NDLI: Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia.

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Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia.

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Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rochette, Pierre-Alexandre Bourget, Amélie Sanabria-Solano, Carolina Lahmidi, Soumia Lavallée, Gabriel Ouellet Pearson, Angela
Description	Country affiliation: Canada Author Affiliation: Rochette PA ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.); Bourget A ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.); Sanabria-Solano C ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.); Lahmidi S ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.); Lavallée GO ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.); Pearson A ( Université INRS, INRS-Institut Armand-Frappier, 531 boulevard des Prairies, Laval, Québec H7V 1B7, Canada.)
Abstract	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 1âlog10, 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.
File Format	HTM / HTML
ISSN	00221317
Issue Number	9
Volume Number	96
e-ISSN	14652099
Journal	Journal of General Virology
Language	English
Publisher	Microbiology Society
Publisher Date	2015-09-01
Publisher Place	Great Britain (UK)
Access Restriction	Subscribed
Subject Keyword	Research Support, Non-u.s. Gov't Cornea Discipline Virology Neurons Humans Cytology Viral Proteins Metabolism Journal Article Virology Herpesvirus 1, Human Herpes Simplex Animals Virus Replication Trigeminal Ganglion Genetics Physiology Mice Mutation Disease Models, Animal
Content Type	Text
Resource Type	Article
Subject	Virology

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