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. 2018 Apr 5;14(5):565–576. doi: 10.7150/ijbs.24562

Figure 2.

Figure 2

EBV-encoded miRNAs regulate host immune responses. In latently infected cells, the viral DNA genome forms in a circular shape (episome). EBV miRNA biogenesis is dependent on the host machinery. EBV miRNAs reduce the levels of viral antigens (LMP1 and LMP2A) to favor viral persistence in host cells. LMP1 acts as a functional mimic of CD40 and can activate MHCs and costimulatory molecules. Thus, LMP1 downregulation by viral miRNAs may block antigen presentation. More importantly, EBV invokes its miRNAs to subvert host immune responses by downregulating multiple cellular genes or pathways. 1) EBV miRNAs can efficiently interfere with MHC class I-mediated antigen presentation by targeting the antigen transporter TAP2. 2) Viral miRNAs inhibit expression of the lysosomal enzymes (IFI30, LGMN and CTSB), restraining the capability to present antigens to CD4+ T cells through MHC class-II. 3) Viral miRNAs control the expression of inflammatory cytokines (IL-6 and IL-12), thereby suppressing cytokine-mediated cellular immune responses. 4) EBV miRNAs also allow virus-infected cells to escape from NK- and T-cell attack by directly targeting the NK-cell attracting ligand, MICB and the T-cell attracting chemokine, CXCL-11. TCR, T-cell receptor; MHC, major histocompatibility complex; NKG2D, natural killer group 2D; MICB, MHC class I chain-related molecule B; CXCR3, C-X-C chemokine receptor type 3; CXCL-11, C-X-C motif chemokine ligand 11; ER, endoplasmic reticulum.