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, Jahrgang 42, Nr. 2, 04.2020, S. 187-200.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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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 -