Abstract

The human foamy virus is a complex retrovirus that codes for several regulatory bel genes in addition to the conventional gag, pol, and env genes. The bel 3 gene is located in the 3' part of the viral genome comparable to that of the superantigen of the mouse mammary tumor virus. Superantigens bound to major histocompatibility complex (MHC) class II molecules have been shown to stimulate T cells in a V beta-specific manner. The recombinant Bel 3 protein purified to near homogeneity was assayed in vitro to determine whether or not it functions as a superantigen that stimulates human T lymphocytes expressing particular V beta T cell receptor (TCR) chains. Therefore, an analysis including all known human V beta elements was performed. The expression of different V beta chains of the TCR was analyzed by reverse transcription of the V beta RNAs and subsequent amplification of the corresponding V beta cDNA elements by polymerase chain reaction in unstimulated, phytohemaggluttinin (PHA)- and Bel 3-stimulated human T lymphocytes. In addition, eight monoclonal antibodies directed against particular V beta family members were used to determine any change in the expression of the remaining known V beta elements upon treatment with PHA and Bel 3. The comparative V beta-specific transcriptional analysis revealed that the in vitro expression of the V beta 18 chain was specifically and strongly expanded in Bel 3-stimulated human T cells, a property characteristic for a superantigen.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.