Table 2.
Cellular targets of Herpesvirus miRNAs (References have to be done last)
Cellular target |
Virus/sub -family |
miRNA | (Proposed) functional consequences |
Reference(s) |
---|---|---|---|---|
BACH1 | KSHV/γ | miR-K11 | Pro-proliferative, increased viability under oxidative stress | [28] [30] [69] |
BCLAF1 | KSHV/γ | Inhibit caspase activity, facilitate lytic reactivation | [31] | |
CASP3 | KSHV/γ | miR-K1, -K3, -K4-3p | Inhibition of apoptosis | [49] |
CDKN1A/p21 | KSHV/γ | miR-K1 | release of cell cycle arrest | [28] |
C/EBPbeta, C/EBPbeta p20 |
KSHV/γ | miR-K11 miR-K3, -K7, |
De-repression of IL6/IL10 secretion; Modulation of macrophage cytokine response |
[71] [56] |
IKBKE | KSHV/γ | miR-K11 | Suppression of antiviral immunity via IFN signaling | [55] [28] |
IRAK1 | KSHV/γ | miR-K9 | Decreased activity of TLR/IL1R signaling cascade | [57] |
MAF1 | KSHV/γ | miR-K1, -K6-5p, -K11 | Induce endothelial cell reprogramming | [59] |
MICB | KSHV/γ | miR-K7 | Immune evasion | [70] |
MYD88 | KSHV/γ | miR-K5 | Decreased activity of TLR/IL1R signaling cascade | [57] |
NFIB | KSHV/γ | miR-K3 | Promote latency | [64] |
NFKBIA | KSHV/γ | miR-K1 | Promote latency | [62] |
RBL2 | KSHV/γ | miR-K4-5p | De-repression of DNA methyl transferases (DNMT1, 3a, 3b) | [65] |
SMAD5 | KSHV/γ | miR-K11 | Resistance to growth inhibitory effects | [67] |
TGFBRII | KSHV/γ | miR-K10a, -K10b | Resistance to growth inhibitory effects | [42] |
THBS1 | KSHV/γ | miR-K1, -K3-3p, -K6-3p, -K11 | Pro-angiogenic | [29] |
TNFRSF10B/TWEAKR | KSHV/γ | miR-K10a | Reduced induction of inflammatory response and apoptosis | [48] |
CXCL-11 | EBV/γ | miR-BHRF1-3 | Immune modulation | [58] |
MICB | EBV/γ | miR-BART2-5p | Immune evasion | [70] |
PUMA | EBV/γ | miR-BART5 | Anti-apoptotic | [50] |
Listed are targets that have been functionally confirmed at least by luciferase reporter repression upon ectopic miRNA expression, and de-repression of the reporter upon target site mutation; KSHV = Kaposi’s sarcoma-associated herpesvirus, EBV = Epstein-Barr virus.