IOVS Read the Free BMJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
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
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gordon, Y. J.
Right arrow Articles by Becker, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gordon, Y. J.
Right arrow Articles by Becker, Y.

Investigative Ophthalmology & Visual Science, Vol 24, 599-602, Copyright © 1983 by Association for Research in Vision and Ophthalmology

ARTICLES AND REPORTS

HSV-1 thymidine kinase promotes virulence and latency in the mouse

YJ Gordon, DM Gilden and Y Becker

The relationship between thymidine kinase (TK) activity and virulence was studied in the mouse using three HSV-1 strains: (1) NIH TK+ (100% activity), (2) NIH TK+/- (25% TK activity), and (3) NIH TK- (0% TK activity). Following corneal inoculation, keratitis, virus titers (eye, trigeminal ganglia brain), survival, and latency were determined for each strain. The most virulent strain, NIH TK+ (30% survival) produced the worst keratitis, highest CNS titers, and established latency in 78% of surviving mice. NIH TK+/- demonstrated dose-dependent intermediate virulence (57-90% survival) and established latency in 80% of mice. NIH TK-, the most avirulent strain (93-100% survival) produced eye virus titers equal to the other strains but did not appear to invade the CNS or establish latency. These results indicate that TK gene activity is essential for HSV-1 murine neurovirulence (ie, efficient CNS invasion, replication and establishment of latency), but not for ocular replication.


This article has been cited by other articles:


Home page
 J. Virol.Home page
J. A. Murphy, R. J. Duerst, T. J. Smith, and L. A. Morrison
Herpes Simplex Virus Type 2 Virion Host Shutoff Protein Regulates Alpha/Beta Interferon but Not Adaptive Immune Responses during Primary Infection In Vivo
J. Virol., September 1, 2003; 77(17): 9337 - 9345.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
W. D. Hunter, R. L. Martuza, F. Feigenbaum, T. Todo, T. Mineta, T. Yazaki, M. Toda, J. T. Newsome, R. C. Platenberg, H. J. Manz, et al.
Attenuated, Replication-Competent Herpes Simplex Virus Type 1 Mutant G207: Safety Evaluation of Intracerebral Injection in Nonhuman Primates
J. Virol., August 1, 1999; 73(8): 6319 - 6326.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1983 by the Association for Research in Vision and Ophthalmology