Serum starvation impacts rhinovirus spread from cell to cell.

Single-cell studies of virus infection have found significant heterogeneity in virus and host gene expression as well as the kinetics of progeny particle release. However, such studies have yet to examine how the resulting virus descendants spread and infect nearby cells. We monitored reporter-gene expression from a recombinant rhinovirus in cell monolayers infected at low multiplicity of infection; we found that the second round of infection consistently exhibited a shorter delay in fluorescence signal appearance relative to the first round, indicating an acceleration in infection spread. We examined how the efficiency and timing of infection spread from initial to subsequent single infected cells depended on serum starvation, inhibition of protein synthesis, cell cycle arrest, and receptor expression. The sensitivity of this method to external factors and its ability to track viral protein expression in individual cells emphasize its potential in studying the role of host cell factors in infection spread.