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Journal of Virology, January 2004, p. 520-523, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.520-523.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Failure of Thymidine Kinase-Negative Herpes Simplex Virus To Reactivate from Latency following Efficient Establishment

Shih-Heng Chen,1 Angela Pearson,2 Donald M. Coen,2 and Shun-Hua Chen1*

Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China,1 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 021152

Received 7 July 2003/ Accepted 17 September 2003

Thymidine kinase-negative mutants of herpes simplex virus did not reactivate from latency in mouse trigeminal ganglia, even when their latent viral loads were comparable to those that permitted reactivation by wild-type virus. Thus, reduced establishment of latency does not suffice to account for the failure to reactivate.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China. Phone: 886-6-2353535, ext. 5633. Fax: 886-6-208-2705. E-mail: shunhua{at}mail.ncku.edu.tw.


Journal of Virology, January 2004, p. 520-523, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.520-523.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




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  • Chen, S.-H., Lin, Y.-W., Griffiths, A., Huang, W.-Y., Chen, S.-H. (2006). Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia. J. Gen. Virol. 87: 3495-3502 [Abstract] [Full Text]