Retrovirology Laboratory, Infectious Diseases Division, Federal University of São Paulo (UNIFESP), Rua Pedro de Toledo 669, Vila Clementino, Sao Paulo, SP, 04039-032, Brazil.
Laboratory of Bioinformatics and Computational Biology, A.C. Camargo Cancer Center, Rua Taguá, 440, São Paulo, SP, 01508-010, Brazil.
Sci Rep. 2021 Nov 26;11(1):22993. doi: 10.1038/s41598-021-02463-0.
DNA methylation is one of the epigenetic modifications that configures gene transcription programs. This study describes the DNA methylation profile of HIV-infected individuals with distinct characteristics related to natural and artificial viremia control. Sheared DNA from circulating mononuclear cells was subjected to target enrichment bisulfite sequencing designed to cover CpG-rich genomic regions. Gene expression was assessed through RNA-seq. Hypermethylation in virologic responders was highly distributed closer to Transcription Start Sites (p-value = 0.03). Hyper and hypomethylation levels within TSS adjacencies varied according to disease progression status (Kruskal-Wallis, p < 0.001), and specific differentially methylated regions associated genes were identified for each group. The lower the promoter methylation, the higher the gene expression in subjects undergoing virologic failure (R = - 0.82, p = 0.00068). Among the inversely correlated genes, those supporting glycolysis and its related pathways were hypomethylated and up-regulated in virologic failures. Disease progression heterogeneity was associated with distinct DNA methylation patterns in terms of rates and distribution. Methylation was associated with the expression of genes sustaining intracellular glucose metabolism in subjects undergoing antiretroviral virologic failure. Our findings highlight that DNA methylation is associated with latency, disease progression, and fundamental cellular processes.
DNA 甲基化是一种表观遗传修饰,可配置基因转录程序。本研究描述了具有与天然和人工病毒血症控制相关的不同特征的 HIV 感染个体的 DNA 甲基化谱。来自循环单核细胞的剪切 DNA 经过靶向富集亚硫酸氢盐测序处理,旨在覆盖富含 CpG 的基因组区域。通过 RNA-seq 评估基因表达。病毒学应答者中的高甲基化高度分布在转录起始位点(p 值=0.03)附近。TSS 附近的高甲基化和低甲基化水平根据疾病进展状态而变化(Kruskal-Wallis,p<0.001),并为每个组鉴定了特定的差异甲基化区域相关基因。在经历病毒学失败的受试者中,启动子甲基化越低,基因表达越高(R=-0.82,p=0.00068)。在反向相关基因中,支持糖酵解及其相关途径的基因在病毒学失败中低甲基化和上调。疾病进展异质性与不同的 DNA 甲基化模式相关,涉及速率和分布。甲基化与抗逆转录病毒病毒学失败的受试者中维持细胞内葡萄糖代谢的基因表达相关。我们的研究结果强调了 DNA 甲基化与潜伏期、疾病进展和基本细胞过程有关。