SARS-CoV-2 reprograms host chromatic network to induce immune dysfunction
A recent study conducted at the University of Texas Science Center, Houston, in the USA, has revealed that upon infection, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) alters the host chromatin architecture to suppress antiviral interferon-responsive genes and augment inflammatory genes. The study is currently available on the bioRxiv* preprint server.
SARS-CoV-2, the causative pathogen of coronavirus disease 2019 (COVID-19), is an enveloped, positive-sense, single-stranded RNA virus that primarily attacks epithelial cells in the human respiratory tract. From the perspective of viral evolution, it is well known that mutations appearing in SARS-CoV-2 spike protein under positive selection pressure are primarily responsible for increasing viral fitness into host cells. However, it is equally important to understand how SARS-CoV-2 modulates the host chromatin network to facilitate immune evasion and induce persistent clinical consequences.
The entire mammalian chromatin network contains several layers of architectures, including A/B compartments, Topological Associating Domains (TADs), and chromatin loops, which collectively regulate vital nuclear functions, including gene transcription, replication, recombination, and DNA damage repair.
In the current study, the scientists have investigated how SARS-CoV-2 affects the three-dimensional …
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