Endogenous retroviruses

Maksakova, Irina A.; Mager, Dixie L.; Reiss, Daphne

doi:10.1007/s00018-008-8494-3

Cited by 150 publications

(77 citation statements)

References 187 publications

(273 reference statements)

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“…4), while the lack of enrichment in other cell populations could exemplify the indirect mechanism regulating HML-2 expression in HIV-1-infected patients. The differences in the magnitude of HML-2 transcription in cell subsets could be due to cell-specific transcription factors, methylation patterns, or other epigenetic changes, which are believed to control endogenous retrovirus expression in differentiated tissues (60,61). Based on these results, it appears that differential expression from multiple cell sources may lead to the 2-fold difference in HML-2 expression in HIV-infected versus control individuals.…”

Section: Discussionmentioning

confidence: 96%

HIV-1 Infection Leads to Increased Transcription of Human Endogenous Retrovirus HERV-K (HML-2) ProvirusesIn Vivobut Not to Increased Virion Production

Bhardwaj

Maldarelli

Mellors

et al. 2014

J Virol

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Recent studies suggest that human endogenous retrovirus group K (HERV-K) provirus expression plays a role in the pathogenesis of HIV-1 infection. In particular, RNA from the HML-2 subgroup of HERV-K proviruses has been reported to be highly expressed at the cellular level and detectable in the plasma of HIV-1-infected patients, suggestive of virion production and, perhaps, replication. In this study, we developed an HML-2-specific quantitative-PCR assay that detects 51 of the 89 known HML-2 proviruses in the human genome. Plasma and peripheral blood mononuclear cells (PBMCs) from HIV-negative controls and HIV-1-infected patients were collected for analysis of HML-2 RNA expression. Contrary to previous reports, we did not detect high levels of HML-2 RNA in the plasma of HIV-1-infected patients, but we did observe a significant increase of HML-2 RNA in total PBMCs compared to HIV-negative controls. The level of HML-2 expression in PBMCs does not appear to be related to patient use of antiretrovirals or to HIV-1 plasma RNA, cellular RNA, or cellular DNA levels. To investigate the source of HML-2 RNA expression, patient PBMCs were sorted into CD3 ؉ CD4 ؉ , CD3 ؉ CD8 ؉ , CD3 ؊ CD14 ؉ , and CD3 ؊ CD20 ؉ cell subsets and then analyzed for HML-2 RNA levels. No single cell subset was enriched for HML-2 RNA expression in HIV-1-infected patients, but there appears to be substantial variability in the level of HML-2 expression depending on the cell type. IMPORTANCEHere, we report that human endogenous retrovirus group K (HERV-K) (HML-2) proviruses are expressed at significantly higher levels in peripheral blood mononuclear cells (PBMCs) from patients with HIV-1 infection than in those from uninfected individuals. However, contrary to previous reports, this expression did not lead to detectable virions in the plasma of these patients. In addition, we found that HML-2 proviruses were expressed in multiple blood cell types from HIV-1-infected individuals, and the magnitude of HML-2 expression was not related to HIV-1 disease markers in this patient cohort. These findings may have implications for HML-2-based therapies targeting HIV-1 infection.

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Section: Discussionmentioning

confidence: 96%

HIV-1 Infection Leads to Increased Transcription of Human Endogenous Retrovirus HERV-K (HML-2) ProvirusesIn Vivobut Not to Increased Virion Production

Bhardwaj

Maldarelli

Mellors

et al. 2014

J Virol

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“…As other retrotransposons, IAPs are generally maintained in the silenced state by repressive epigenetic modifications (reviewed in [8]). A major contributor for IAP silencing is DNA (5-cytosine) methylation.…”

Section: Epigenetic Regulation Patterns Of Iaps Differ Among Tissuesmentioning

confidence: 99%

“…A recent study has estimated that there could be at least 32 previously identified germline mutations caused by IAPs in mice, which account for roughly 5 per cent of all such incidents reported so far [8]. These include two well analysed loci, namely, the agouti viable yellow (A VY ) and the Axin-fused (Axin FU ) alleles, which arise from IAP insertions in the promoter and intronic regions of the agouti and the Axin loci, respectively [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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Is there a role for endogenous retroviruses to mediate long-term adaptive phenotypic response upon environmental inputs?

Sharif

Shinkai

Koseki

2013

Phil. Trans. R. Soc. B

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Endogenous retroviruses (ERVs) are long terminal repeat-containing virus-like elements that have colonized approximately 10 per cent of the present day mammalian genomes. The intracisternal A particles (IAPs) are a class of ERVs that is currently highly active in the rodents. IAP elements can influence the transcription profile of nearby genes by providing functional promoter elements and modulating local epigenetic landscape through changes in DNA methylation and histone (H3K9) modifications. Despite the potential role for IAPs in gene regulation, the precise genomic locations where these elements are integrated are not well understood. To address this issue, we have identified more than 400 novel IAP insertion sites within/near annotated genes by searching the murine genome, which suggests that the impact of IAP elements on local and/or global gene regulation could be more profound than was previously expected. On the basis of our independent analyses and already published reports, here we argue that IAPs and ERV elements in general could have an evolutionary role for modulating phenotypic plasticity upon environmental inputs, and that this could be mediated through specific stages of embryonic development such as placentation during which the epigenetic constraints on IAP elements are partially relaxed.

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“…Treatment of cells with a chemical inhibitor specific for G9a increases the efficiency of iPS cell generation [56]. Although the molecular significance of silencing is unknown, ES cells are considered to be a good model for studying the relationship between DNA methylation and histone modifications, because of their high level of de novo DNA methyltransferase activity [57]. Endogenous retroviruses (ERVs) are transcriptionally silenced in ES cells.…”

Section: Distinct Histone Modification Profile In Pluripotent Cellsmentioning

confidence: 99%

Epigenetic regulation in pluripotent stem cells: a key to breaking the epigenetic barrier

Watanabe

Yamada

Yamanaka

2013

Phil. Trans. R. Soc. B

111

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The differentiation and reprogramming of cells are accompanied by drastic changes in the epigenetic profiles of cells. Waddington's classical model clearly describes how differentiating cells acquire their cell identity as the developmental potential of an individual cell population declines towards the terminally differentiated state. The recent discovery of induced pluripotent stem cells as well as of somatic cell nuclear transfer provided evidence that the process of differentiation can be reversed. The identity of somatic cells is strictly protected by an epigenetic barrier, and these cells acquire pluripotency by breaking the epigenetic barrier by reprogramming factors such as Oct3/4, Sox2, Klf4, Myc and LIN28. This review covers the current understanding of the spatio-temporal regulation of epigenetics in pluripotent and differentiated cells, and discusses how cells determine their identity and overcome the epigenetic barrier during the reprogramming process.

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Endogenous retroviruses

Cited by 150 publications

References 187 publications

HIV-1 Infection Leads to Increased Transcription of Human Endogenous Retrovirus HERV-K (HML-2) ProvirusesIn Vivobut Not to Increased Virion Production

HIV-1 Infection Leads to Increased Transcription of Human Endogenous Retrovirus HERV-K (HML-2) ProvirusesIn Vivobut Not to Increased Virion Production

Is there a role for endogenous retroviruses to mediate long-term adaptive phenotypic response upon environmental inputs?

Epigenetic regulation in pluripotent stem cells: a key to breaking the epigenetic barrier

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