Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

Abstract

Abbreviations : RABV (rabies virus), HSV-1 (herpes simplex virus type 1), mAb monoclonal antibody, HCMV ( Human cytomegalovirus) 2 Abstract HLA-G and E are non classical human MHC class I molecules. They may promote tolerance leading to virus and tumour 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 and -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-1infection. Thus, neurotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially.3

Pseudoloma neurophilia: A Retrospective and Descriptive Study of Nervous System and Muscle Infections, with New Implications for Pathogenesis and Behavioral Phenotypes

“…9 Inflammation of neuron cell bodies in the absence of directly observable pathogens in the cell body has some precedent in mammals: Human neurons express atypical MHC-I molecules in response to infection by rabies or herpesviruses, and rodent neurons in vitro can internalize and express foreign ovalbumin antigens via MHC-I complexes that leads to cytotoxic T-cell-mediated killing. 22,23 Histopathologically, most of the inflammatory cells surrounding cell bodies in zebrafish with P. neurophilia resembled microglial cells rather than T cells (Figs. 4 and 5).…”

HLA-G polymorphisms in women with squamous intraepithelial lesions harboring human papillomavirus

“…22 Although removal of the 92 bases produces a more stable mRNA, the presence of þ 14 bp has been associated with a lower mRNA production. 20 Some virus including Epstein-Barr virus, rabies virus and cytomegalovirus may upregulate HLA-G expression; 13,[23][24][25] however, the function of HPV in HLA-G expression has not been determined. Recently, we reported that cervical lesions may express HLA-G molecules that may differ according to the severity of SIL in HPV-infected women.…”

HLA-G: A Versatile Biomarker

“…HLA-G was reported to be expressed on cells infected with rabies virus [13,14], influenza virus [15], and herpes B virus [16]. In our lab, we have shown that herpes B virus infected human cells induce increased surface expression of HLA-G but HSV-1 infected cells do not show similar HLA-G expression [16].…”