Polyomaviruses

A medically important polyomavirus, the JC virus, causes progressive multifocal leukoencephalopathy (PML), a demyelinating disease that has become more frequent as a sequel to HIV infections, but is otherwise rare. The same applies to the BK virus, which affects bone marrow transplantation patients. Electron microscopy or PCR are the main diagnostic tools.

Pathogens. The polyomaviruses can be divided into two groups: in one group are the SV40 and SV40-like viruses (Fig. 1) such as human pathogen JC and BK viruses. In the other are the true polyomaviruses such as the carcinogenic murine polyomavirus. The designations JC and BK are the initials of the first patients in whom these viral types were identified. There are also a number of other zoopathic oncogenic polyomaviruses. The name polyoma refers to the ability of this organism to produce tumors in many different organs.

Pathogenesis and clinical picture. The JC and BK viruses are widespread: over 80% of the adult population shows antibodies to them, despite which, clinical manifestations like PML are very rare. The viruses can be reactivated by a weakening of the immune defense system. The JC virus attacks the macroglia, especially in AIDS patients, to cause progressive multifocal PML, a demyelinating process in the brain with disseminated foci that is fatal within one year. The BK virus can cause hemorrhagic cystitis in bone marrow transplantation patients.

Fig. 1 Section through viral conglomerations in the nucleus of the host cell (TEM).

Diagnosis. The JC and BK viruses can be grown in cultures, albeit with great difficulty and not for diagnostic purposes. Both can be detected with PCR and the BK virus can be seen under the electron microscope in urine. Antibody assays are practically useless due to the high level of generalized contamina­tion.

Epidemiology. Despite the high level of generalized contamination, the trans­mission routes used by the human polyomaviruses have not been clarified.