Table 3.

Interaction of the P53 isoforms with EBV.

p53 family	Interaction with the EBV genes or oncoproteins	EBV transformed cells/malignant tissue used
p53	EBNA3C repress the transcriptional activity of p53 through130-190 region or by direct interaction with Gemim3	B cell lymphoma cell
	USP7 lowers the p53 level through the binding with EBNA1,	Osteosarcoma cell
	LMP-1 inhibits the transcription activation of p53 through the interaction of NF-κB pathway, stimulate A20 expression and inhibit p53, interact with IRF5.	Large cell lung carcinoma and Osteogenic sarcoma, Non-small-cell lung cells
	C terminal region of BZLF-1 binds with the p53 and alter its expression	Lymphoid and T-lymphoblastoid cell
p63	ΔNp63α interact with BARF1 and transactivate many folds.	Gastric Carcinoma cell
	LMP-2A increases and stabilized the expression of ΔNp63α via the modulation of itch.	human keratinocyte cell
	EBNA5 has a direct interaction with the p63 in EBV positive Burkitt's lymphoma cell.	Burkitt's lymphoma cell
	EBNA2 interact with p63 through 310 to 336 amino acid sequence.	B cell lymphoma cell
	EBNA1 interact with the p63, but the mechanism of their interaction is still unknown.	Breast cancer tissue
p73	EBNA3C directly interfere with the p73 in the nucleus and stabilized ΔNp73.	B-cell
	LMP-1 binds with p73 through the displacement of polycomb 2 complex component EZH2 and epigenetic changes via activation of JNK-1	B cell
	Aberrant methylation in the exon 1 and SNPs in the p73 are associated with the EBV interaction.	Gastric Carcinoma and chronic lymphocytic leukemia