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Infection with an H2 recombinant herpes simplex virus vector results in expression of MHC class I antigens on the surfaces of human neuroblastoma cells in vitro and mouse sensory neurons in vivo

Infectious Diseases Laboratories, Institute of Medical and Veterinary Science, Frome Road, Adelaide, South Australia 5000, Australia¹

Author for correspondence: Tony Simmons. Fax +61 8 222 3543. e-mail tony.simmons{at}imvs.sa.gov.au

The majority of neurons in herpes simplex virus (HSV)-infected murine sensory ganglia are transiently induced to express MHC-I antigens at the cell surface, whereas only a minority are themselves productively infected. The aim of the current work was to determine whether MHC-I antigens can be expressed on the surfaces of infected neurons in addition to their uninfected neighbours. To address this aim a recombinant HSV type 1 strain, S-130, was used to deliver a mouse H2K^d gene, under control of the HCMV IE-1 promoter/enhancer, into human neuroblastoma cells in vitro and mouse primary sensory neurons in vivo. S-130 expressed H2K^d antigens on the surfaces of IMR-32 cells, a human neuroblastoma cell line that expresses very low levels of MHC-I constitutively. In K562 cells, which do not express MHC-I constitutively, H2K^d and ₂-microglobulin (₂m) were shown to be co-expressed at the cell surface following S-130 infection. This observation was taken as evidence that class I heavy chain (C) molecules encoded by the expression cassette in the HSV genome were transported to the cell surface as stable complexes with ₂m. Significantly, after introduction of S-130 into flank skin, H2K^d antigens were detected on the surfaces of primary sensory neurons in ganglia innervating the inoculation site. Our data show that HSV-infected murine primary sensory neurons and human neuroblastoma cells are capable of expressing cell-surface MHC-I molecules encoded by a transgene. From this, we infer that up-regulation of C expression is, in principle, sufficient to overcome potential impediments to neuronal cell surface expression of MHC-I complexes.

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