Table 1 Functional outcomes of epigenetic regulation in viral infections
From: Control of viral infections by epigenetic-targeted therapy
Target class | Target | Inhibitor | Virus studied | Functional outcome |
|---|---|---|---|---|
HDM | JMJD2 | ML324 | HCMV | Repression of viral IE gene expression and viral yields [95, 97] |
DMOG | HCMV | Decrease in the expression of HCMV IE genes UL37, UL72, and US3 [97] | ||
DMOG and ML342 | HSV-1 | Significant decreased in the viral titers in trigeminal ganglia of HSV-1 latently infected mice [97] | ||
LSD1 | OG-L002 | HCMV | Repression of HCMV IE expression [96] | |
TCP | HCMV | Decrease in the expression of HCMV IE genes UL37, UL72, and US3 [97] | ||
HSV-1 | Repression of HSV IE gene expression and genome replication in vivo | |||
Decrease in the severity of a virus-induced encephalitis and corneal blindness in mouse models | ||||
Blockage of viral reactivation in trigeminal ganglia | ||||
Adenovirus | Reduction in E1A gene expression [96] | |||
HDAC | Class II HDAC4 | MC1568 | HCMV | Induction of transient expression of the viral lytic IE antigens without full virus reactivation [104] |
Histone deacetylase | Sodium butyrate | HSV-1 | Production of infectious progeny in quiescently infected cells [154] | |
EBV, KSHV | Latency reversal [179] | |||
TSA, SAHA, VPA, and suberoylanilide hydroxamic acid | HSV-1 | Reduction in the number of HSV-1 genomes that initiate replication [164] | ||
TSA, VPA | HBV | Increase in HBV transcripts | ||
Cytoplasmic accumulation of HBV replicative intermediates | ||||
Increase in secreted HBV viral particles [128] | ||||
SAHA | HCV | Suppression of HCV replication without affecting cell viability [135] | ||
Histone deacetylase 3 | RGFP966 | HCV | Reduction of viral replication in Huh7 cells and an in vivo model of humanized transgenic mice [141] | |
Histone deacetylase 6 | Tubastatin A | HCV | Suppression of HCV replication in HepG2 cells [137] | |
Pan-histone deacetylase | SAHA + TPA | HIV | Purging HIV-1 proviruses in HIV-1 latently infected cells via ERK and AP-1 pathways [26] | |
HMT | EZH2 | (DZnep) | HCMV | Significant activation of the lytic transcriptional program [85] |
GSK126 and GSK343 | HSV-1 | Blockage of lytic viral replication in latently infected ganglion explant model [169] | ||
Suv39H | Chaetocin | HIV | HIV-1 recovery in resting CD4+ T cells [36] | |
G9a | BIX-01294 | HIV | HIV-1 recovery in resting CD4+ T cells [36] | |
HAT | p300/CBP | C646 | HBV | Reduction in HBV transcription in a dose-dependent manner [111] |
DNMT | DNMT | Azacitidine | HBV | Tumor growth inhibition and decreased aggressiveness in vitro and in vivo [123] |
HCV | Inhibition of HCV infection [150] | |||
Viral protein | Tat (transactivator of transcription) | Didehydro-cortistatin A (dCA) | HIV | Reduction of residual levels of viral transcription in several models of HIV latency |
Establishment of a nearly permanent state of latency [42] | ||||
Suppression of viral rebound after ART interruption in HIV+ humanized BLT mice [43] |