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Epigenetic crosstalk in chronic infection with HIV-1

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Epigenetic crosstalk in chronic infection with HIV-1. / Lange, Ulrike C; Verdikt, Roxane; Ait-Ammar, Amina; Van Lint, Carine.

In: SEMIN IMMUNOPATHOL, Vol. 42, No. 2, 04.2020, p. 187-200.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Lange, UC, Verdikt, R, Ait-Ammar, A & Van Lint, C 2020, 'Epigenetic crosstalk in chronic infection with HIV-1', SEMIN IMMUNOPATHOL, vol. 42, no. 2, pp. 187-200. https://doi.org/10.1007/s00281-020-00783-3

APA

Lange, U. C., Verdikt, R., Ait-Ammar, A., & Van Lint, C. (2020). Epigenetic crosstalk in chronic infection with HIV-1. SEMIN IMMUNOPATHOL, 42(2), 187-200. https://doi.org/10.1007/s00281-020-00783-3

Vancouver

Lange UC, Verdikt R, Ait-Ammar A, Van Lint C. Epigenetic crosstalk in chronic infection with HIV-1. SEMIN IMMUNOPATHOL. 2020 Apr;42(2):187-200. https://doi.org/10.1007/s00281-020-00783-3

Bibtex

@article{4624f56b8f6f4e439354102039f64575,
title = "Epigenetic crosstalk in chronic infection with HIV-1",
abstract = "Human immunodeficiency virus 1 (HIV-1) replicates through the integration of its viral DNA into the genome of human immune target cells. Chronically infected individuals thus carry a genomic burden of virus-derived sequences that persists through antiretroviral therapy. This burden consists of a small fraction of intact, but transcriptionally silenced, i.e. latent, viral genomes and a dominant fraction of defective sequences. Remarkably, all viral-derived sequences are subject to interaction with host cellular physiology at various levels. In this review, we focus on epigenetic aspects of this interaction. We provide a comprehensive overview of how epigenetic mechanisms contribute to establishment and maintenance of HIV-1 gene repression during latency. We furthermore summarize findings indicating that HIV-1 infection leads to changes in the epigenome of target and bystander immune cells. Finally, we discuss how an improved understanding of epigenetic features and mechanisms involved in HIV-1 infection could be exploited for clinical use.",
author = "Lange, {Ulrike C} and Roxane Verdikt and Amina Ait-Ammar and {Van Lint}, Carine",
year = "2020",
month = apr,
doi = "10.1007/s00281-020-00783-3",
language = "English",
volume = "42",
pages = "187--200",
journal = "SEMIN IMMUNOPATHOL",
issn = "1863-2297",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Epigenetic crosstalk in chronic infection with HIV-1

AU - Lange, Ulrike C

AU - Verdikt, Roxane

AU - Ait-Ammar, Amina

AU - Van Lint, Carine

PY - 2020/4

Y1 - 2020/4

N2 - Human immunodeficiency virus 1 (HIV-1) replicates through the integration of its viral DNA into the genome of human immune target cells. Chronically infected individuals thus carry a genomic burden of virus-derived sequences that persists through antiretroviral therapy. This burden consists of a small fraction of intact, but transcriptionally silenced, i.e. latent, viral genomes and a dominant fraction of defective sequences. Remarkably, all viral-derived sequences are subject to interaction with host cellular physiology at various levels. In this review, we focus on epigenetic aspects of this interaction. We provide a comprehensive overview of how epigenetic mechanisms contribute to establishment and maintenance of HIV-1 gene repression during latency. We furthermore summarize findings indicating that HIV-1 infection leads to changes in the epigenome of target and bystander immune cells. Finally, we discuss how an improved understanding of epigenetic features and mechanisms involved in HIV-1 infection could be exploited for clinical use.

AB - Human immunodeficiency virus 1 (HIV-1) replicates through the integration of its viral DNA into the genome of human immune target cells. Chronically infected individuals thus carry a genomic burden of virus-derived sequences that persists through antiretroviral therapy. This burden consists of a small fraction of intact, but transcriptionally silenced, i.e. latent, viral genomes and a dominant fraction of defective sequences. Remarkably, all viral-derived sequences are subject to interaction with host cellular physiology at various levels. In this review, we focus on epigenetic aspects of this interaction. We provide a comprehensive overview of how epigenetic mechanisms contribute to establishment and maintenance of HIV-1 gene repression during latency. We furthermore summarize findings indicating that HIV-1 infection leads to changes in the epigenome of target and bystander immune cells. Finally, we discuss how an improved understanding of epigenetic features and mechanisms involved in HIV-1 infection could be exploited for clinical use.

U2 - 10.1007/s00281-020-00783-3

DO - 10.1007/s00281-020-00783-3

M3 - SCORING: Review article

C2 - 32047948

VL - 42

SP - 187

EP - 200

JO - SEMIN IMMUNOPATHOL

JF - SEMIN IMMUNOPATHOL

SN - 1863-2297

IS - 2

ER -