Epigenome reprogramming after SARS-CoV-2 infection Chromatin SARSCoV2 Coronavirus Disease COVID NatureMicrobiol UTHealthHouston MDAndersonNews SanDiegoBiomed
By Neha MathurMar 27 2023Reviewed by Lily Ramsey, LLM In a recent article in published in the journal Nature Microbiology, researchers in Texas, United States performed a three-dimensional evaluation of severe acute respiratory syndrome coronavirus 2 infected human cells to show a direct cell-autonomous effect elicited by SARS-CoV-2 on the host chromatin.
The A and B compartments superimpose transcriptionally active euchromatin and relatively inactive heterochromatin, respectively. However, studies have barely investigated these effects. In addition, the team evaluated the epigenetic features of the altered chromatin regions to understand the vulnerability to compartmental changes due to infection. To this end, they used chromatin immunoprecipitation methods to generate data on representative histone markers and polymerase II in A549-ACE2 cells. This analysis covered four histone markers, viz., H3K27ac, H3K4me3, H3K9me3, and H3K27me3.
Further, a P curve showed that SARS-CoV-2 elicited modest and enhanced interactions in middle-to-long-distance contacts and far-positioned regions, respectively. Further analysis showed that the 'B-ing' and 'A-ing' genomic regions were historically enriched in active chromatin markers and repressive histone markers, especially H3K27me3. Unexpectedly, SARS-CoV-2 infection selectively modified the H3K4me3 marker of phytochrome interacting factors gene promoters, suggesting unappreciated mechanisms at these promoters that confer deviating inflammation in COVID-19.
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