Inactivation of the HIV LTR by DNA CpG methylation: evidence for a role in latency.

Bednarik, Daniel P.; Cook, Judith Α.; Pitha, Paula M.

doi:10.1002/j.1460-2075.1990.tb08222.x

Cited by 138 publications

(78 citation statements)

References 50 publications

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“…Several studies support the idea that the latent state of integrated provirus is stabilized by the establishment of some suppressive epigenetic marks, such as DNA methylation or a specific histone code, particularly at the viral promoter (Bednarik et al, 1990;Ishida et al, 2006;Jiang et al, 2007;Mok and Lever, 2007). Latency with persistence of the entire virus, especially in the case of HIV, is very important because it provides a reservoir of viruses that are potentially harmful and able to trigger a carcinogenic process.…”

Section: Human Immune Deficiency Virusesmentioning

confidence: 97%

“…Several models have been proposed to explain proviral silencing (Mok and Lever, 2007;Han et al, 2008;Duverger et al, 2009;Richman et al, 2009). Although DNA methylation of the HIV 5 0 -LTR is known to suppress viral gene expression (Bednarik et al, 1990), more complex processes have been discovered that govern this transcriptional feature.…”

Section: Human Immune Deficiency Virusesmentioning

confidence: 99%

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Viral epigenomes in human tumorigenesis

Fernández

Esteller

2010

Oncogene

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Viruses are associated with 15-20% of human cancers worldwide. In the last century, many studies were directed towards elucidating the molecular mechanisms and genetic alterations by which viruses cause cancer. The importance of epigenetics in the regulation of gene expression has prompted the investigation of virus and host interactions not only at the genetic level but also at the epigenetic level. In this study, we summarize the published epigenetic information relating to the genomes of viruses directly or indirectly associated with the establishment of tumorigenic processes. We also review aspects such as viral replication and latency associated with epigenetic changes and summarize what is known about epigenetic alterations in host genomes and the implications of these for the tumoral process. The advances made in characterizing epigenetic features in cancer-causing viruses have improved our understanding of their functional mechanisms. Knowledge of the epigenetic changes that occur in the genome of these viruses should provide us with markers for following cancer progression, as well as new tools for cancer therapy.

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Section: Human Immune Deficiency Virusesmentioning

confidence: 97%

Section: Human Immune Deficiency Virusesmentioning

confidence: 99%

Viral epigenomes in human tumorigenesis

Fernández

Esteller

2010

Oncogene

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“…17 This is in contrast to gene expression in exogenous human retroviruses from transiently transfected constructs and from proviruses in cells that have not undergone long-term culture. In these cells, TSA, sodium butyrate and tumour necrosis factor-a could all readily reactivate latent HIV-1, 21 whereas 5AzaC could reactivate both latent HIV-1 22,23 and HTLV-1. 24 In this study, we explored the relative proportion of integrated HIV-1-based vectors that are expressed using a construct with deletions introduced to ensure single round infection kinetics.…”

Section: Introductionmentioning

confidence: 97%

Stable gene expression occurs from a minority of integrated HIV-1-based vectors: transcriptional silencing is present in the majority

2007

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“…Epigenetic modification of particular CpG residues within regulatory regions of eukaryotic genes influence the transcriptional activity, with a correlation between gene expression and hypomethylation (for review, see Razin & Cedar, 1991). DNA methylation seems to be involved in cellular senescence (Klein et al, 1991) and genomic imprinting (Reik et al, 1987) as well as in viral latency as described recently for human immunodeficiency virus (HIV) (Bednarik et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

The Effect of DNA Methylation on Gene Regulation of Human Papillomaviruses

Rösl

Arab

Klevenz

et al. 1993

Journal of General Virology

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Integration of human papillomaviruses (HPVs) into the host genome is considered to be an early and important event in HPV-linked cervical carcinogenesis. Consequently, the viral DNA potentially becomes a target for cellular control mechanisms normally acting on the corresponding integration site. Besides resulting position effects, host-specific DNA methylation may play a functional role in HPV gene regulation. To elucidate the influence of such a kind of epigenetic modification on viral transcription, in vitro methylation studies on HPV-18 upstream regulatory region (URR)-controlled reporter plasmids were carded out. Selective methylation of the viral URR results in a down-regulation of the transcriptional activity, which can be attributed to nonrandom distribution of methyl-acceptor sites clustered within the constitutive enhancer region. In vivo competition experiments show that suppression is not directly mediated by steric hindrance of methyl residues with transcription factors, but rather is due to the association with methyl-CpG DNA-binding proteins. Using a restriction enzyme accessibility assay on both the DNA and chromatin levels, it could be demonstrated that, in vivo, extensively methylated viral DNA is nucleosomally organized, characteristic of transcriptionally inactive chromatin. These data suggest that DNA methylation is an important regulatory pathway in the modulation of HPV expression and as a consequence the proliferation rate of virus-infected cells.

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Inactivation of the HIV LTR by DNA CpG methylation: evidence for a role in latency.

Cited by 138 publications

References 50 publications

Viral epigenomes in human tumorigenesis

Viral epigenomes in human tumorigenesis

Stable gene expression occurs from a minority of integrated HIV-1-based vectors: transcriptional silencing is present in the majority

The Effect of DNA Methylation on Gene Regulation of Human Papillomaviruses

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