Post-exposure vaccination improves gammaherpesvirus neutralization.
Herpesvirus carriers transmit infection despite making virus-specific antibodies. Thus, their antibody responses are not necessarily optimal. An important question for infection control is whether vaccinating carriers might improve virus neutralization. The antibody response to murine gamma-herpesvirus-68 (MHV-68) blocks cell binding, but fails to block and even enhances an IgG Fc receptor-dependent infection of myeloid cells. Viral membrane fusion therefore remains intact. Although gH/gL-specific monoclonal antibodies can block infection at a post-binding step close to membrane fusion, gH/gL is a relatively minor antibody target in virus carriers. We show here that gH/gL-specific antibodies can block both Fc receptor-independent and Fc receptor-dependent infections, and that vaccinating virus carriers with a gH/gL fusion protein improves their capacity for virus neutralization both in vitro and in vivo. This approach has the potential to reduce herpesvirus transmission.
Gillet
Laurent
L
Division of Virology, Department of Pathology, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
May
Janet S
JS
Stevenson
Philip G
PG
D000818:Animals; D057134:Antibodies, Neutralizing / Q000276:immunology*; D002460:Cell Line; D006224:Cricetinae; D005434:Flow Cytometry; D018142:Gammaherpesvirinae / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D014765:Viral Vaccines / Q000008:administration & dosage* / Q000276:immunology
D057134:Antibodies, Neutralizing; D007074:Immunoglobulin G; D014765:Viral Vaccines