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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Virology. 2017 Dec;512:113–123. doi: 10.1016/j.virol.2017.09.015

Figure 8.

Figure 8

Model for how pri-miR-BHRF1-2 and 1-3 regulate EBV gene expression in cis. In the context of WT EBV infection (left side), pri-miR-BHRF1-2 and 1-3 form part of the 3′UTR of EBNA-LP mRNAs. Cleavage of these pri-miRNAs by Drosha leads to a decrease in EBNA-LP transcript levels and, hence, EBNA-LP transcription factor expression. This in turn leads to a lower level of expression of EBNA-LP regulated transcripts, such as LMP1, and their encoded proteins. In contrast, when pri-miR-BHRF1-2 and 1-3 are deleted (right side), in the EBV Δ123 mutant, EBNA-LP and its downstream viral gene targets are overexpressed, resulting in reduced B cell transformation and slower LCL growth.