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Journal of Virology, October 2008, p. 9870-9879, Vol. 82, No. 20
0022-538X/08/$08.00+0     doi:10.1128/JVI.00566-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Lymphoid-Related CD11c+ CD8{alpha}+ Dendritic Cells Are Involved in Enhancing Herpes Simplex Virus Type 1 Latency{triangledown}

Kevin R. Mott,1 David UnderHill,2 Steven L. Wechsler,3,4,5 and Homayon Ghiasi1*

Center for Neurobiology & Vaccine Development, Ophthalmology Research Laboratories,1 Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048,2 The Eye Institute, University of California Irvine, School of Medicine, Irvine, California 92697,3 Department of Microbiology and Molecular Genetics, University of California Irvine, School of Medicine, Irvine, California 92697,4 The Center for Virus Research, University of California, Irvine, Irvine, California 926975

Received 13 March 2008/ Accepted 24 July 2008

The mechanism(s) by which herpes simplex virus type 1 (HSV-1) latency is established in neurons is not known. In this study, we examined the effect of dendritic cells (DCs) on the level of HSV-1 latency in trigeminal ganglia (TGs) of ocularly infected BALB/c and C57BL/6 mice. We found that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which increases the number of DCs, increased the amount of latency in infected mice. Conversely, depletion of DCs was associated with reduced latency. Latency was also significantly reduced in Flt3L–/– and CD8–/– mice. Interestingly, immunization of Flt3L–/– but not CD8–/– mice with Flt3L DNA increased latency. Transfer experiments using DCs expanded ex vivo with Flt3L or granulocyte-macrophage colony-stimulating factor suggested that increased latency was associated with the presence of lymphoid-related (CD11c+ CD8{alpha}+) DCs, while reduced latency was associated with myeloid-related (CD11c+ CD8{alpha}–) DCs. Modulation of DC numbers by Flt3L DNA immunization or depletion did not alter acute virus replication in the eye or TG or eye disease in ocularly infected mice. Our results suggest that CD11c+ CD8{alpha}+ DCs directly or indirectly increase the amount of HSV-1 latency in mouse TGs.

* 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 30 July 2008.

Journal of Virology, October 2008, p. 9870-9879, Vol. 82, No. 20
0022-538X/08/$08.00+0     doi:10.1128/JVI.00566-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Dunne, P. J., Moran, B., Cummins, R. C., Mills, K. H. G. (2009). CD11c+CD8{alpha}+ Dendritic Cells Promote Protective Immunity to Respiratory Infection with Bordetella pertussis. J. Immunol. 183: 400-410 [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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