Furthermore, we recently showed that the higher level of constitutive lytic infection in early passage LCLs with T2 versus T1 EBV infection is due not only to the universal presence of the NFATc1-responsive form of the Zp promoter (Zp-V3) in all T2 strains, but also a much higher level of the activated forms of both NFATc1 and NFATc2 in T2 LCLs [27]. This evidence concerns the gene NFATC1 and Epstein-Barr virus infection.