Establishment of novel cell lines latently infected with human immunodeficiency virus 1

Oh, You Take; Kim, Kyung Chang; Hong, Kee-Jong; Lee, Hak Sung; Jang, Dae Ho; Lee, Joo Shil; Choi, Seo‐Hyun; Kim, Sung Soon; Choi, Boseung

doi:10.4149/av_2011_02_155

Cited by 4 publications

(9 citation statements)

References 13 publications

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“…However, the expression level of LAT and SLA was decreased only in two types of cells and slightly increased in another cells. The functional significance of identified genes such as ZAP70 and LAT was confirmed in our previous experiments [20,25]. When the expression of ZAP70 was knock-downed by siRNA, the HIV-1 P24 viral antigen production was decreased.…”

Section: Resultssupporting

confidence: 62%

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Genome-wide analysis of histone modifications in latently HIV-1 infected T cells

Park¹,

Lim

Ham³

et al. 2014

Aids

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Objectives:The transcriptional silencing of HIV type 1 (HIV-1) provirus in latently infected cells is a major hurdle on the pathway to HIV-1 elimination. The epigenetic mechanisms established by histone modifications may affect the transcriptional silencing of HIV-1 and viral latency. A systematic epigenome profiling could be applicable to develop new epigenetic diagnostic markers for detecting HIV-1 latency.Design:The HIV-1 latency cell lines (NCHA1, NCHA2 and ACH2] were compared with CD4+ T-cell line (A3.01).Methods:The histone modification profiles obtained from chromatin immunoprecipiation followed by sequencing (ChIP-Seq) for histone H3K4me3 and H3K9ac were systematically examined and differential gene expression patterns along with levels of histone modifications were used for network analysis.Results:The HIV-1 latency gave rise to downregulation of histone H3K4me3 and H3K9ac levels in 387 and 493 regions and upregulation in 451 and 962 sites, respectively. By network analysis, five gene clusters were associated with downregulated histone modifications and six gene clusters came up with upregulated histone modifications. Integration of gene expression with epigenetic information revealed that the cell cycle regulatory genes such as CDKN1A (p21) and cyclin D2 (CCND2) identified by differentially modified histones might play an important role in maintaining the HIV-1 latency.Conclusion:The transcriptional regulation by epigenetic memory should play a key role in the evolution and maintenance of HIV-1 latency accompanied by modulation of signalling molecules in the host cells.

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Section: Resultssupporting

confidence: 62%

“…The HIV-1 virus particles in our HIV-1 latency cell models were actively generated upon activation [25]. The overall histone modification patterns near HIV-1 integrated sites were not significantly different from those of control in this study.…”

Section: Discussionmentioning

confidence: 65%

Genome-wide analysis of histone modifications in latently HIV-1 infected T cells

Park¹,

Lim

Ham³

et al. 2014

Aids

View full text Add to dashboard Cite

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“…A latent reservoir of HIV-1 is maintained in resting memory CD4+ T cells by multiple factors and contributes to the re-emergence of viremia upon discontinuation of highly active antiretroviral therapy [1]. Oh et al [2] established novel HIV-1 latently infected cell lines, NCHA cells, by limiting dilution cloning after the infection of A3.01 cells with pNL4-3 strain. NCHA cells have a more stable latent state than ACH2 cells which were derived from A3.01 cells.…”

Section: Tablementioning

confidence: 99%

“…Reference cell lines, A3.01, ACH2 [14], and J1.1 cells [3], were obtained from the National Institutes of Health AIDS Research and Reference Reagent Program. NCHA cells were established in our laboratory [2]. The HIV-1 reactivating capacities and cytotoxicities of HDACi, DNMTi, and HMTi were examined in HIV-1 latently infected cells.…”

Section: Tablementioning

confidence: 99%

“…Reuse et al [19] have also reported that no synergistic reactivation of latent virus was observed when 5′-Aza-CdR was combined with VPA. As 12-O-tetradecanoylphorbol-13-acetate (TPA), a global T-cell activator, can powerfully express HIV-1 proviruses [2], we assessed the combined effect of TPA and EMAs. The combined use of SAHA and TPA showed a more significant synergistic effect in HIV-1 reactivation than TPA alone in all HIV-1 latently infected cells (fig.…”

Section: Tablementioning

confidence: 99%

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Histone Deactylase Inhibitor SAHA Induces a Synergistic HIV-1 Reactivation by 12-O-Tetradecanoylphorbol-13-Acetate in Latently Infected Cells

et al. 2013

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Objectives: Recent studies have reported that human immunodeficiency virus type 1 (HIV-1) proviruses are strongly suppressed in the unique epigenetic environments caused by chromatin modifications such as acetylation and methylation. Therefore, optimized therapeutic strategies directed against the virus reservoir using these epigenetic modifying agents (EMAs) should cure HIV infection. Methods: Cytotoxicity and HIV-1 reactivation were determined using the PrestoBlue™ Cell Viability Reagent and p24 HIV ELISA, respectively. Results: EMAs, including histone deacetylase inhibitors (VPA and SAHA), DNA methyltransferase inhibitor (5′-Aza-CdR), histone methyltransferase inhibitor (ADOX) and 12-O-tetradecanoylphorbol-13-acetate (TPA), were used to reactivate proviruses in HIV-1 latently infected cells. The effect of monotreatment with these EMAs on HIV-1 reactivation was VPA or SAHA > 5′-Aza-CdR > ADOX. Even though cotreatment with these potential HIV-1 reactivating agents did not show any significant reactivation effects in HIV-1 latently infected cells, employing SAHA under TPA treatment demonstrated a dramatic synergistic effect on purging HIV-1 proviruses in all HIV-1 latently infected cells via the ERK and AP-1 pathways. Conclusions: These results suggest that the combined approaches of EMAs, cotreatment of SAHA and TPA, could provide an effective way to lead a decline of HIV-1 reservoirs in patients.

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Synergistic reactivation of latent HIV-1 provirus by PKA activator dibutyryl-cAMP in combination with an HDAC inhibitor

et al. 2017

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Establishment of novel cell lines latently infected with human immunodeficiency virus 1

Cited by 4 publications

References 13 publications

Genome-wide analysis of histone modifications in latently HIV-1 infected T cells

Genome-wide analysis of histone modifications in latently HIV-1 infected T cells

Histone Deactylase Inhibitor SAHA Induces a Synergistic HIV-1 Reactivation by 12-O-Tetradecanoylphorbol-13-Acetate in Latently Infected Cells

Synergistic reactivation of latent HIV-1 provirus by PKA activator dibutyryl-cAMP in combination with an HDAC inhibitor

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