The stable 2-kilobase latency-associated transcript of herpes simplex virus type 1 can alter the assembly of the 60S ribosomal subunit and is exported from nucleus to cytoplasm by a CRM1-dependent pathway.

During latency of herpes simplex virus type 1 in the neurons of the peripheral nervous system, the major transcript detected is the 2-kb latency-associated transcript (LAT) intron. During lytic infection, this intron has been shown to associate with ribosomes, suggesting a role in modifying the translational machinery of infected cells. In this study we show, using LAT-transfected cells, that the interaction of the intron with the 60S ribosomal subunit leads to irreversible changes in the sedimentation profile of this subunit in the nucleus. Furthermore, the 2-kb LAT intron is transported to the cytoplasm as part of the 60S ribosomal subunit, using a CRM1-dependent pathway.