The purpose of the study was to test the therapeutic effects of novel vaccines for reducing weight gain and increasing weight loss in diet induced obesity (DIO) model. Male C57BL/6 J mice, fed a 60% Kcal fat diet for 8 weeks prior to the start of the study, were vaccinated via the intraperitoneal route with two formulations (JH17 & JH18) of chimeric-somatostatin vaccines at 1 and 22 days of the study. Control mice were injected with PBS. All mice continued to be feed the 60% Kcal fat diet for the 6 week study. Body weights were measured two times a week and food intake was measured weekly. At week 6, mice were euthanized and a terminal bleed was made and antibody levels to somatostatin and levels of insulin-like growth factor 1 (IGF-1) were determined. Vaccination with both vaccine formulations induced a statistically significant body weight change over the study period, as compared with PBS controls. Percentage of baseline body weight was also significantly affected by vaccination during the study period. Vaccinates finished the study at 104% and 107% of baseline weight, JH17 & JH18 respectively, while untreated controls reached 115% of baseline weight. Food intake per mouse was similar in all mouse groups during the entire study. Control mice did not demonstrate any antibody titers to somatostatin, while all vaccinated mice had measurable antibody responses (> 1:500,000 titer). IGF-1 levels were not statistically significant among the groups, but were elevated in the JH18 vaccinates (mean 440.4 ng/mL) when compared with PBS controls (mean 365.6 ng/mL). Vaccination with either JH17 or JH18 chimeric –somatostatin vaccines produced a statistically significant weight loss as compared with PBS controls (P < 0.0001), even though the DIO mice with continually fed a 60% Kcal fat diet. The weight loss/lower weight gain observations were even more significant, as all mice consumed similar amounts of food for the entire study. The presence of high levels of anti-somatostatin antibodies at 6 weeks was correlative with the weight observations and confirmed the success of vaccination.

Macrophages form S- and K-strain Leghorn chickens, susceptible and restant to Marek's disease (MD) respectively, were studied to determine the macrophage contribution to the dynamics of MD infection, tumorigenesis and genetic resistance to this disease. In vitro studies demonstrated that macrophages from bothstrains were similar in their responses toward JM strain of Marek's disease virus (MDV) and JM-1 tumor cells. Macrophages were observed to phagocytize JM virus, but the interiorized virus was not seen to replicate within the macrophage or induce antigenic changes of the cell membrane. Clearance of JM-1 tumor cells was by both cytolytic and phagocytic mechanism. In vivo selective suppression of macrophage functions by antimacrophage serum or trypan blue inoculations resulted in significantly elevated viral titers and increased tumorigenesis, as compared to infected, non-suppressed or non-infected control groups. Results from this study indicate that genetic susceptibility or resistance to MD, as exhibited by S- and K-strain chickens, respectively, is not controlled at the macrophage level. The role of the macrophage in MD infection appears to be specifically surveillance.

This is a review of the current knowledge of feline leukemia virus (FeLV) associated with immune depression observed in cats. It will focus on the clinical and experimental observations associated with feline retroviral infection and presence in vivo and in vitro. We will briefly describe retroviral-associated acquired immune deficiency syndrome associated with FeLV infection in the cat and specific cellular pathology associated with FeLV latency. In addition, we will focus on the action of FeLV-p15E in vitro and describe possible mechanisms of the FeLV-associated immunosuppression observed both in vivo and in vitro. Lastly, we will evaluate the current status of immunoprevention of FeLV. We will not attempt an in-depth analysis of the current literature; our focus is to review current findings as they relate to feline AIDS and immunotherapy.

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A temperature-sensitive (ts) mutant of avian reovirus isolate Maine 1-203 was obtained at 41 C. The 19th passage of this mutant (ts 19) was utilized for in vitro studies comparing its replication in macrophage cultures with that of its parent strain and an apathogenic S1133 virus. In vivo studies were initiated to determine the ts mutant's pathogenicity for day-old chicks, safety and protective levels for 6-day-old chicks, and interference with Marek's disease, Newcastle, and infectious bronchitis vaccinations. Although the results of in vitro trials indicated no difference among the three reoviruses in the in vitro pathogenicity for macrophage cultures, in vivo studies found the mutant to differ from its parent strain in pathogenicity for day-old chicks. When the ts mutant was administered at 6 days of age, it was a safe and effective vaccine against viral arthritis, with no resulting suppression of other vaccine responses.