%0 Journal Article %T Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia. %+ Institut Armand Frappier (INRS-IAF) %A Rochette, Pierre-Alexandre %A Bourget, Amélie %A Sanabria-Solano, Carolina %A Lahmidi, Soumia %A Lavallée, Gabriel Ouellet %A Pearson, Angela %Z We thank D. Favreau and P. Talbot (INRS-Institut Armand-Frappier) for assistance with the setup of LA-N-5 neuronal cultures. DNA sequencing was carried out by the McGill University and Génome Québec Innovation Centre. P.-A. R. is the recipient of scholarships from the Fondation Armand-Frappier (FAF) and the Fonds pour la Recherche en Santé du Québec. A. B. was the recipient of scholarships from the FAF and the Canadian Institutes for Health Research (CIHR). G. O. L and C. S.-S are recipients of scholarships from the FAF. This work was supported by an operating grant from CIHR (MOP 82924), by Institut Pasteur International Network–Paribas funds, and infrastructure and equipment grants from the Canada Foundation for Innovation (9991) and the National Science and Engineering Research Council (300745) to A. P. %< avec comité de lecture %@ 0022-1317 %J Journal of General Virology %I Microbiology Society %V 96 %N 9 %P 2794-805 %8 2015-09-01 %D 2015 %R 10.1099/vir.0.000189 %M 25986633 %K Animal - Large DNA Viruses %Z Life Sciences [q-bio] %Z Life Sciences [q-bio]/Microbiology and Parasitology/VirologyJournal articles %X Herpes simplex virus 1 (human herpesvirus 1) initially infects epithelial cells of the mucosa and then goes on to infect sensory neurons leading ultimately to a latent infection in trigeminal ganglia (TG). UL24 is a core herpesvirus gene that has been identified as a determinant of pathogenesis in several Alphaherpesvirinae, although the underlying mechanisms are unknown. In a mouse model of ocular infection, a UL24-deficient virus exhibited a reduction in viral titres in tear films of 1 log10, whilst titres in TG are often below the level of detection. Moreover, the efficiency of reactivation from latency was also severely reduced. Herein, we investigated how UL24 contributed to acute infection of TG. Our results comparing the impact of UL24 on viral titres in eye tissue versus in tear films did not reveal a general defect in virus release from the cornea. We also found that the impairment of replication seen in mouse primary embryonic neurons with a UL24-deficient virus was not more severe than that observed in an epithelial cell line. Rather, in situ histological analyses revealed that infection with a UL24-deficient virus led to a significant reduction in the number of acutely infected neurons at 3 days post-infection (p.i.). Moreover, there was a significant reduction in the number of neurons positive for viral DNA at 2 days p.i. for the UL24-deficient virus as compared with that observed for WT or a rescue virus. Our results supported a model whereby UL24 functions in the dissemination of acute infection from the cornea to neurons in TG. %G English %L pasteur-01352640 %U https://riip.hal.science/pasteur-01352640 %~ RIIP %~ INRS-IAF