This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lafon, M. Articles by Carosella, E. D. Search for Related Content PubMed PubMed Citation Articles by Lafon, M. Articles by Carosella, E. D.

 Previous Article  |  Next Article 

Journal of Virology, December 2005, p. 15226-15237, Vol. 79, No. 24
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.24.15226-15237.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Modulation of HLA-G Expression in Human Neural Cells after Neurotropic Viral Infections

Unité de Neuroimmunologie Virale, Institut Pasteur, Paris, France,¹ Service de Recherche en Hémato-Immunologie, CEA-DSV-DRM, Hôpital Saint Louis, IUH, Paris, France²

Received 30 June 2005/ Accepted 7 September 2005

HLA-G is a nonclassical human major histocompatibility complex class I molecule. It may promote tolerance, leading to acceptance of the semiallogeneic fetus and tumor immune escape. We show here that two viruses—herpes simplex virus type 1 (HSV-1), a neuronotropic virus inducing acute infection and neuron latency; and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection—upregulate the neuronal expression of several HLA-G isoforms, including HLA-G1 and HLA-G5, the two main biologically active isoforms. RABV induces mostly HLA-G1, and HSV-1 induces mostly HLA-G3 and HLA-G5. HLA-G expression is upregulated in infected cells and neighboring uninfected cells. Soluble mediators, such as beta interferon (IFN-ß) and IFN-, upregulate HLA-G expression in uninfected cells. The membrane-bound HLA-G1 isoform was detected on the surface of cultured RABV-infected neurons but not on the surface of HSV-1-infected cells. Thus, neuronotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially. HLA-G may therefore be involved in the escape of certain viruses from the immune response in the nervous system.

This article has been cited by other articles:

• Moreau, P., Contu, L., Alba, F., Lai, S., Simoes, R., Orru, S., Carcassi, C., Roger, M., Rabreau, M., Carosella, E. D. (2008). HLA-G Gene Polymorphism in Human Placentas: Possible Association of G*0106 Allele with Preeclampsia and Miscarriage. Biol. Reprod. 79: 459-467 [Abstract] [Full Text]  
• Lafon, M., Megret, F., Meuth, S. G., Simon, O., Velandia Romero, M. L., Lafage, M., Chen, L., Alexopoulou, L., Flavell, R. A., Prehaud, C., Wiendl, H. (2008). Detrimental Contribution of the Immuno-Inhibitor B7-H1 to Rabies Virus Encephalitis. J. Immunol. 180: 7506-7515 [Abstract] [Full Text]  
• Carosella, E. D., Favier, B., Rouas-Freiss, N., Moreau, P., LeMaoult, J. (2008). Beyond the increasing complexity of the immunomodulatory HLA-G molecule. Blood 111: 4862-4870 [Abstract] [Full Text]  
• Hooks, J. J., Nagineni, C. N., Hooper, L. C., Hayashi, K., Detrick, B. (2008). IFN-{beta} Provides Immuno-Protection in the Retina by Inhibiting ICAM-1 and CXCL9 in Retinal Pigment Epithelial Cells. J. Immunol. 180: 3789-3796 [Abstract] [Full Text]  
• Naji, A., Le Rond, S., Durrbach, A., Krawice-Radanne, I., Creput, C., Daouya, M., Caumartin, J., LeMaoult, J., Carosella, E. D., Rouas-Freiss, N. (2007). CD3+CD4low and CD3+CD8low are induced by HLA-G: novel human peripheral blood suppressor T-cell subsets involved in transplant acceptance. Blood 110: 3936-3948 [Abstract] [Full Text]