Polyoma virus middle T is essential for virus replication and persistence as well as for tumor induction in mice.
A mutant strain of polyoma virus encoding a truncated middle T protein has been studied for its ability to replicate and induce tumors following inoculation into newborn mice. Virus replication in the acute period prior to expected onset of tumors as well as persistence of virus in older animals were followed. The mutant virus proved to be defective in replication and persistence and failed to induce tumors. These results demonstrated that middle T plays an essential role in productive viral infection in the animal. Since the mutant virus encodes normal large and small T proteins, the results also indicate that functions associated with these T antigens, including large T binding of the retinoblastoma tumor suppressor gene product and the ability to immortalize, are insufficient to cause development of tumors in this system.
Freund
R
R
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.
Sotnikov
A
A
Bronson
R T
RT
Benjamin
T L
TL
D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D000952:Antigens, Polyomavirus Transforming / Q000494:pharmacology*; D007668:Kidney / Q000382:microbiology; D051379:Mice; D008809:Mice, Inbred C3H; D009154:Mutation; D009374:Neoplasms, Experimental / Q000382:microbiology*; D011120:Polyomavirus / Q000254:growth & development*; D014412:Tumor Virus Infections / Q000473:pathology*; D014779:Virus Replication
D000952:Antigens, Polyomavirus Transforming