Cell surface expression of H2 antigens on primary sensory neurons in response to acute but not latent herpes simplex virus infection in vivo

CD8(+) T lymphocytes and class I major histocompatibility complex (MHC-I) m olecules profoundly influence the severity of neuronal herpes simplex virus (HSV) infection in experimentally infected mice. Paradoxically, neurons ar e classically regarded as MHC-I deficient. However, it is shown here that H 2-encoded heavy chains (alpha Cs) and their associated light chain, beta 2 microglobulin, are present on the surfaces of primary sensory neurons recov ered from sensory ganglia within 1 to 2 weeks of HSV infection. During this time, some neurons are found to be tightly associated with T cells in vivo . Prior data showed that termination of productive HSV infection in the per ipheral nervous system is not dependent on cell-mediated lysis of infected neurons. Consistent with these data, immunogold electron microscopy showed that the density of cell surface H2 on neurons is an order of magnitude low er than on satellite glia, which is predicted to favor a noncytolytic CD8 c ell response.