IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1167/iovs.08-2430 on January 17, 2009
 (Investigative Ophthalmology and Visual Science. 2009;50:2855-2861.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-2430
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Table
Right arrow All Versions of this Article:
iovs.08-2430v1
50/6/2855    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Clement, C.
Right arrow Articles by Hill, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Clement, C.
Right arrow Articles by Hill, J. M.

Heat-Induced Reactivation of HSV-1 in Latent Mice: Upregulation in the TG of CD83 and Other Immune Response Genes and Their LAT-ICP0 Locus

Christian Clement,1 Partha S. Bhattacharjee,1,2 Herbert E. Kaufman,1,3,4,5 and James M. Hill1,3,4,5

1From the Department of Ophthalmology, LSU Eye Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana; the 2Department of Biology, Xavier University of Louisiana, New Orleans, Louisiana; and the Departments of 3Pharmacology and 4Microbiology and the 5Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana.

PURPOSE. To determine changes in host gene expression in HSV-1 latent trigeminal ganglia (TG) after hyperthermic stress.

METHODS. Scarified corneas of 6-week-old female BALB/c mice were inoculated with either HSV-1 17Syn+ (high phenotypic reactivator) or 17{Delta}Pst(LAT–) (low phenotypic reactivator) at 104 plaque-forming units/eye. At 28 days after infection, viral reactivation was induced in some of the infected mice with hyperthermic stress, and the mice were killed after 1 hour. Heat-treated uninfected mice served as the control. Labeled cRNA derived from TG-isolated total RNA was hybridized to 430 2.0 chips containing 14,000 mouse genes. Gene expression was confirmed by quantitative real-time PCR.

RESULTS. There was no difference in gene expression in the non–heat-treated mice. Gene expression in the TG of each of the heat-treated mouse groups (17Syn+, 17{Delta}Pst(LAT–) and uninfected) yielded upregulation of more than twofold of a group of the same genes, designated as heat stress–induced gene expression. Twenty-nine genes (0.2%) were significantly upregulated (2- to 17-fold) when the heat stress–induced gene expression was subtracted from the gene expression of 17Syn+ latent TG relative to 17{Delta}Pst(LAT–) latent TG 1 hour after mouse hyperthermic stress. Nine host adaptive immunity genes comprising Ig molecules, CD83, CD8A, ADA, and CCL8 were the largest subset upregulated, and all were confirmed by real-time PCR. Others identified included genes involved in hypothalamic-pituitary gland functions.

CONCLUSIONS. Hyperthermic stress–induced reactivation of the HSV-1 high phenotypic reactivator can upregulate gene expression involved in B-cell function and in T-cell function. CD83 is implicated in HSV-1 latency, suggesting it could also be involved in immune-mediated mechanisms of viral reactivation.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the Association for Research in Vision and Ophthalmology