This popped up in Pubmed last week, though it says it was published in September. I didn't see any discussion on it so thought I'd post it, since it looks like a cool study. The study is done on poliovirus, but there is some discussion on other picornaviruses as well. Full text here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246951/ Nonlytic viral spread enhanced by autophagy components Sara Whitney Bird, Nathaniel D. Maynard, [...], and Karla Kirkegaard SIGNIFICANCE The cell-to-cell spread of viruses that are not surrounded by membranes was thought to occur only by destruction of the infected cell, as no obvious path for a cytoplasmic particle to penetrate the plasma membrane exists. Nonetheless, it is known that spread within tissues in human infections is not always accompanied by obvious cell death. Here we use quantitative single-cell analysis to show that poliovirus can spread to a neighboring cell prior to bursting and killing the originally infected cell. This type of spread is dependent on components of the autophagy pathway, a recycling pathway that is found in all eukaryotes. This finding identifies targets to block the spread of viruses and other toxic cytoplasmic assemblages. ABSTRACT The cell-to-cell spread of cytoplasmic constituents such as nonenveloped viruses and aggregated proteins is usually thought to require cell lysis. However, mechanisms of unconventional secretion have been described that bypass the secretory pathway for the extracellular delivery of cytoplasmic molecules. Components of the autophagy pathway, an intracellular recycling process, have been shown to play a role in the unconventional secretion of cytoplasmic signaling proteins. Poliovirus is a lytic virus, although a few examples of apparently nonlytic spread have been documented. Real demonstration of nonlytic spread for poliovirus or any other cytoplasmic constituent thought to exit cells via unconventional secretion requires demonstration that a small amount of cell lysis in the cellular population is not responsible for the release of cytosolic material. Here, we use quantitative time-lapse microscopy to show the spread of infectious cytoplasmic material between cells in the absence of lysis. siRNA-mediated depletion of autophagy protein LC3 reduced nonlytic intercellular viral transfer. Conversely, pharmacological stimulation of the autophagy pathway caused more rapid viral spread in tissue culture and greater pathogenicity in mice. Thus, the unconventional secretion of infectious material in the absence of cell lysis is enabled by components of the autophagy pathway. It is likely that other nonenveloped viruses also use this pathway for nonlytic intercellular spread to affect pathogenesis in infected hosts.