Crosstalk between Hepatitis B Virus and the 3D Genome Structure

Dias, João Diogo; Sarica, Nazim; Cournac, Axel; Koszul, Romain; Neuveut, Christine

doi:10.3390/v14020445

Cited by 9 publications

(8 citation statements)

References 107 publications

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“…However, for HPV, HBV, and HTLV-1, insertion-induced changes in chromatin organization are becoming increasingly evident [19,[24][25][26]. The HBV, EBV, HPV, and HTLV-1 genomes contain binding sites for the transcriptional repressor and chromatin regulator CCCTC-binding factor (CTCF) [26,[73][74][75], which mediates the formation of loops in the human genome and establishes boundaries between hetero-and euchromatin [76]. Chromosome conformation capture (Hi-C) studies on human cervical cancer biopsies harboring HPV integrations into the RIG CCDC106, as well as HPV provirusharboring cell lines, showed changes within host genomic topologically associating domains (TADs) as well as altered TAD borders in the vicinity of the integration site [25,77,78].…”

Section: Box 1 Chromatin Remodeling Resulting From Viral Integrationmentioning

confidence: 99%

Potential multi-modal effects of provirus integration on HIV-1 persistence: lessons from other viruses

Linden

Jones

2022

Trends in Immunology

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Section: Box 1 Chromatin Remodeling Resulting From Viral Integrationmentioning

confidence: 99%

Potential multi-modal effects of provirus integration on HIV-1 persistence: lessons from other viruses

Linden

Jones

2022

Trends in Immunology

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“…Notably, inactivation of p53 also suppresses the p53-driven stress response (129). Other viruses such as HTLV-I and HBV express "promiscuous transactivators" that empower specific TFs and chromatin modifiers typically acting at active promoters and enhancers, respectively (134)(135)(136)(137). Yet other viruses, such as influenza A virus (IAV), inhibit transcription termination, and ensuing readthrough transcription over extended chromatin segments exerts itself the ProA antisilencing function, switching entire domains from B to A (138).…”

Section: Viruses Drive Global Genome Opening By Switching or Tuning S...mentioning

confidence: 99%

ProA and ProB repeat sequences shape genome organization, and enhancers open domains

Bonnet,

Hulo,

Mourad

et al. 2023

Preprint

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SUMMARYThere is a growing awareness that repeat sequences (RepSeq) - the main constituents of the human genome - are also prime players in its organization. Here we propose that the genome should be envisioned as a supersystem with three main subsystems, each composed of functionally redundant, cooperating elements. We define herein ProA and ProB RepSeqs as sequences that promote either the A/euchromatin or the B/heterochromatin compartment. ProA and ProB RepSeqs shape A/B partitioning, such that the relative proportions of ProA and ProB RepSeqs determine the propensity of a chromosome segment to adopt either an A or a B configuration. In human, core ProA RepSeqs are essentially made of Alu elements, whereas core ProB RepSeqs consist of young L1 and some Endogenous Retroviruses (ERVs) as well as a panel of AT-rich microsatellites and pericentromeric and telomeric satellites. Additionally, RepSeqs with more indefinite character and, importantly, their derivatives known as “transcriptional enhancers”, can shift between ProA and ProB functions and thus act to open or close specific chromatin domains depending on the cellular context. In this framework, genes and their promoters appear as a special class of RepSeqs that, in their active, transcribed state, reinforce the openness of their surroundings. Molecular mechanisms involve cooperativity between ProB elements, presumably underpinned by the condensate-like properties of heterochromatin, which ProA elements oppose in several ways. We provide strong arguments that altered CpG methylation patterns in cancer including a marked loss in the B compartment, result primarily from a global imbalance in the process of CpG methylation and its erasure. Our results suggest that the resulting altered methylation and impaired function of ProB RepSeqs globally weaken the B compartment, rendering it more plastic, which in turn may confer fate plasticity to the cancer cell.

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“…It cannot only directly influence the gene expression by integrated into the proximal locus of the target gene 69 , 70 , 71 , 72 but also perform a function by distal interaction or disrupting the 3D genome structure. 73 , 74 , 75 , 76 …”

Section: D Genome and Common Virus Infectionmentioning

confidence: 99%

“…All in all, HBV can affect the host gene expression by various mechanisms. It cannot only directly influence the gene expression by integrated into the proximal locus of the target gene 69–72 but also perform a function by distal interaction or disrupting the 3D genome structure 73–76 …”

Section: D Genome and Common Virus Infectionmentioning

confidence: 99%

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

Liang

Wang

Wang³

et al. 2022

Journal of Medical Virology

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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.

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Crosstalk between Hepatitis B Virus and the 3D Genome Structure

Cited by 9 publications

References 107 publications

Potential multi-modal effects of provirus integration on HIV-1 persistence: lessons from other viruses

Potential multi-modal effects of provirus integration on HIV-1 persistence: lessons from other viruses

ProA and ProB repeat sequences shape genome organization, and enhancers open domains

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

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