JC and BK viruses are small, nonenveloped double-stranded DNA tumour viruses . There are currently 10 known human polyomaviruses, most of them not associated with human disease.
JC and BK viruses are ubiquitous. Infection probably occurs early in life and a persistent/latent infection is extablished. By adulthood, 70-90% of individuals have antibodies to both JCV and BKV. There is serological evidence for reactivation of JC and/or BK in 5 to 10% of women during pregnancy, and virus can often be isolated from the urine. Whether human intrauterine infection with JC or BK occurs is still unresolved.The exact route of transmission is still unknown but probably occurs by aerosol inhalation or oral ingestion of virus.
Primary polyomavirus infections have not been associated with any specific clinical syndromes. Most infections seem to be subclinical although some children develop mild respiratory symptoms.
Progressive multifocal leucoencephalopathy ?
JC virus is thought to persist in a number of organs, including kidney, bone marrow and brain. In brain, JC virus sets up a true latent infection but may be reactivated, especially under conditions of severe immunosuppression.
Progressive Multifocal Leucoencephalopathy (PML) is a unique demyelinating disease caused by JC virus cytolytic infection of the oligodendrocytes. The majority of PML occurs in patients with AIDS with only sporadic cases of PML developing without an underlying immune disorder. Natalizumab, used in the treatment of MS, acts by preventing extravasation of T- cells and is associated with PML, suggesting the importance of immunosurveillance in the CNS.
The pathology of PML is distinctive with multiple foci of demyelination of varying size from pinpoint lesions to areas of several centimetres. The lesions may occur anywhere but are usually in the cerebral hemispheres, less often in the cerebellum and brain stem and rarely in the spinal cord. The oligodendrocytes in the peripheral zone surrounding an area of demyelination are grossly abnormal. The nuclei of abnormal oligodendrocytes are packed with JC virions. Typically, PML initially evolves gradually, with impairment of mental function and disturbance of speech and vision. Movement may also be affected. The disease then progresses rapidly and the patient becomes severely disabled, demented, blind and paralysed with finally coma and death.
The clinical diagnosis of PML is confirmed by finding JC virus DNA in CSF.
References
1. Jiang M et al. Minireview. The role of polyomaviruses in human disease. Virology 2009;384:266-273.
2. Bloomgren G et al . Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Eng J Med 2012;366:1870-80
For further information contact the laboratory (contact via Lablink: 22000 or (09) 307-8995 or 0800 522 7587) ,or:
the Virology team
virology@adhb.govt.nz
Laboratory Notes
CSF- send to VIM , store at room temperature
CSF required. Send in a sterile container at room temperature.