Human polyomaviruses (HPyVs) are members of a genus of DNA viruses in the Polyomaviridae family. Fourteen HPyV species have been identified. JC virus (JCV) was first reported in the 1970s as well as another HPyV, BK virus (BKV). BKV was isolated in tissue culture from the urine of a kidney transplant recipient with ureteral stenosis; JCV was isolated from the brain tissue of a patient with Hodgkin lymphoma and progressive multifocal leukoencephalopathy.
From LabPlus Test Guide:
JCV and BKV 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 JCV and/or BKV in 5 to 10% of women during pregnancy, and virus can often be isolated from the urine. Whether human intrauterine infection with JCV or BKV occurs is still unresolved. The exact route of transmission is still unknown but probably occurs by aerosol inhalation or oral ingestion of virus.
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 JCV 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.
PLEASE NOTE: Serology testing for JCV is not performed in NZ. Antibody testing for MS patients is available from Unilabs Denmark, the patient MUST be enrolled appropriately before sending any samples. Virology/Serology does not deal with these samples or the results. Please contact CHLResearch@cdhb.health.nz for more information.
Microbiology - Virology
Referred to LabPlus Auckland for testing
Chilled (2 - 8 degrees Celsius)
Detection of virus does not always correspond to clinically important disease.
Due to the sensitivity of some JC PCR assays a positive test for JC supports diagnosis, but a negative result does not exclude it. Repeating the PCR on a specimen obtained later in the course of disease may assist with diagnosis in some patients in whom the initial PCR is negative.
Nucleic acid extraction and PCR for JC virus.
$245.19 (Exclusive of GST)
Testing performed by LabPlus Auckland
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