Table 1.

Mechanisms Involved in EBV Latency.

Mechanism	Effect	References
ROS Expression	B cell immortalization	[104,105,106]
-	Required for normal LMP1 expression	[106]
-	STAT3 phosphorylation	[106,107]
BHLF1	Maintenance of type III latency	[108]
PAX5	EBNA-1 localization to oriP and TR-DNA	[119]
-	Association of transcription enhancers from oriP and TR-DNA	[119]
CAF1	Inhibits lytic gene expression and increases histone presence at multiple points on the EBV genome.	[120]
HIRA	Histone loader involved in maintaining latency	[120]
ATRX	Histone loader involved in maintaining latency	[120]
DAXX	Histone loader involved in maintaining latency	[120]
MYC	Acts on BZLF1 promoter to prevent oriLyt and TR-DNA from looping	[110]
SMC1A	Contributes to latency by promoting MYC expression	[110]
Facilitated Chromatic Transcription Complex	Contributes to latency by promoting MYC expression	[110]
CXCR4	Maintenance of latency; stimulates LMP2A and EBNA-1	[112]
SUMOylation/SIM-interacting motifs	Facilitates oriP mini genome maintenance and the binding of EBNA-1 to His-tagged SUMO1 and SUMO2 proteins	[116]
-	EBNA-1 targets proteins with SUMO2 modifications for degradation	[116]
-	Inhibits BZLF1 expression	[116]
miRNAs	Inhibition of B cell receptor activation by diminishing NF-κB and/or AP-1 signaling	[123]