Loss of structural specificity in 3D genome organization upon viral infection is predicted by polymer physics.

Loss of structural specificity in 3D genome organization upon viral infection is predicted by polymer physics.

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

Original Article

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