S. No L1 genomic-regulators Existing anti-latency strategy acting here¥ Potential HIV cure approach 1 Piwi-interacting RNAs (piRNAs) methylation of L1 sequences siRNA, DNA methylase inhibitors , HIV-1 targeted piRNA L1 methylation is maintainance by DNMT1, DNMT3A, and DNMT3B. DNA methylase inhibitors, HIV-1 targeted DNMT1, DNMT3A, and DNMT3B Methyl CpG binding protein 2 (MECP2) DNA methylase inhibitors, HIV-1 targeted MECP2 2 L1 silencing by histone alterations, including deacetylation of H4 and dimethylation of H3K9. histone deacetylase inhibitors Deacetylation of H4 and dimethylation of H3K9 3 Lymphoid-specific helicase (HELLS). - HIV-1 targeted HELLS 4 Retinoblastoma protein-containing complex (RB1) - HIV-1 targeted RB1 5 Three prime repair exonuclease 1 (TREX1) and excision repair cross complementing 1 (ERCC). CRE-recombinase, homing endonucleases (HEs), and zinc finger nucleases (ZFN) HIV-1 targeted TREX1 and ERCC HIV directed CRE, HEs, ZFN, TALENs & CRISPER/Cas 6 Apolipoprotein B mRNA editing enzyme, catalytic proteins APOBEC3A, APOBEC3B, and APOBEC1. - HIV-1 directed APOBEC3A, APOBEC3B, and APOBEC1 Anti/Counter-HIV-1 evasion of RFs by NEF, VPU, VPR ¥Note that except for the action of CRE-recombinase, homing endonucleases (HE), TALENS and CRISPER/Cas9 and zinc finger nucleases (ZFN); most existing anti-latency agents-aiming to awaken latent HIV for HAART targeting, indeed act in opposition to the natural L1 genomic regulators. Wherever dashes are, there were no existing anti-latency models based on these pathways found.

Table 1: Active L1 genomic-regulators and their corresponding anti-latency strategies.

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