JCvirus

JC virus (JCV) is a small, nonenveloped double-stranded DNA virus in the polyomavirus family. It is named after the patient John Cunningham from whom it was first isolated in 1971 in association with progressive multifocal leukoencephalopathy (PML). JCV is widespread in humans, with seroprevalence increasing with age.

Most primary infections are asymptomatic and occur in childhood. After initial infection, the virus establishes latency, principally in the kidneys and lymphoid tissue, with possible persistence in bone marrow and other sites. Reactivation can occur during immunosuppression, allowing viral replication and spread to the brain.

JC virus has a preference for oligodendrocytes, leading to demyelination of the central nervous system. The most important clinical manifestation is PML, a progressive, focal neurologic disorder characterized by weakness, sensory loss, visual deficits, ataxia, and cognitive or language changes. On MRI, PML shows multifocal, white-matter lesions that are often periventricular or subcortical, T2 hyperintense, non-enhancing, and without mass effect.

Diagnosis relies on detection of JCV DNA in cerebrospinal fluid by PCR, supported by MRI findings; brain biopsy is rarely needed. Serology can indicate prior exposure but does not distinguish active disease.

Treatment centers on restoring immune function and reducing immunosuppression where possible. In HIV-associated PML, antiretroviral therapy is used; in natalizumab- or rituximab-associated PML, stopping the drug and switching therapy is recommended. There is no widely approved antiviral therapy; prognosis is variable and often poor, though immune reconstitution can stabilize or improve outcomes. IRIS can complicate recovery and may require corticosteroids.

JCV remains a significant cause of demyelinating disease in immunocompromised patients. Vaccination is not available; prevention focuses on monitoring and adjusting immunosuppressive therapies; ongoing research seeks targeted antivirals and vaccines.