The 80s TV show MacGyver featured a main character who was always able to get himself out of dangerous situations with just his wits and clever use of whatever materials happened to be lying around. In much the same way, EBV has figured out how to harness a host B cell’s DNAm machinery to modulate its own infection cycle in order to survive.
Researchers at the German Research Center for Environmental Health in Munich have been studying EBV as model of human tumor viruses and viral latency. Some of their newly published results shed new light on the infection and life cycle of these microscopic MacGyvers. Here is what they discovered:
- EBV must first establish a latent B cell infection in order to keep them alive long enough to produce new viral particles
- EBV DNA is unmethylated upon infection, but becomes methylated over time by the host B cell
- The BZLF1-encoded protein, Zta (a cousin to AP-1), induces the viral lytic cycle, but it prefers binding sites that are methylated. So the lytic phase gets delayed until enough methylation has occurred.
In this way, the EBV virus has created its own time-dependent, epigenetic switch to control its biphasic life cycle. How very MacGyver-like…even if they don’t have the sweet mullet hair-do!
Catch the entire episode at PNAS, January 2010