The chicken major histocompatibility (B) complex (MHC) affects disease outcome significantly. One of the best characterized systems of MHC control is the response to the oncogenic retrovirus, Rous sarcoma virus (RSV). Genetic selection altered the tumor growth pattern, either regressively or progressively, with the data suggesting control by one or a few loci. Particular MHC genotypes determine RSV tumor regression or progression indicating the crucial B complex role in Rous sarcoma outcome. Analysis of inbred lines, their crosses, congenic lines, and noninbred populations has revealed the anti-RSV response of many B complex haplotypes. Tumor growth disparity among lines identical at the MHC but differing in their background genes suggested a non-MHC gene contribution to tumor fate. Genetic complementation in tumor growth has also been demonstrated for MHC and non-MHC genes. RSV tumor expansion reflects both tumor cell proliferation and viral replication generating new tumor cells. In addition, the B complex controls tumor growth induced by a subviral DNA construct encoding only the RSV v-src oncogene. Immunity to subsequent tumors and metastasis also exhibit MHC control. Genotypes that regressed either RSV or v-src DNA primary tumors had enhanced protection against subsequent homologous challenge. Regressor B genotypes had lower tumor metastasis compared with progressor types. Together, the data indicate that B complex control of RSV tumor fate is strongly defined by the response to a v-src-determined function. Differential RSV tumor outcomes among various B genotypes may include immune recognition of a tumor-specific antigen or immune system influences on viral replication.
The influence of the major histocompatibility (B) complex on acquired immunity to the avian coccidium Eimeria tenella was studied in 217 F4 segregants (B2B2, B2B5, B5B5) of a cross between inbred lines 6(1) (B2B2) and 15(1) (B5B5) and segregating haplotype combinations of UNH105 (B23B23, B23B24, B24B24), a noninbred line of New Hampshire chickens. Chickens were immunized at 6 weeks of age with 500 oocysts daily for 5 days, then challenged 14 days later with 10 000 oocysts. Responses to infection were evaluated by cecal lesion scores, body weight gain, delayed wattle reaction (DWR), and spleen weight. The F4 segregants of genotypes B2B5 and B5B5 exhibited greater immunity to challenge than B2B2 chickens. B5B5 chickens showed a significantly greater DWR following immunization and larger spleens 6 days after the challenge than either of the other genotypes. However, both B2B5 and B5B5 chickens demonstrated significantly lower lesion scores than B2B2 chickens. There were no significant differences in weight gain among these genotypes. Among 139 line UNH105 segregants, B23B23 hosts had significantly lower lesion scores than B24B24 chickens. No other differences in immune response among line UNH105 genotypes were detected.
Incorporation of amphotericin B into liposomes significantly altered its toxicity, tissue distribution, and efficacy. Compared with intravenously administered amphotericin B-desoxycholate, liposome-amphotericin B showed a reduced acute toxicity and a maximal tolerable dose 9 times greater than amphotericin B-desoxycholate. Liposome-amphotericin B also produced higher tissue and lower serum concentrations than amphotericin B-desoxycholate, and was significantly more effective in prolonging survival of mice infected with Histoplasma capsulatum.
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