On the flip side, strategies to disrupt the BORF2-A3B interaction, such as competitive peptidomimetics of A3B L1 and/or L7, may restore A3B’s natural ability to restrict the replication of EBV and potentially also related herpesviruses and thus contribute to treating lytic phase diseases such as infectious mononucleosis, cold sores, and genital lesions. The gene discussed is APOBEC3B; the disease is infectious mononucleosis.