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CpG Methylation Controls Reactivation of HIV from Latency

Figure 1

Methylation profiles of latent promoters of HIV-1 LTR-driven vectors integrated in Jurkat cells.

(A) CpG methylation levels of the 5′ LTR of latent HIV-1 LTR-driven retroviral vector pEV731 coding the HIV-1 protein Tat and EGFP in Jurkat clonal cell lines A2, A8, G10, and H12, and of the latent complete EGFP-coding HIV-1 in the JNLGFP cell line. Methylation levels are presented as a mean±standard error of percentages of methylated CpGs in cloned HIV-1 promoters for each cell line. Only DNA sequences with at least 95% conversion of cytosines outside CpGs were taken into account. Levels of EGFP expression (mean±standard error) in all five cell lines are shown bellow. Significance of the difference in methylation levels between cell lines was calculated by non-parametric, two-side Mann-Whitney test. (B) Methylation pattern of the 5′ LTR in the H12 cell line. Analysis of ten promoter molecules is shown as a linear array of open circles representing nonmethylated CpG residues and closed circles representing methylated CpG residues. Shown in the rectangle representing the LTR regions U3, R, and U5 of the pEV731 vector is the distribution of CpG dinucleotides. (C) Integration site of the latent HIV-1 “mini-virus” in the H12 cell line. Gray rectangles represent the exons of ubiquilin. See Table S2 for the flanking sequences. mCpG, methylated CpG residues.

Figure 1

doi: https://doi.org/10.1371/journal.ppat.1000554.g001