Fig 6. T2 EBV-infected LCLs have increased lytic infection compared to T1 EBV-infected LCLs.

A) Immunoblot analysis of LCLs (from the same donor) derived from two different T1 strains (Akata and Mutu) and two different T2 strains (AG876 and BL5) was performed using antibodies against EBNA2 (EBV latency protein), LMP1 (EBV latency protein), and actin. Kem I and Kem III serve as negative and positive controls, respectively, for presence of EBNA2 and LMP1. B) Nuclear and cytoplasmic extracts from T1 and T2 EBV-infected LCLs were subjected to immunoblot analysis using antibodies against EBNA-LP, Tubulin (cytoplasmic fraction control), and EBNA2 (as a nuclear fraction control). C) Immunoblot analysis of LCLs using antibodies against EBNA2, Z (immediate-early lytic protein), BRLF1(R) (immediate-early lytic protein), BMRF1 (early lytic protein), p18 VCA (late lytic protein), and actin. D) RNA isolated from T1 (Akata) or T2 (AG876) EBV-infected LCLs was subjected to qPCR analysis using primers against 18S rRNA, BARTs (EBV miRNA transcript), BZLF1 (immediate-early lytic gene), and BcLF1 (late lytic gene). The primers for EBV genes recognize both T1 and T2 EBV; results were normalized to the level of the cellular 18S transcript.