Noroviruses, a major cause of gastroenteritis in man, have evolved a mechanism that relies on the interaction of translation initiation factors with the virus-encoded VPg protein covalently linked to the 5′ end of the viral RNA.

and those that can eliminate infected cells, thereby reducing persistent and latent reservoirs of the virus.

In order to illustrate the differences leading to faster transport of RABV compared to NGF, we proceeded to inquire whether internalization of these ligands occurs over similar time frames. To this end, we performed a series of live imaging experiments using TIRF microscopy, and tracked fluorescent RABV or NGF particles at the axonal growth cone. Distinct features of the TIRF evanescent wave allow us to limit our view to the basal surface, an ideal set up for viewing internalization processes occurring at axon tips.

FIG 3  Cellular translation initiation factors colocalize to viral factories. (A, B) CV-1 cells were infected with T3D or T1L at an MOI of 1. At 18 h p.i., RPM-labeled cells were coimmunostained for μNS and eIF4E (A) or eIF3A (B). Scale bars, 10 µm. (C) CV-1 cells were infected with T3D, MOI of 3, for the times indicated. Protein levels were assessed by immunoblotting. M = mock.

In mice and other animal model systems, the virus establishes latency in some neurons but multiplies in others (4). Ultimately, in mice, after an interval of 4 wk, only latent virus can be detected in the peripheral ganglia (5).