Summary. In-vitro culture of Haemophilus somnus in liquid or solid media supplemented with bovine blood or serum resulted in non-immune binding of immunoglobulin (Ig) by the organism. This binding was independent of the antigencombining site of the Ig molecule, since binding of an IgG preparation specific for the hapten dinitrophenol was unaffected by the presence of the homologous antigen. Quantitative comparison of the binding of Ig fragments Fab and Fc demonstrated that the non-immune binding occurred in the Fc region of bovine IgG. The isotypes of Ig that became bound to H. somnus included both bovine IgG subclasses (IgG1 and IgG2), which were bound equally, and bovine IgM.
SllmmaryRas protooncogenes are activated by characteristic point mutations in a wide variety of malignancies. The expressed p21 ~ proteins are oncogenic by virtue of single substituted amino acids, usually at position 12 or 61 of the 189-residue p21 ~ protein. In the current study, the ability of class I major histocompatibility complex (MHC)-restricted T cells to recognize the altered segment of a transforming p21 ~ protein and to lyse cells transformed by the corresponding ras oncogene was examined. Synthetic ms peptides encompassing the common activating substitution of leucine for glutamine at position 61 were constructed with an amino acid motif appropriate for binding to the H-2K b murine class I MHC molecule. Cytotoxic T lymphocytes (CTL) spedfic for bound ms leucine 61 peptide were elicited by in vitro immunization of normal lymphocytes with synthetic peptides. The ras peptide-induced CTL specifically lysed syngeneic fibroblasts transformed by an activated ras gene encoding oncogenic p21 ~ protein containing the same single amino acid substitution. Thus, in some circumstances, mutated p21 ~ protein can serve as a tumor-specific antigen.
The duration of HIV infection is usually unknown for most patients entering into HIV care. Data on the frequency at which resistance mutations are detected in these patients are needed to support practical guidance on the use of resistance testing in this clinical situation. Furthermore, little is known about HIV subtype diversity in much of the United States. Therefore, we analyzed the prevalence of drug resistance mutations and nonsubtype B strains of HIV among antiretroviral-naïve individuals presenting for HIV care in New York State between September 2000 and January 2004. Sequences were obtained using a commercial HIV genotyping assay. Seventeen of 151 subjects (11.3%; 95% confidence interval 7.2%-17.3%) had at least one drug-resistance mutation, including 5 subjects with fewer than 200 CD4(+) T cells, indicative of advanced infection. Nucleoside reverse transcriptase inhibitor, non-nucleoside reverse transcriptase inhibitor, and protease inhibitor resistance mutations were detected in 6.6%, 5.3%, and 0.7% of subjects, respectively. Subjects from New York City-based clinics were less likely to have resistant virus than subjects from clinics elsewhere in New York State. Nonsubtype B strains of HIV were detected in 9 (6.0%) individuals and were associated with heterosexual contact. Two nonsubtype B strains from this cohort also carried drug-resistance mutations. These data indicate that drug-resistant virus is frequently detected in antiretroviral-naïve individuals entering HIV care in New York State. Furthermore, a diverse set of nonsubtype B strains were identified and evidence suggests that nonsubtype B strains, including those carrying drug-resistance mutations, are being transmitted in New York State.
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