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

ABSTRACT: 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., SARSCoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and...

Full description

Autores:
Granados Alzate, María Camila
Alfaro García, Jenny Paola
Gallego Gómez, Juan Carlos
Vicente Manzanares, Miguel
Tipo de recurso:
Review article
Fecha de publicación:
2021
Institución:
Universidad de Antioquia
Repositorio:
Repositorio UdeA
Idioma:
eng
OAI Identifier:
oai:bibliotecadigital.udea.edu.co:10495/45426
Acceso en línea:
https://hdl.handle.net/10495/45426
Palabra clave:
Cell Plasticity
Plasticidad de la Célula
Cellular Reprogramming
Reprogramación Celular
Epithelial-Mesenchymal Transition
Transición Epitelial-Mesenquimal
Gene Regulatory Networks
Redes Reguladoras de Genes
Neoplasms
Neoplasias
Systems Biology
Biología de Sistemas
Virus Diseases
Virosis
Viruses
Virus
https://id.nlm.nih.gov/mesh/D014780
https://id.nlm.nih.gov/mesh/D000066670
https://id.nlm.nih.gov/mesh/D065150
https://id.nlm.nih.gov/mesh/D058750
https://id.nlm.nih.gov/mesh/D053263
https://id.nlm.nih.gov/mesh/D009369
https://id.nlm.nih.gov/mesh/D049490
https://id.nlm.nih.gov/mesh/D014777
Rights
openAccess
License
https://creativecommons.org/licenses/by/4.0/
Description
Summary:ABSTRACT: 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., SARSCoV-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.