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HSV1感染中的表观遗传调控机制研究进展

吴长静 邹雨芳 黄新伟

吴长静, 邹雨芳, 黄新伟. HSV1感染中的表观遗传调控机制研究进展[J]. 昆明医科大学学报, 2024, 45(1): 172-178. doi: 10.12259/j.issn.2095-610X.S20240129
引用本文: 吴长静, 邹雨芳, 黄新伟. HSV1感染中的表观遗传调控机制研究进展[J]. 昆明医科大学学报, 2024, 45(1): 172-178. doi: 10.12259/j.issn.2095-610X.S20240129
Changjing WU, Yufang ZOU, Xinwei HUANG. Advances in Epigenetic Regulatory Mechanisms in HSV1 Infection[J]. Journal of Kunming Medical University, 2024, 45(1): 172-178. doi: 10.12259/j.issn.2095-610X.S20240129
Citation: Changjing WU, Yufang ZOU, Xinwei HUANG. Advances in Epigenetic Regulatory Mechanisms in HSV1 Infection[J]. Journal of Kunming Medical University, 2024, 45(1): 172-178. doi: 10.12259/j.issn.2095-610X.S20240129

HSV1感染中的表观遗传调控机制研究进展

doi: 10.12259/j.issn.2095-610X.S20240129
基金项目: 国家自然科学基金资助项目(82260486)
详细信息
    作者简介:

    吴长静(1999~),女,山东德州人,在读硕士研究生,主要从事病毒感染机制研究工作

    通讯作者:

    黄新伟,E-mail:532768282@qq.com

  • 中图分类号: R392.9

Advances in Epigenetic Regulatory Mechanisms in HSV1 Infection

  • 摘要: 1型单纯疱疹病毒(HSV1)是一类最为常见的人类传染病原体,感染后可导致一系列程度不同的疾病。HSV1在中枢神经系统的潜伏感染及偶发重激活是其病理发生的关键,也为抗病毒治疗带来了巨大的挑战。目前,关于HSV1感染的建立、维持和重激活的机制并未完全阐明,但普遍认为表观遗传调控可能在其中扮演重要作用。越来越多研究表明,病毒裂解期和潜伏感染期的基因组呈现不同的染色质结构,其富含的多种翻译后修饰组蛋白赋予病毒基因转录激活或抑制特征。此外,病毒潜伏相关转录本LATs也可能参与基因组表观遗传修饰调控。
  • 图  1  HSV1基因的级联表达和表观修饰

    VP16:病毒蛋白16;IE:即早期基因;E:早期基因;L:晚期基因UL:基因组长片段区;US:基因组短片段区;RL:长片段重复区;RS:短片段重复区;图片来源于Figdraw[2]

    Figure  1.  Cascade expression and epigenetic modification of HSV1 gene

    图  2  LAT上CTCF结合位点和LAT的表观调控

    CTCF结合位点,包括CTRL1,CTRL2,CTa’ m,CTRS1,CTRS2,CTRS3与CTUS1[42]

    Figure  2.  CTCF binding sites and epigenetic regulation of LAT on LAT

  • [1] Arduino P G,Porter S R. Herpes simplex virus type 1 infection: Overview on relevant clinico-pathological features[J]. Journal of Oral Pathology & Medicine:Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology,2008,37(2):107-121.
    [2] Schang L M,Hu M,Cortes E F,et al. Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy[J]. Antiviral Research,2021,192(1):105103-105139.
    [3] Steiner I,Benninger F. Update on herpes virus infections of the nervous system[J]. Current Neurology and Neuroscience Reports,2013,13(12):414-421. doi: 10.1007/s11910-013-0414-8
    [4] Lehman I R,Boehmer P E. Replication of herpes simplex virus DNA[J]. The Journal of Biological Chemistry,1999,274(40):28059-28062. doi: 10.1074/jbc.274.40.28059
    [5] Knipe D M,Cliffe A. Chromatin control of herpes simplex virus lytic and latent infection[J]. Nature Reviews Microbiology,2008,6(3):211-221. doi: 10.1038/nrmicro1794
    [6] Zhu S,Viejo-Borbolla A. Pathogenesis and virulence of herpes simplex virus[J]. Virulence,2021,12(1):2670-2702. doi: 10.1080/21505594.2021.1982373
    [7] Cliffe A R,Garber D A,Knipe D M. Transcription of the herpes simplex virus latency-associated transcript promotes the formation of facultative heterochromatin on lytic promoters[J]. J Virol,2009,83(16):8182-8190. doi: 10.1128/JVI.00712-09
    [8] Stevens J G,Wagner E K,Devi-rao G B,et al. RNA complementary to a herpesvirus alpha gene mRNA is prominent in latently infected neurons[J]. Science (New York,NY),1987,235(4792):1056-1059.
    [9] Zwaagstra J C,Ghiasi H,Slanina S M,et al. Activity of herpes simplex virus type 1 latency-associated transcript (LAT) promoter in neuron-derived cells: Evidence for neuron specificity and for a large LAT transcript[J]. J Virol,1990,64(10):5019-5028. doi: 10.1128/jvi.64.10.5019-5028.1990
    [10] Farrell M J,Dobson A T,Feldman L T. Herpes simplex virus latency-associated transcript is a stable intron[J]. Proceedings of the National Academy of Sciences of the United States of America,1991,88(3):790-794.
    [11] Pan D,Flores O,Umbach J L,et al. A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency[J]. Cell Host & Microbe,2014,15(4):446-456.
    [12] Umbach J L,Nagel M A,Cohrs R J,et al. Analysis of human alphaherpesvirus microRNA expression in latently infected human trigeminal ganglia[J]. J Virol,2009,83(20):10677-10683. doi: 10.1128/JVI.01185-09
    [13] Umbach J L,Kramer M F,Jurak I,et al. MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs[J]. Nature,2008,454(7205):780-783. doi: 10.1038/nature07103
    [14] Jiang X,Brown D,Osorio N,et al. Increased neurovirulence and reactivation of the herpes simplex virus type 1 latency-associated transcript (LAT)-negative mutant dLAT2903 with a disrupted LAT miR-H2[J]. Journal of Neurovirology,2016,22(1):38-49. doi: 10.1007/s13365-015-0362-y
    [15] Perng G C,Jones C,Ciacci-Zanella J,et al. Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript[J]. Science (New York,NY),2000,287(5457):1500-1503.
    [16] Javier R T,Stevens J G,Dissette V B,et al. A herpes simplex virus transcript abundant in latently infected neurons is dispensable for establishment of the latent state[J]. Virology,1988,166(1):254-257. doi: 10.1016/0042-6822(88)90169-9
    [17] Leib D A,Bogard C L,Kosz-Vnenchak M,et al. A deletion mutant of the latency-associated transcript of herpes simplex virus type 1 reactivates from the latent state with reduced frequency[J]. J Virol,1989,63(7):2893-2900. doi: 10.1128/jvi.63.7.2893-2900.1989
    [18] Vanni E A H,Foley J W,Davison A J,et al. The latency-associated transcript locus of herpes simplex virus 1 is a virulence determinant in human skin[J]. PLoS Pathog,2020,16(12):e1009166-e1009196. doi: 10.1371/journal.ppat.1009166
    [19] Moore L D,Le T,Fan G. DNA methylation and its basic function[J]. Neuropsychopharmacology:Official Publication of the American College of Neuropsychopharmacology,2013,38(1):23-38. doi: 10.1038/npp.2012.112
    [20] Kouzarides T. Chromatin modifications and their function[J]. Cell,2007,128(4):693-705. doi: 10.1016/j.cell.2007.02.005
    [21] Leinbach S S, Summers W C. The structure of herpes simplex virus type 1 DNA as probed by micrococcal nuclease digestion [J]. The Journal of General Virology, 1980, 51(Pt 1): 45-59.
    [22] Deshmane S L,Fraser N W. During latency,herpes simplex virus type 1 DNA is associated with nucleosomes in a chromatin structure[J]. J Virol,1989,63(2):943-947. doi: 10.1128/jvi.63.2.943-947.1989
    [23] Muggeridge M I,Fraser N W. Chromosomal organization of the herpes simplex virus genome during acute infection of the mouse central nervous system[J]. J Virol,1986,59(3):764-767. doi: 10.1128/jvi.59.3.764-767.1986
    [24] Huang J,Kent J R,Placek B,et al. Trimethylation of histone H3 lysine 4 by set1 in the lytic infection of human herpes simplex virus 1[J]. J Virol,2006,80(12):5740-5746. doi: 10.1128/JVI.00169-06
    [25] Kent J R,Zeng P Y,Atanasiu D,et al. During lytic infection herpes simplex virus type 1 is associated with histones bearing modifications that correlate with active transcription[J]. J Virol,2004,78(18):10178-10186. doi: 10.1128/JVI.78.18.10178-10186.2004
    [26] Paulus C,Nitzszhe A,Nevels M. Chromatinisation of herpesvirus genomes[J]. Reviews in Medical Virology,2010,20(1):34-50. doi: 10.1002/rmv.632
    [27] Lee J S,Raja P,Knipe D M. Herpesviral ICP0 protein promotes wwo waves of heterochromatin removal on an early viral promoter during lytic infection[J]. mBio,2016,7(1):e02007-e02015.
    [28] Gao C,Chen L,Tang S B,et al. The epigenetic landscapes of histone modifications on HSV-1 genome in human THP-1 cells[J]. Antiviral Research,2020,176(1):104730-104741. doi: 10.1016/j.antiviral.2020.104730
    [29] Kubat N J,Tran R K,Mcanany P,et al. Specific histone tail modification and not DNA methylation is a determinant of herpes simplex virus type 1 latent gene expression[J]. J Virol,2004,78(3):1139-1149. doi: 10.1128/JVI.78.3.1139-1149.2004
    [30] Oh J,Fraser N W. Temporal association of the herpes simplex virus genome with histone proteins during a lytic infection[J]. J Virol,2008,82(7):3530-3537. doi: 10.1128/JVI.00586-07
    [31] Gross S,Catez F,Masumoto H,et al. Centromere architecture breakdown induced by the viral E3 ubiquitin ligase ICP0 protein of herpes simplex virus type 1[J]. PloS One,2012,7(9):e44227-e44240. doi: 10.1371/journal.pone.0044227
    [32] Wagner L M,Deluca N A. Temporal association of herpes simplex virus ICP4 with cellular complexes functioning at multiple steps in PolII transcription[J]. PloS One,2013,8(10):e78242-e78254. doi: 10.1371/journal.pone.0078242
    [33] Herrera F J,Triezenberg S J. VP16-dependent association of chromatin-modifying coactivators and underrepresentation of histones at immediate-early gene promoters during herpes simplex virus infection[J]. J Virol,2004,78(18):9689-9696. doi: 10.1128/JVI.78.18.9689-9696.2004
    [34] Cliffe A R,Knipe D M. Herpes simplex virus ICP0 promotes both histone removal and acetylation on viral DNA during lytic infection[J]. J Virol,2008,82(24):12030-12038. doi: 10.1128/JVI.01575-08
    [35] Arbuckle J H,Vogel J L,Efstathiou S,et al. Deletion of the transcriptional coactivator HCF-1 in vivo impairs the removal of repressive heterochromatin from latent HSV genomes and suppresses the initiation of viral reactivation[J]. mBio,2023,14(1):e0354222-e0354238. doi: 10.1128/mbio.03542-22
    [36] Bloom D C,Giordani N V,Kwiakkowski D L. Epigenetic regulation of latent HSV-1 gene expression[J]. Biochim Biophys Acta,2010,1799(3-4):246-256. doi: 10.1016/j.bbagrm.2009.12.001
    [37] Neumann D M,Bhattacharjee P S,GIORDANI N V,et al. In vivo changes in the patterns of chromatin structure associated with the latent herpes simplex virus type 1 genome in mouse trigeminal ganglia can be detected at early times after butyrate treatment[J]. J Virol,2007,81(23):13248-13253. doi: 10.1128/JVI.01569-07
    [38] Amelio A L,Giordani N V,Kubat N J,et al. Deacetylation of the herpes simplex virus type 1 latency-associated transcript (LAT) enhancer and a decrease in LAT abundance precede an increase in ICP0 transcriptional permissiveness at early times postexplant[J]. J Virol,2006,80(4):2063-2068. doi: 10.1128/JVI.80.4.2063-2068.2006
    [39] Kubat N J,Amelio A L,Giordani N V,et al. The herpes simplex virus type 1 latency-associated transcript (LAT) enhancer/rcr is hyperacetylated during latency independently of LAT transcription[J]. J Virol,2004,78(22):12508-12518. doi: 10.1128/JVI.78.22.12508-12518.2004
    [40] Kwiatkowski D L,Thompson H W,Bloom D C. The polycomb group protein Bmi1 binds to the herpes simplex virus 1 latent genome and maintains repressive histone marks during latency[J]. J Virol,2009,83(16):8173-8181. doi: 10.1128/JVI.00686-09
    [41] Wang Q Y,Zhou C,Johnson K E,et al. Herpesviral latency-associated transcript gene promotes assembly of heterochromatin on viral lytic-gene promoters in latent infection[J]. Proceedings of the National Academy of Sciences of the United States of America,2005,102(44):16055-16059.
    [42] Amelio A L,Mcanany P K,Bloom D C. A chromatin insulator-like element in the herpes simplex virus type 1 latency-associated transcript region binds CCCTC-binding factor and displays enhancer-blocking and silencing activities[J]. J Virol,2006,80(5):2358-2368. doi: 10.1128/JVI.80.5.2358-2368.2006
    [43] Lang F,Li X,Vladimirova O,et al. CTCF interacts with the lytic HSV-1 genome to promote viral transcription[J]. Scientific Reports,2017,7(1):39861-39876. doi: 10.1038/srep39861
    [44] Washington S D,Musarrat F,ERTEL M K,et al. CTCF binding sites in the herpes simplex virus 1 genome display site-specific CTCF occupation,protein recruitment,and insulator function[J]. J Virol,2018,92(8):e00156-e00171.
    [45] Washington S D,Singh P,Johns R N,et al. The CCCTC binding factor,CTRL2,modulates heterochromatin deposition and the establishment of herpes shimplex virus 1 latency in vivo[J]. J Virol,2019,93(13):e00415-e00419.
    [46] Bedadala G R,Pinnoji R C,Palem J R,et al. Thyroid hormone controls the gene expression of HSV-1 LAT and ICP0 in neuronal cells[J]. Cell Res,2010,20(5):587-598. doi: 10.1038/cr.2010.50
    [47] Grams T R,Edwards T G,Bloom D C. HSV-1 LAT promoter deletion viruses exhibit strain-specific and LAT-dependent epigenetic regulation of latent viral genomes in human neurons[J]. J Virol,2023,97(2):e01935-e01951.
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  • 收稿日期:  2023-09-01
  • 网络出版日期:  2023-12-21
  • 刊出日期:  2024-01-25

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