[Specificity of monoclonal antibodies obtained with the Paster PV rabies virus strain].
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Biomedical subjects
G Libeau
Publications and source records attributed to G Libeau.
Production of monoclonal antibodies against the Pasteur (P.V.) strain of rabies virus: problems and results.
Assuming the fact that the highest specific secreting hybrids number has been recorded with Iq secreting spleen cells, we did some immunizing protocols to maximize the ELISA reacting antibodies: for this Balb/c mice were primed intra-peritoneally with vaccine containing inactivated rabies (P.V. strain). Half of them were boosted intravenously with the same concentrated purified and live virus. We performed a series of hybridizations, at different times (i.e. 10, 15, 20, 75 days), between the rabies committed splenocytes and the SP 2/0 non secreting myeloma cells. Successful hybrids secreting antibody to rabies virus have only been obtained at the earliest and the latest time of fusion, essentially with the intravenous booster. They were initially screened by ELISA test for PV binding and about 65% of the colonies were generally positive. Clones directed against nucleocapsids were revealed by immunofluorescence of the rabies infected fixed cells, and those directed against glycoprotein by the neutralizing test and rabies infected live cells. From the early fusion we also produced hybrids secreting IgG (60%) or IgM (40%). At that time IgG/IgM distribution of specific hybrids do not correlate to that seen for ELISA reacting antibodies. It suggests that the IgG secreting spleen cells are the preferential fusion partners or the most vigorous ones.
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Anti-trypanosome specific immune responses in bovids of differing susceptibility to African trypanosomiasis.
A clone of Trypanosoma brucei brucei (DiTat 1.1) was injected into 32 bovids of various breeds, 11 animals being kept as controls. Five animals, Simmental-Ndama F1 crosses, were extremely sensitive. They showed overt symptoms and one died on day 18 of infection despite treatment with a trypanocidal drug. Seven other animals became ill but recovered progressively and cleared the infection. Twenty animals, of breeds generally considered to be trypanosensitive as well as ones from trypanotolerant breeds, did not show symptoms apart from anaemia and cleared the infection. Putative protective antibody, i.e. directed against exposed determinants on the coat variant-specific glycoprotein, was detected by agglutination, complement-mediated lysis and inhibition of infectivity. All animals showed a primary immune response consisting of IgM whose kinetics and amplitude were indistinguishable between animals of differing sensitivity. The response was long-lasting, whether the animals had been treated or not with a trypanocidal drug 3 weeks after infection, and antibody of IgG1 and IgG2 types were detected in certain sensitive as well as resistant animals after 2 months. Some animals were rechallenged with DiTat 1.1 either 1 year after the primary infection or 6 months after inoculation of irradiated trypanosomes. Peak titres of antibody were lower than was the case following primary infection but higher levels of mercaptoenthanol-resistant antibodies were seen. In no case was there any difference in the response of sensitive or tolerant animals. Our results do not support the idea that resistance of certain bovids to African trypanosomiasis is due to a better protective antibody response.
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[Deleterious effect of levamisole on experimental trypanosomiasis in mice].
One outbred strain, NMRI, and 4 inbred strains of mice, BALB/c A/J, CBA and C57B1/6, of widely differing susceptibilities to infection by Trypanosoma (Nannomonas) congolense, stock Dinderesso/80/CRTA/3, were treated throughout the course of infection with levamisole, an immunomodulating drug. Under the regime used this drug is capable of restoring depressed immune responses. Surprisingly, levamisole was not beneficial to the course of infection. In all of the strains except BALB/c, levamisole treatment increased mortality and in three of the strains parasitaemia was enhanced. The authors discuss possible reason for these findings which highlight the fact that the protective immune mechanisms operating in African trypanosomiasis are still poorly understood.
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