Communications Biology (Jul 2022)
A model for network-based identification and pharmacological targeting of aberrant, replication-permissive transcriptional programs induced by viral infection
- Pasquale Laise,
- Megan L. Stanifer,
- Gideon Bosker,
- Xiaoyun Sun,
- Sergio Triana,
- Patricio Doldan,
- Federico La Manna,
- Marta De Menna,
- Ronald B. Realubit,
- Sergey Pampou,
- Charles Karan,
- Theodore Alexandrov,
- Marianna Kruithof-de Julio,
- Andrea Califano,
- Steeve Boulant,
- Mariano J. Alvarez
Affiliations
- Pasquale Laise
- DarwinHealth Inc
- Megan L. Stanifer
- Department of Infectious Diseases, Molecular Virology, Heidelberg University Hospital
- Gideon Bosker
- DarwinHealth Inc
- Xiaoyun Sun
- DarwinHealth Inc
- Sergio Triana
- Structural and Computational Biology Unit, European Molecular Biology Laboratory
- Patricio Doldan
- Department of Infectious Diseases, Virology, Heidelberg University Hospital
- Federico La Manna
- Department for BioMedical Research, Urology Research Laboratory, University of Bern
- Marta De Menna
- Department for BioMedical Research, Urology Research Laboratory, University of Bern
- Ronald B. Realubit
- Department of Systems Biology, Columbia University Irving Medical Center
- Sergey Pampou
- Department of Systems Biology, Columbia University Irving Medical Center
- Charles Karan
- Department of Systems Biology, Columbia University Irving Medical Center
- Theodore Alexandrov
- Structural and Computational Biology Unit, European Molecular Biology Laboratory
- Marianna Kruithof-de Julio
- Department for BioMedical Research, Urology Research Laboratory, University of Bern
- Andrea Califano
- Department of Systems Biology, Columbia University Irving Medical Center
- Steeve Boulant
- Department of Molecular Genetics and Microbiology, University of Florida, College of Medicine
- Mariano J. Alvarez
- DarwinHealth Inc
- DOI
- https://doi.org/10.1038/s42003-022-03663-8
- Journal volume & issue
-
Vol. 5,
no. 1
pp. 1 – 12
Abstract
Master Regulator proteins, controlling the transcriptional identity of infected cells, can serve as drug targets for inhibiting virus replication, here demonstrated in a SARSCoV-2 infection model.
