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. 2010 Apr 14;84(12):6130–6138. doi: 10.1128/JVI.00364-10

FIG. 6.

FIG. 6.

Regulation and function of IRFs in EBV latency. The only three IRFs with oncogenic properties, IRF7 (39, 73), -2 (72), and -4 (35, 69), as well as IRF5 (35, 40, 70), are all expressed at much higher levels in EBV type 3 latency. Both IRF4 (35, 69) and IRF7 (73) are induced by EBV LMP1, and IRF5 is induced by both TLR7 and LMP1 (16, 35), whereas IRF2 is induced through an unknown mechanism and negatively regulates the EBNA1 Q promoter in latency 3 (72). Moreover, IRF7 and likely IRF4 are activated by LMP1 (24, 38, 69). The activated IRF7 induces expression of LMP1, TAP2 and type I IFNs (39, 68, 74) but negatively regulates the EBV EBNA1 Q promoter and BART gene P1 promoter (11, 71). However, IRF5 (40) as well as A20 that is also induced by LMP1 (19, 29) negatively regulates LMP1-promoted IRF7 activity in EBV latency 3. In addition, like its role in antiviral responses (37), IRF4 may negatively regulate TLR7 activation of IRF5 in the EBV context.