Herpes simplex virus type 1 corneal infection results in periocular disease by zosteriform spread

Journal of Virology
B C SummersD A Leib

Abstract

In humans and animal models of herpes simplex virus infection, zosteriform skin lesions have been described which result from anterograde spread of the virus following invasion of the nervous system. Such routes of viral spread have not been fully examined following corneal infection, and the possible pathologic consequences of such spread are unknown. To investigate this, recombinant viruses expressing reporter genes were generated to quantify and correlate gene expression with replication in eyes, trigeminal ganglia, and periocular tissue. Reporter activity peaked in eyes 24 h postinfection and rapidly fell to background levels by 48 h despite the continued presence of viral titers. Reporter activity rose in the trigeminal ganglia at 60 h and peaked at 72 h, concomitant with the appearance and persistence of infectious virus. Virus was present in the periocular skin from 24 h despite the lack of significant reporter activity until 84 h postinfection. This detection of reporter activity was followed by the onset of periocular disease on day 4. Corneal infection with a thymidine kinase-deleted reporter virus displayed a similar profile of reporter activity and viral titer in the eyes, but little or no detectable activity was ob...Continue Reading

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Citations

Nov 28, 2012·Proceedings of the National Academy of Sciences of the United States of America·Andrew H KarabaRichard Longnecker
Apr 11, 2013·Antimicrobial Agents and Chemotherapy·Arun KapoorRavit Arav-Boger
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