cc49fe1
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