Mutual functional antagonism of the simian virus 40 T antigen and the hepatitis B virus trans activator.
The hepatitis B virus X protein (pX) trans activates transcription of a wide variety of viral and cellular genes, apparently by interacting with multiple cellular transcription factors. It has been shown previously that the simian virus 40 early-region gene products (large-T and small-t antigens) prevent trans activation by pX. We show here that this phenomenon can be ascribed solely to the large-T antigen and that T antigen binds to pX in vitro. Mapping studies reveal that the region of large-T antigen around residues 125 and 126 is critical for this binding and also for the ability of T antigen to prevent trans activation by pX. Furthermore, pX in turn interferes with two of the known functions of T antigen, transcriptional trans activation and simian virus 40 DNA replication. We propose that pX and T antigen inactivate each other by forming a nonfunctional complex in vivo.
Seto
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Department of Pathology, Veterans Affairs Medical Center, San Francisco, California.
Yen
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D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000037:antagonists & inhibitors* / Q000378:metabolism; D002478:Cells, Cultured; D006511:Hepatitis B Antigens / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009154:Mutation; D010957:Plasmids; D011233:Precipitin Tests; D013539:Simian virus 40 / Q000276:immunology*; D015534:Trans-Activators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015533:Transcriptional Activation; D014162:Transfection; D054334:Viral Regulatory and Accessory Proteins
D000952:Antigens, Polyomavirus Transforming; D006511:Hepatitis B Antigens; D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein