When 3D genome technology meets viral infection, including SARS‐CoV‐2

Abstract

Mammalian chromosomes undergo varying degrees of compression to form three‐dimensional genome structures. These three‐dimensional structures undergo dynamic and precise chromatin interactions to achieve precise spatial and temporal regulation of gene expression. Most eukaryotic DNA viruses can invade their genomes into the nucleus. However, it is still poorly understood how the viral genome is precisely positioned after entering the host cell nucleus to find the most suitable location and whether it can specifically interact with the host genome to hijack the host transcriptional factories or even integrate into the host genome to complete its transcription and replication rapidly. Chromosome conformation capture technology can reveal long‐range chromatin interactions between different chromosomal sites in the nucleus, potentially providing a reference for viral DNA‐host chromatin interactions. This review summarized the research progress on the three‐dimensional interaction between virus and host genome and the impact of virus integration into the host genome on gene transcription regulation, aiming to provide new insights into chromatin interaction and viral gene transcription regulation, laying the foundation for the treatment of infectious diseases.

Multi-omics analysis reveals the dynamic interplay between Vero host chromatin structure and function during vaccinia virus infection

“…The architecture of the genome, including its compartmentalization, chromatin contacts, conformation, and accessibility, is as fundamental to understanding the function of a particular genomic locus as its sequence. Indeed, investigation of 3D chromatin structure may be paramount to deciphering disease-states, aberrant cellular behavior, and the impact of environmental perturbations, including pathogen exposures, all of which have functional implications, including dysregulation of gene expression 13 , 47 – 50 . Further, pathogen-induced changes in host chromatin features may have far-reaching implications for development of appropriate and efficacious counter measures including vaccine development.…”

Vaccinia virus infection induces concurrent alterations in host chromatin architecture, accessibility, and gene expression

“…The architecture of the genome, including its compartmentalization, chromatin contacts, conformation, and accessibility, is as fundamental to understanding the function of a particular genomic loci as its sequence. Indeed, investigation of 3D chromatin structure may be paramount to deciphering disease-states, aberrant cellular behavior, and the impact of environmental perturbations, including pathogen exposures, all of which have functional implications, including dysregulation of gene expression 13,47–50 . Further, pathogen-induced changes in host chromatin features may have far-reaching implications for development of appropriate and efficacious countermeasures including vaccine development.…”

Genome-wide chromatin interaction profiling reveals a vital role of super-enhancers and rearrangements in host enhancer contacts during BmNPV infection

“…This study is the first to identify SEs in the silkworm and reveal their roles in vital biological processes, which expand the knowledge of SEs in insects. Nevertheless, considering the robust activating ability of SEs and the close relation between enhancer–gene contacts and the variable chromatin state in diverse conditions ( Dawson and Kouzarides 2012 ; Jia et al 2017 ; Li et al 2018 , 2019 ; Sun et al 2018 ; Zhang and Cao 2019 ; Braga et al 2020 ; Chang et al 2020b ; Vidaurre and Chen 2021 ; Liang et al 2022 ), the dynamic changes of the enhancer regulatory network and the roles of SEs in insect disease, development, sex determination, and biological and abiotic stresses remain to be further investigated. In mammalian cells, the regulatory pattern of SEs is different from that of TEs ( Whyte et al 2013 ; Sabari et al 2018 ).…”

“…In eukaryotic cells, the genome is dynamic and nonrandomly organized in the nucleus. Therefore, the chromatin epigenomic signatures and three-dimensional (3D) architecture are dynamically remodeled during different processes or under different conditions, such as embryonic development ( Li et al 2018 ; Li et al 2019 ), cell differentiation ( Vidaurre and Chen 2021 ), aging ( Sun et al 2018 ; Braga et al 2020 ), carcinogenesis ( Dawson and Kouzarides 2012 ; Jia et al 2017 ), abiotic stress ( Chang et al 2020b ), and pathogen infection ( Zhang and Cao 2019 ; Liang et al 2022 ). Consequently, the interaction regulatory network between enhancers and their target genes varies under diverse circumstances, making it possible to adjust the expression of genes with specific functions spatially and temporally to adapt to the changing status.…”