The epigenetic landscapes of histone modifications on HSV-1 genome in human THP-1 cells

Gao, Chuan; Chen, Lin; Tang, Shan-Bo; Long, Qiaoyun; He, Jiali; Zhang, Na-An; Shu, Hong‐Bing; Chen, Zhenxia; Wu, Min; Li, Lianyun

doi:10.1016/j.antiviral.2020.104730

Cited by 12 publications

(21 citation statements)

References 32 publications

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“…A series of recent publications have started to provide evidence that the HSV-1 DNA is uniquely chromatinized and regulated by somewhat different epigenetic mechanisms than most cellular DNA ( Table 1 ). ChIP-seq was used to map the interactions between HSV-1 DNA and total histone H3, or H3 with specific PTM characteristic of transcription or silencing ( Gao et al, 2020 ). The levels of viral DNA that co-immunoprecipitated with total H3, or with H3 with the different PTM, varied with infection time.…”

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

“…Early in infection, from 1 to 2 h, the interactions with histone H3 bearing PTM associated with non-transcribed genes, such as H3K27me3 and H3K9me3, were enriched, while those associated with transcribed genes, like H3K27ac, were depleted. The former two PTM were relatively depleted later on, from 8 to 12 h, to be replaced with PTM characteristic of highly transcribed genes, such as H3K27ac or, to a lesser extent, H3K4me3 ( Gao et al, 2020 ).…”

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

“…In contrast, and as expected, the PTM on the cellular genome correlated with other PTM characteristic of the same transcription state and counter-correlated with those of the opposed transcription state. Transcription and PTM levels in any HSV-1 gene resolved and clustered according to time after infection, not individual gene transcription level ( Gao et al, 2020 ). The changes in the histone PTM thus occur synchronously through the entire HSV-1 genome, and regardless of the levels of transcription of any individual gene, as the infection progresses.…”

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

“…ATAC-seq or MCN protection assays have also shown no preferential accessibility to transcribed over non-transcribed genes ( Dremel and DeLuca, 2019 ; McSwiggen et al, 2019 ), and ChIP-seq has shown no good correlation between specific histone PTM and the level of transcription of a given gene, but rather global changes in PTMs along the entire viral genomes that correlate with the global level of transcription of the genomes ( Dremel and DeLuca, 2019 ; Gao et al, 2020 ). Using high resolution imaging, Dr. O’Hare has shown that the HSV-1 genomes must decondense for transcription to occur ( Sekine et al, 2017 ), which is consistent with them becoming competent by increased chromatin dynamics.…”

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

“…8 ) ( Hu et al, 2019 ); recently reviewed in ( Kobiler and Afriat, 2021 ). These dynamics themselves appear to be in part determined by global enrichment in particular PTM in the viral chromatin, in that the PTM change along infection as HSV-1 DNA accessibility does ( Gao et al, 2020 ; Hu et al, 2019 ).…”

Section: The Unique Characteristics Of the Hsv-1 Chromatin And Its Epigenetic Regulation Indicate A Potential Role For Epigenetic Targetsmentioning

confidence: 99%

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Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy

Schang

Cortes

et al. 2021

Antiviral Research

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The ability to establish, and reactivate from, latent infections is central to the biology and pathogenesis of HSV-1. It also poses a strong challenge to antiviral therapy, as latent HSV-1 genomes do not replicate or express any protein to be targeted. Although the processes regulating the establishment and maintenance of, and reactivation from, latency are not fully elucidated, the current general consensus is that epigenetics play a major role. A unifying model postulates that whereas HSV-1 avoids or counteracts chromatin silencing in lytic infections, it becomes silenced during latency, silencing which is somewhat disrupted during reactivation. Many years of work by different groups using a variety of approaches have also shown that the lytic HSV-1 chromatin is distinct and has unique biophysical properties not shared with most cellular chromatin. Nonetheless, the lytic and latent viral chromatins are typically enriched in post translational modifications or histone variants characteristic of active or repressed transcription, respectively. Moreover, a variety of small molecule epigenetic modulators inhibit viral replication and reactivation from latency. Despite these successes in culture and animal models, it is not obvious how epigenetic modulation would be used in antiviral therapy if the same epigenetic mechanisms governed viral and cellular gene expression. Recent work has highlighted several important differences between the viral and cellular chromatins, which appear to be of consequence to their respective epigenetic regulations. In this review, we will discuss the distinctiveness of the viral chromatin, and explore whether it is regulated by mechanisms unique enough to be exploited in antiviral therapy.

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Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

Section: Uniqueness Of the Hsv-1 Chromatinmentioning

confidence: 99%

Section: The Unique Characteristics Of the Hsv-1 Chromatin And Its Epigenetic Regulation Indicate A Potential Role For Epigenetic Targetsmentioning

confidence: 99%

See 3 more Smart Citations