Modulation of HLA-G and HLA-E expression in human neuronal cells after rabies virus or herpes virus simplex type 1 infections.

Françoise Mégret (1) , Christophe Prehaud (1) , Mireille Lafage (1) , Philippe Moreau (2) , Nathalie Rouas-Freiss (2) , Edgardo D Carosella (2) , Monique Lafon (1)

1 Neuro-Immunologie Virale
2 SRHI - UMR_E 05 - Service de Recherche en Hémato-Immunologie

Human Leukocyte Antigen (HLA)-G and E are nonclassical human MHC class I molecules. They may promote tolerance leading to virus and tumor immune escape. We recently described that the herpes simplex virus type 1 (HSV-1), a neurotropic virus inducing chronic infection and neuron latency, and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection, up-regulate HLA-G expression in human neurons (NT2-N). Surface expression was only detected after RABV infection. We investigated here whether RABV and HSV-1 up-regulate HLA-E expression in human neuronal precursors (Ntera-2D/1). We found that RABV, not HSV-1, up-regulates HLA-E expression, nevertheless HLA-E could not be detected on the surface of RABV-infected Ntera-2D/1. Altogether these data suggest that HLA-G and not HLA-E could contribute to the immune escape of RABV. In contrast, there was no evidence that these molecules are used by latent HSV-1 infection. Thus, neurotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially.

Domaines: Virologie

Françoise Mégret, Christophe Prehaud, Mireille Lafage, Philippe Moreau, Nathalie Rouas-Freiss, et al.. Modulation of HLA-G and HLA-E expression in human neuronal cells after rabies virus or herpes virus simplex type 1 infections.. Human Immunology, 2007, 68 (4), pp.294-302. ⟨10.1016/j.humimm.2006.12.003⟩. ⟨pasteur-00202632⟩