Notes

restricted antigen expressed on the BALB/c sarcoma Meth A
Because induction of the antibody required many vaccinations with irradiated and unirradiated Meth A cells over a prolonged period, we have investigated methods of improving the efficiency of producing Meth A antibody in BALB/c mice. Three general approaches were used: immunizing with irradiated Meth A cells mixed with adjuvants, immunizing with irradiated Meth A cells modified by treatment with chemicals, or administration of tumor cell vaccines in conjunction with low dose cyclophosphamide. These vaccine preparations were injected subcutaneously into groups of BALB/c mice five to six times at 2-wk intervals. chitosan supplement from all mice were screened for reactivity to Meth A by complement-dependent cytotoxicity, protein A, and mixed hemadsorption assays. Twenty-three vaccine preparations containing adjuvants or modified cells were tested in individual groups of mice. Mice in some groups receiving adjuvants and in all groups receiving modified cells produced antibody, but only after four to six vaccinations.

In contrast, nine of the 14 mice immunized with irradiated Meth A cells (unmodified and without adjuvant) in conjunction with 10 or 100 mg/kg body weight of cyclophosphamide, and all nine of the mice receiving 25 mg/kg cyclophosphamide made Meth A antibodies after only one or two vaccinations. The titer of antibodies produced after one treatment with cyclophosphamide and irradiated Meth A cells was at least as high as that achieved after five or six vaccinations in our other trials. The specificity of these antibodies for the Meth A antigen was established by absorption analysis. We conclude that treatment with cyclophosphamide before vaccination is highly effective in augmenting the humoral immune response to the Meth A antigen.Bursal Disease Virus in chickens.by destruction of antibody producing B cells in the Bursa of Fabricius and poses a potential threat to the poultry industry. We have examined the protective efficacy of a subunit DNA vaccine against IBDV infection in chickens in this study.

An immunodominant VP2 gene fragment (VP252-417) was cloned into CMV promoter based DNA vaccine vector pVAX1 and in vitro expression of the DNA encoded antigens was confirmed by transfection of CHO cells with vaccine constructs followed by RT-PCR and western blot analysis using IBDV-antiserum. Two weeks old chickens were immunized intramuscularly with pVAXVP252-417 and the in vivo transcription of the plasmid DNA was confirmed by RT-PCR analysis of DNA injected muscle tissue at different intervals of post immunization. Tissue distribution analysis revealed that the plasmid DNA was extensively distributed in muscle, spleen, kidney, liver, and bursa tissues. Chickens immunized with pVAXVP252-417 developed high titer (1:12,000) of anti-VP252-417 antibodies. Further, chicken splenocytes from pVAXVP252-417 immunized group showed a significantly high proliferation to the whole viral and recombinant antigen (P<0.01) compared to control groups, which implies that pVAXVP252-417 codes for immunogenic fragment which has epitopes capable of eliciting both B and T cell responses. This is evident by the fact that, pVAXVP252-417 immunized chicken conferred 75% protection against virulent IBDV (vIBDV) challenge compared to the control group.

Thus, the present study confirms that the immunodominant VP2 fragment can be used as a potential DNA vaccine against IBDV infection in against variant 2 avian infectious bronchitis virus challenge.Mass and Dutch variants as vaccine boosters after H120 priming on inhibiting variant 2 viral load in the kidneys (as the target organ) and reducing fecal shedding. Ciliostasis score and antibody response were investigated as well. A total of 150 specific-pathogen-free (SPF) chicken were divided into six groups. All groups were vaccinated with a single dose of attenuated H120 vaccine except for two (no vaccine groups). Then, chitosan supplement benefits received booster vaccines with inactivated polyvalent vaccines. At the 42 day of age, all groups were challenged with variant 2 viruses except for one (no vaccine group).
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