Immunology of herpesvirus infection: immunity to herpes simplex virus in eye infections.

A gereral, overall pattern of the temporal relationship and interaction between cell and antibody-mediated immune responses following herpes simplex virus infection of the rabbit cornea can be synthesized from our studies. Cell-mediated immunity (CMI) appears early following infection, at a time when mononuclear and lymphocytic cellular proliferation occur at the limbus. Interaction between specifically immune lymphocytes with virus antigens are detected by lymphocyte blastogenesis and migration inhabiting factor. During stromal keratitis, a second phase of CMI involves transient virus-specific cytotoxic lymphocytes, which destroy cells that display viral-induced antigens on their surface. Chemotatic factors generated by viral antigens alone or with antiviral antibody or by virus-sensitized lymphocytes play a role in attracting polymorphonuclear leukocytes to the cornea during stromal keratitis. Soluble mediators of CMI secreated by activated lymphocytes act both specifically and nonspecifically on virus-infected cells, allowing cell destruction and making intracellular virus available for neutralization by antiviral antibody. Cell-mediated immunity in the acute infection, diminishes with the appearance of significant antiviral antibody titers. The late phase of the corneal immune response results from a local antigen-antibody interaction and is characterized by cells predominantly of the plasmacytic type. The presence of complement-dependent cytotoxic antibodies capable of destroying virus-infected cells provide an additional factor in restriction of infection.