A new mechanism to inhibit Epstein-Barr virus infection; the virus responsible for kissing disease and several types of cancer.

Most people are infected with Epstein-Barr virus (EBV); a herpesvirus that establishes a lifetime infection with no current treatments or vaccines. While usually asymptomatic, EBV can cause mononucleosis or “kissing disease” on initial infection, and persistent infection can cause several types of lymphomas and carcinomas. A proteomics experiment in Dr. Lori Frappier’s lab identified an interaction between an EBV protein (BORF2) and a cellular DNA mutating enzyme called APOBEC3B. In collaboration with Reuben Harris’s lab at the University of Minnesota, the team showed that BORF2 inactivates and relocalizes APOBEC3B away from replicating EBV genomes.  They further showed that BORF2was necessary to protect EBV genomes from mutation by APOBEC3B, which impairs the infectivity of the virus. The finding was unexpected, since it was not previously known that herpesviruses are susceptible to genome editing and need a mechanism to protect themselves from cellular editing enzymes. This provides a new opportunity to inhibit EBV infection by interfering with the BORF2-APOBEC3B interaction.  It also provides a novel way of inhibiting APOBEC3B, which itself is associated with some human cancers including breast cancer.This study was published in Nature Microbiology.

Read the study here: https://www.nature.com/articles/s41564-018-0284-6