A polypeptide encoded within the murine AIDS defective virus stimulates primary proliferation of CD8+ T-cells.

The murine AIDS (MAIDS) is a retrovirus-induced disease that shows severe immunodeficiency with abnormal lymphoproliferation in susceptible strains of mice. To clarify the antigenicity of gag gene products of the LP-BM5 defective virus, which is known as the causative virus of MAIDS, we expressed and purified the gag p12 gene product (P12) by using a baculovirus expression vector system. The P12 protein strongly stimulated the proliferation of normal C57BL/6 (B6) lymph node T-cells in vitro. Furthermore, a 25-mer synthetic polypeptide within the P12 sequence gave rise to the similar or even higher activation of T-cells. The phenotype of responding T-cells was found to be CD8+ CD44low, indicating that naive CD8+ T-cells respond against a peptide encoded within a MAIDS defective virus gag p12 gene. Finally, the expression of T-cell receptor (TcR) V beta on the responding CD8+ T-cells was analyzed. Although CD8+ T-cells with the particular V beta chains were expanded in response to the 25-mer peptide, this polypeptide does not seem to be a superantigen, since this response is MHC class I-restricted and the V beta preference is not striking. The presentation pathway of this highly antigenic polypeptide will be discussed.