Comparison of four test kits for feline leukemia virus antigen.

The sensitivity and specificity of 4 commercial FeLV ELISA kits, using blood, were compared with results of virus isolation from blood and immunofluorescent antibody (IFA) testing on blood. Significant differences were not found among the 4 ELISA kits. Marked decrease in sensitivity of the ELISA kits was detected when virus isolation was used as the standard of positivity rather than the IFA test. Virus isolation was a more sensitive indicator of early infection, with marked discrepancy among results obtained by virus isolation, ELISA, and the IFA test. Results became progressively more concordant as infection became fully established. Cats FeLV-positive by virus isolation alone were more likely to eliminate viremia. All cats FeLV-positive by IFA testing remained persistently viremic. Virus isolation, ELISA, and IFA testing appear to differ in their prognostic value. The use of blood rather than serum for the ELISA resulted in several discordant results. Six cats were FeLV-positive by ELISA when blood was tested but were FeLV-negative when serum was tested. Positive ELISA results were obtained for 4 of these cats when serum was tested, using extended incubation to increase sensitivity. It is possible that blood may actually be more sensitive than serum for use of the ELISA method.

Comparison of the efficacy of three commercial feline leukemia virus vaccines in a natural challenge exposure.

Forty-seven kittens were exposed for 31 weeks to 12 FeLV-positive carrier cats. The carrier cats were infected with 2 laboratory strains of FeLV and at least 2 strains of street virus. Eleven nonvaccinated control kittens and 12 vaccinated kittens were allotted to 3 groups. After 31 weeks of exposure, the following kittens were persistently blood FeLV positive by ELISA and immunofluorescence antibody (IFA) testing: 7 of the 11 control kittens, 0 of 12 kittens inoculated with vaccine A, 5 of 12 kittens inoculated with vaccine B, and 6 of 12 kittens inoculated with vaccine C. Only the kittens inoculated with vaccine A were significantly (P less than 0.05) different from the control group. After 23 weeks of exposure, culture was done to identify FeLV in the bone marrow of the kittens. Feline leukemia virus was isolated from the bone marrow of 9 of 11 control kittens. Virus was isolated from the bone marrow of 5 of 12 kittens inoculated with vaccine A, 11 of 12 kittens inoculated with vaccine B, and 10 of 12 kittens inoculated with vaccine C. Of the 17 cats that had FeLV isolated only from culture of bone marrow (negative results of blood virus isolation, ELISA, and IFA testing), 13 eliminated the virus from the bone marrow by week 31 of exposure. After 31 weeks of exposure, FeLV was isolated from the bone marrow of 8 of 11 control kittens, 0 of 12 kittens inoculated with vaccine A, 7 of 12 kittens inoculated with vaccine B, and 7 of 12 kittens inoculated with vaccine C.

Antibody response of kittens after vaccination followed by exposure to feline leukemia virus-infected cats.

Protein (western) blot analysis and virus-neutralization assay were used to evaluate the antibody response of specific-pathogen-free kittens to FeLV vaccination and followed by natural exposure. Several kittens had barely detectable reactions to specific FeLV antigens prior to vaccination or exposure. Correlation was not found between protection against persistent viremia and antibody response after vaccination as measured by western blot analysis or virus neutralization assay. A statistically significant (P less than 0.01) difference in the antibody response against p27 antigen after natural exposure to FeLV was observed between persistently viremic kittens and transiently viremic or aviremic kittens. Measurable (P less than 0.05) virus neutralizing antibody titer after FeLV exposure was found only in a small number of kittens that were protected against persistent viremia. Lack of association between humoral response and vaccination-induced protection against persistent FeLV infection suggests an important role for cell-mediated immunity in such protection.

Role of hypothermia in ethanol-induced conditioned taste aversion.

Two experiments examined the effect of ambient temperature during ethanol exposure on development of conditioned taste aversion to saccharin. In both studies, male albino rats receiving saccharin-ethanol (1.5 g/kg, IP) pairings followed by 6-h exposure to a 32 degrees C environment developed a weaker saccharin aversion than did rats experiencing ethanol at room temperature. Exposure to the warm environment reduced ethanol-induced hypothermia, but enhanced ethanol's motor-impairing effect. The influence of ambient temperature on ethanol-induced taste aversion may be due to changes in body temperature, neural sensitivity, or elimination rate. Although alternative accounts cannot be entirely dismissed, this outcome suggests that ethanol-induced hypothermia plays a role in determining strength of conditioned taste aversion and thus may be involved in the regulation of oral ethanol intake in rats.