Challenges in Quantifying Cytosine Methylation in the HIV Provirus

ABSTRACT DNA methylation is an epigenetic mechanism most commonly associated with transcriptional repression. While it is clear that DNA methylation can silence HIV proviral expression in in vitro latency models, its correlation with HIV persistence and expression in vivo is ambiguous, particularly...

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Main Authors: Sarah A. LaMere, Antoine Chaillon, Christina Huynh, Davey M. Smith, Sara Gianella
Format: Article
Language:English
Published: American Society for Microbiology 2019-02-01
Series:mBio
Subjects:
Online Access:https://journals.asm.org/doi/10.1128/mBio.02268-18
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author Sarah A. LaMere
Antoine Chaillon
Christina Huynh
Davey M. Smith
Sara Gianella
author_facet Sarah A. LaMere
Antoine Chaillon
Christina Huynh
Davey M. Smith
Sara Gianella
author_sort Sarah A. LaMere
collection DOAJ
description ABSTRACT DNA methylation is an epigenetic mechanism most commonly associated with transcriptional repression. While it is clear that DNA methylation can silence HIV proviral expression in in vitro latency models, its correlation with HIV persistence and expression in vivo is ambiguous, particularly in persons living with HIV (PLWH) receiving antiretroviral therapy (ART). Several factors potentially contribute to discrepancies between results in the literature, including differences in integration sites, functional proviral load, sampling bias, and stochastic PCR amplification. Recent studies into genomic features of cytosine methylation sites in mammalian genes offer potentially significant insights into this mechanism. Here, we discuss the importance of these factors in the context of the HIV.
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spelling doaj.art-b7390ba0885f4d55bdc9305fde4be5172022-12-21T21:25:24ZengAmerican Society for MicrobiologymBio2150-75112019-02-0110110.1128/mBio.02268-18Challenges in Quantifying Cytosine Methylation in the HIV ProvirusSarah A. LaMere0Antoine Chaillon1Christina Huynh2Davey M. Smith3Sara Gianella4Department of Medicine, University of California San Diego, La Jolla, California, USADepartment of Medicine, University of California San Diego, La Jolla, California, USADepartment of Medicine, University of California San Diego, La Jolla, California, USADepartment of Medicine, University of California San Diego, La Jolla, California, USADepartment of Medicine, University of California San Diego, La Jolla, California, USAABSTRACT DNA methylation is an epigenetic mechanism most commonly associated with transcriptional repression. While it is clear that DNA methylation can silence HIV proviral expression in in vitro latency models, its correlation with HIV persistence and expression in vivo is ambiguous, particularly in persons living with HIV (PLWH) receiving antiretroviral therapy (ART). Several factors potentially contribute to discrepancies between results in the literature, including differences in integration sites, functional proviral load, sampling bias, and stochastic PCR amplification. Recent studies into genomic features of cytosine methylation sites in mammalian genes offer potentially significant insights into this mechanism. Here, we discuss the importance of these factors in the context of the HIV.https://journals.asm.org/doi/10.1128/mBio.02268-18HIV latencycytosine methylationepigenetic silencingnon-CpG methylation
spellingShingle Sarah A. LaMere
Antoine Chaillon
Christina Huynh
Davey M. Smith
Sara Gianella
Challenges in Quantifying Cytosine Methylation in the HIV Provirus
mBio
HIV latency
cytosine methylation
epigenetic silencing
non-CpG methylation
title Challenges in Quantifying Cytosine Methylation in the HIV Provirus
title_full Challenges in Quantifying Cytosine Methylation in the HIV Provirus
title_fullStr Challenges in Quantifying Cytosine Methylation in the HIV Provirus
title_full_unstemmed Challenges in Quantifying Cytosine Methylation in the HIV Provirus
title_short Challenges in Quantifying Cytosine Methylation in the HIV Provirus
title_sort challenges in quantifying cytosine methylation in the hiv provirus
topic HIV latency
cytosine methylation
epigenetic silencing
non-CpG methylation
url https://journals.asm.org/doi/10.1128/mBio.02268-18
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