Antibody and Cell‐Mediated Immune Responses to Feline Herpesvirus 1 Following Inactivated Vaccine and Challenge

Abstract

Summary Specific‐pathogen‐free cats were immunized with a betapropiolactone‐inactivated feline herpesvirus 1 (FHV1) vaccine, with or without alhydrogel adjuvant, and antibody and cell mediated immune responses were measured. Maximal antibody titres were obtained in 2 cats vaccinated with 2 doses of adjuvanted vaccine. Antibody persisted at low levels for at least 10 months in 3 of 4 vaccinated cats and there was a strong anamnestic antibody response in the 4 vaccinated cats following FHV1 challenge 10 months after vaccination. FHV1 antigen specific lymphocyte blastogenesis (LB), was detected following vaccination and challenge. A cell‐mediated plaque reduction (CMPR) assay was developed using both autologous kitten kidney (AKK) cells, prepared by unilaterally nephrectomizing cats, and a feline embryo (FEmb) cell line. Leukocyte suspensions enriched for T lymphocytes mediated a major histocompatabily (MHC)‐restricted, cytotoxic T (Tc) lymphocyte response. Buffy coat cells, with added plasma, mediated and MHC — unrestricted CMPR response which was interpreted as an antibody dependent cell mediated cytotoxicity (ADCC). Both null cells, presumably a feline killer (K) cell, and neutrophils were effector cells in ADCC. In 51Cr release cell mediated cytotoxicity (CMC) assay leukocytes from vaccinated cats were cytotoxic for both AKK‐ and FEmb‐FHV1 infected target cell suspensions when tested 10 months post‐vaccination and 3 days before FHV1 challenge. CMC was augmented in the vaccinated cats and a significant primary response was observed in an unvaccinated control cat on day 4 post challenge. The levels of cytotoxicity were higher in AKK than in FEmb cells and effector cells enriched for T lymphocytes were more cytotoxic for AKK cells indicative of a MHC‐restricted Tc lymphocyte response. Zusammenfassung Antikörper‐ und zellvermittelte Reaktionen gegen Katzenherpesvirus 1 nach Impfung mit inaktivierter Vakzine und Testinfektion Spf‐Katzen wurden mit betapropiolakton‐inaktivierter Katzenherpesvirus‐1(FHV 1)‐Vakzine mit oder ohne Alhydrogel geimpft. Anschließend wurde die antikörper‐ und zellvermittelte Immunreaktion gemessen. Die maximalen Antikörpertiter hatten zwei Katzen, die mit 2 Dosen der Adjuvans‐Vakzine geimpft worden waren. In drei von vier geimpften Katzen konnten geringe Antikörpertiter noch mindestens zehn Monate nach der Impfung festgestellt werden. 10 Monate nach der Impfung löste eine Belastung mit FHV 1 eine starke anamnestische Antikörperreaktion in den vier geimpften Katzen aus. FHV 1‐antigenspezifische Lymphozytenblastogenese (LB) konnte bei geimpften und belasteten Katzen nachgewiesen werden. Ein zellvermittelter Plaque‐Reduktionstest (CMPR) wurde mit autologen, von einseitig nephrektomierten Katzen gewonnenen Welpennierenzellen (AKK), und einer Katzenembryozellinie entwickelt. Leukozytensuspensionen, die mit T‐Lymphozyten angereichert waren, vermittelten eine auf den MHC begrenzte zytotoxische T‐Lymphozytenreaktion. In Plasma aufgeschwemmte “Buffycoat” Zellen vermittelten einen MHC, der nicht auf di...

Vaccines in Veterinary Medicine: A Brief Review of History and Technology

“…It is clear that the presence of neutralizing, vaccine-derived antibody will reduce mucosal virus replication, virus shedding, and viremia in kittens vaccinated with modified live feline herpes vaccines. [20][21][22] However, regulated CD41 and CD81 cellular responses are required to control tissue damage and reactivation of disease. 23 In this case, antibody may be a protective correlate of infection while cellular immunity is a protective correlate of disease.…”

“…The ability of modified live vaccines to generate a very rapid onset of cytokines and interferons (and rapid antigen focusing in dendritic cells in lymphoid tissues) is associated with a rapid onset of protection, even though antibody responses may not be detectable in serum for up to 2 weeks. [20][21][22] Therefore, the early response of multiple cytokines and concurrent activation of the innate immune system may serve as early correlates of protection. There are also documented cases in which functional immunity outlasts detectable circulating antibody; this is true with many herpesvirus infections.…”