Although virologists long assumed that lone viruses independently infect target cells, in the case of poliovirus and other enteroviruses, several viral particles can cluster within lipid vesicles—from which they collectively enter target cells, improving overall infectivity and yields, the NIH researchers report. Nihal Altan-Bonnet at the National Heart Lung and Blood Institute at the National Institutes of Health (NIH) in Bethesda, Md., and her collaborators focused on poliovirus, a particular type of enterovirus.

This group also includes rhinovirus, Coxsackie viruses, and enterovirus 68, which is linked to a recent outbreak leading to paralysis among some infected children. In HeLa cells after replication and assembly, poliovirus congregates in clusters that are surrounded by double-membrane phosphatidylserine vesicles, ranging from 250 to 350 nm in diameter. Both rhinovirus and Coxsackie virus also form similar vesicles after infecting cells. The vesicles fuse with the plasma membrane of the host cell, and the viruses are released into the extracellular environment within this package, rather than as separate particles.

Details appeared 12 February 2015 in Cell (doi:10.1016/j.cell.2015.01.032), and the research was featured in the May 2015 issue of Microbe.