Infecting nearly every child by age five, rotaviruses are the major causative agents of severe gastroenteritis in young children. While much is known about the structure of these nonenveloped viruses and their components, the exact mechanism of viral cell entry is still poorly understood. A consensus opinion that appears to be emerging from recent studies is that rotavirus cell entry involves a series of complex and coordinated events following proteolytic priming of the virus. Rotaviruses attach to the cell through sialic acid containing receptors, with integrins and Hsc70 acting as postattachment receptors, all localized on lipid rafts. Unlike other endocytotic mechanisms, this internalization pathway appears to be independent of clathrin or caveola. Equally complex and coordinated is the fascinating structural gymnastics of the VP4 spikes that are implicated in facilitating optimal interface between viral and host components. While these studies only begin to capture the basic cellular, molecular, and structural mechanisms of cell entry, the unusual features they have uncovered and many intriguing questions they have raised undoubtedly will prompt further investigations.