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A Possible Contributory Role of BK Virus Infection in Neuroblastoma Development¹

Department of Pediatrics, University of Tromsø, N-9038 Tromsø, Norway [T. F., G. E. J., A. K.]; Departments of Pathology [P. A. A.] and Virology [P. A. A., J. I. J., S. K. F., S. V., T. T.], University of Tromsø, N-9037 Tromsø, Norway; and Children’s Cancer Research Group, Karolinska Institutet, S-17176 Stockholm, Sweden [P. K.]

The tumor suppressor protein p53 is aberrantly localized to the cytoplasm of neuroblastoma cells, compromising the suppressor function of this protein. Such tumors are experimentally induced in transgenic mice expressing the large tumor (T) antigen of polyomaviruses. The oncogenic mechanisms of T antigen include complex formation with, and inactivation of, the tumor suppressor protein p53.

Samples from 18 human neuroblastomas and five normal human adrenal glands were examined. BK virus DNA was detected in all neuroblastomas and none of five normal adrenal glands by PCR. Using DNA in situ hybridization, polyomaviral DNA was found in the tumor cells of 17 of 18 neuroblastomas, but in none of five adrenal medullas. Expression of the large T antigen was detected in the tumor cells of 16 of 18 neuroblastomas, but in none of the five adrenal medullas. By double immunostaining BK virus T antigen and p53 was colocalized to the cytoplasm of the tumor cells. Immunoprecipitation revealed binding between the two proteins.

The presence and expression of BK virus in neuroblastomas, but not in normal adrenal medulla, and colocalization and binding to p53, suggest that this virus may play a contributory role in the development of this neoplasm.

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