Retroviruses, which cause HIV/AIDS and some forms of leukemia, spread 1,000 times more efficiently when uninfected cells are in physical contact with infected cells. But scientists have been unsure exactly why cell-to-cell contact has such a strong influence on this process.
Walther Mothes, Ph.D., associate professor of microbial pathogenesis, and colleagues used four-dimensional imaging (in 3-D space over time) to track the assembly and movement of individual particles of murine leukemia virus (MLV) in living cells.
As reported in the July issue of PLoS Biology, the study, led by Postdoctoral Fellow Jing Jin, Ph.D., found that MLV expresses an adhesion protein that docks with uninfected cells and recruits other viral proteins to these sites to assemble new viruses. When the team deleted the “tail” of this protein, new viral particles did not assemble at the jumping-off point between cells.
“We are just opening the door to this whole process,” Mothes says. “Our hope is that somewhere down the road we will have a completely new antiviral strategy based on targeting cell-to-cell transmission.”