Publication date: Jan 07, 2025
In the last years, it has been proved that some viruses are able to re-structure chromatin organization and alter the epigenomic landscape of the host genome. In addition, they are able to affect the physical mechanisms shaping chromatin 3D structure, with a consequent impact on gene activity. Here, we investigate with polymer physics genome re-organization of the host genome upon SARS-CoV-2 viral infection and how it can impact structural variability within the population of single-cell chromatin configurations. Using published Hi-C data and molecular dynamics simulations, we build ensembles of 3D configurations representing single-cell chromatin conformations in control and SARS-CoV-2 infected conditions. We focus on genomic length scales of TADs and consider, as a case study, models of real loci containing DDX58 and IL6 genes, belonging, respectively, to the antiviral interferon response and pro-inflammatory genes. Clustering analysis applied to the ensemble of polymer configurations reveals a generally increased variability and a more heterogeneous population of 3D structures in infected conditions. This points toward a scenario in which viral infection leads to a loss of chromatin structural specificity with, likely, a consequent impact on the correct regulation of host cell genes.
Concepts | Keywords |
---|---|
Antiviral | Chromatin |
Genome | Chromatin |
Models | COVID-19 |
Physics | Genome, Human |
Viral | Humans |
Molecular Dynamics Simulation | |
Polymers | |
Polymers | |
SARS-CoV-2 |
Semantics
Type | Source | Name |
---|---|---|
disease | MESH | viral infection |
pathway | REACTOME | Chromatin organization |
disease | IDO | host |
disease | IDO | cell |
disease | MESH | COVID-19 |