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Source: SARS-CoV-2 Induces Human Epigenomic Reprogramming  Jul 23, 2021  2 years, 8 months, 3 weeks, 4 days, 19 hours, 5 minutes ago

BREAKING! University Of Texas Study Discovers That SARS-CoV-2 Alters Human Host Chromatin Complex To Cause Immune Dysfunction!

BREAKING! University Of Texas Study Discovers That SARS-CoV-2 Alters Human Host Chromatin Complex To Cause Immune Dysfunction!
Source: SARS-CoV-2 Induces Human Epigenomic Reprogramming  Jul 23, 2021  2 years, 8 months, 3 weeks, 4 days, 19 hours, 5 minutes ago
An alarming study finding of a recent research conducted by scientist from the University of Texas Science Center, Houston-USA, has revealed that upon infection, the SARS-CoV-2 coronavirus alters the host chromatin architecture to suppress antiviral interferon-responsive genes and augment inflammatory genes. The process that SARS-CoV-2 deploys is similar to what can be termed as epigenomic reprogramming, says the study team.

 
Such altering of the human chromatin also has serious concerning implications about a variety of possible medical and health conditions rising in the long term of those who have been infected with the SARS-CoV-2 coronavirus.
 
There is however no data as yet available indicating if simply spike proteins from the SARS-CoV-2 alone can induce these epigenomic reprogramming  changes alone.(It should noted that the virus spike proteins are being used in a variety of vaccines at the moment.)
 
Numerous viruses can significantly alter host chromatin, but such roles of the SARS-CoV-2 are largely unknown until now.
 
The study team characterized the three-dimensional (3D) genome architecture and epigenome landscapes in human cells after SARS-CoV-2 infection, revealing remarkable restructuring of host chromatin architecture.

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High-resolution Hi-C 3.0 uncovered widespread A compartmental weakening and A-B mixing, together with a global reduction of intra-TAD chromatin contacts. The cohesin complex, a central organizer of the 3D genome, was significantly depleted from intra-TAD regions, supporting that SARS-CoV-2 disrupts cohesin loop extrusion. Calibrated ChIP-Seq verified chromatin restructuring by SARS-CoV-2 that is particularly manifested by a pervasive reduction of euchromatin modifications. Built on the rewired 3D genome/epigenome maps, a modified activity-by-contact model highlights the transcriptional weakening of antiviral interferon response genes or virus sensors (e.g., DDX58) incurred by SARS-CoV-2.
 
On the other hand, pro-inflammatory genes (e.g. IL-6) high in severe infections were uniquely regulated by augmented H3K4me3 at their promoters.
 
The study findings illustrate how the SARS-CoV-2 coronavirus  rewires host chromatin architecture to confer immunological gene deregulation, laying a foundation to characterize the long-term epigenomic impacts of this virus.
 
The study findings were published on a preprint server and are currently being peer reviewed. https://www.biorxiv.org/content/10.1101/2021.07.20.453146v1
 
The SARS-CoV-2 coronavirus, the causative pathogen of COVID-19 disease, is an enveloped, positive-sense, single-stranded RNA virus that primarily attacks epithelial cells in the human resp iratory 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.
 
It is  however equally important to understand how SARS-CoV-2 modulates the host chromatin network to facilitate immune evasion and induce persistent clinical consequences.
 
It is already known that the entire mammalian chromatin network contains several layers of architectures, inc