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Journal of Virology, December 2007, p. 12962-12972, Vol. 81, No. 23
0022-538X/07/$08.00+0     doi:10.1128/JVI.01442-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A Recombinant Herpes Simplex Virus Type 1 Expressing Two Additional Copies of gK Is More Pathogenic than Wild-Type Virus in Two Different Strains of Mice{triangledown}

Kevin R. Mott,1 Guey-Chuen Perng,2 Yanira Osorio,1 Konstantin G. Kousoulas,3 and Homayon Ghiasi1*

Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, CSMC-D2024, 8700 Beverly Blvd., Los Angeles, California 90048,1 Department of Pathology and Laboratory Medicine, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322,2 Division of Biotechnology and Molecular Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 708033

Received 2 July 2007/ Accepted 19 September 2007

The effect of glycoprotein K (gK) overexpression on herpes simplex virus type 1 (HSV-1) infection in two different strains of mice was evaluated using a recombinant HSV-1 virus that expresses two additional copies of the gK gene in place of the latency-associated transcript (LAT). This mutant virus (HSV-gK3) expressed higher levels of gK than either the wild-type McKrae virus or the parental dLAT2903 virus both in vitro (in cultured cells) and in vivo (in infected mouse corneas and trigeminal ganglia [TG] of BALB/c and C57BL/6 mice). gK transcripts were detected in the TG of both HSV-gK3-infected mouse strains on day 30 postinfection (p.i.), while gB transcripts were detected only in the TG of the HSV-gK3-infected C57BL/6 mice, a finding that suggests that increased gK levels promote chronic infection. C57BL/6 mice infected with HSV-gK3 also contained free virus in their TG on day 30 p.i. Both HSV-gK3-infected mouse strains had significantly higher corneal scarring (CS) than did McKrae-infected mice. T-cell depletion studies in C57BL/6 mice suggested that this CS enhancement in the HSV-gK3-infected mice was mediated by a CD8+ T-cell response. Taken together, these results strongly suggest that increased gK levels promote eye disease and chronic infection in infected mice.

* Corresponding author. Mailing address: Center for Neurobiology and Vaccine Development-D2024, Cedars-Sinai Burns and Allen Research Institute, 8700 Beverly Blvd., Los Angeles, CA 90048. Phone: (310) 423-0593. Fax: (310) 423-0302. E-mail: ghiasih{at}CSHS.org

{triangledown} Published ahead of print on 26 September 2007.

Journal of Virology, December 2007, p. 12962-12972, Vol. 81, No. 23
0022-538X/07/$08.00+0     doi:10.1128/JVI.01442-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Mott, K. R., Chentoufi, A. A., Carpenter, D., BenMohamed, L., Wechsler, S. L., Ghiasi, H. (2009). The Role of a Glycoprotein K (gK) CD8+ T-Cell Epitope of Herpes Simplex Virus on Virus Replication and Pathogenicity. IOVS 50: 2903-2912 [Abstract] [Full Text]  
  • Mott, K. R., Bresee, C. J., Allen, S. J., BenMohamed, L., Wechsler, S. L., Ghiasi, H. (2009). Level of Herpes Simplex Virus Type 1 Latency Correlates with Severity of Corneal Scarring and Exhaustion of CD8+ T Cells in Trigeminal Ganglia of Latently Infected Mice. J. Virol. 83: 2246-2254 [Abstract] [Full Text]  
  • Mott, K. R., Ghiasi, H. (2008). Role of Dendritic Cells in Enhancement of Herpes Simplex Virus Type 1 Latency and Reactivation in Vaccinated Mice. CVI 15: 1859-1867 [Abstract] [Full Text]  


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