What is Polyoma virus?

Polyoma Virus: A Comprehensive Overview

Polyomaviruses are small, non-enveloped DNA viruses that can remain latent after primary infection and reactivate during periods of immunosuppression, causing significant disease in immunocompromised individuals. 1

Types and Prevalence

Polyomaviruses are widespread in nature, with several types known to infect humans:

• BK virus (BKV): Infects up to 90% of the general population, typically acquired during childhood 2
• JC virus (JCV): Also widely prevalent in humans
• Merkel cell polyomavirus (MCV): Detected in 43-100% of Merkel cell carcinoma samples 3
• Other human polyomaviruses: KI polyomavirus, WU polyomavirus 4

Pathophysiology

Polyomaviruses typically cause:

1. Primary infection: Usually during childhood, generally asymptomatic
2. Latency: Virus remains dormant in specific tissues
   • BKV: Primarily in the kidney and urinary tract 2
   • JCV: In kidneys, brain, and lymphoid organs
3. Reactivation: Occurs during immunosuppression, leading to clinical disease

Clinical Manifestations

BK Virus

• Hemorrhagic cystitis: Particularly in bone marrow transplant recipients 4
• Nephropathy: Major cause of renal allograft failure in kidney transplant recipients 1
• Ureteral stenosis: Can cause obstruction in transplanted kidneys 2
• Less common: Pneumonitis, retinitis, liver disease, and meningoencephalitis 4

JC Virus

• Progressive multifocal leukoencephalopathy (PML): Fatal demyelinating disease of the CNS in immunocompromised hosts 3
• Potential association with neoplastic disorders: Role still under investigation 1

Merkel Cell Polyomavirus

• Merkel cell carcinoma: Aggressive cutaneous tumor with high mortality rate 3
• Risk factors include:
  • Extensive sun exposure
  • Age ≥65 years (predominantly in whites)
  • Immunosuppression (organ transplants, lymphoproliferative malignancies, HIV) 3

Diagnosis

BK Virus

• Quantitative plasma nucleic acid testing (NAT) 3:
  • Monthly for first 3-6 months after transplantation
  • Every 3 months until end of first post-transplant year
  • When unexplained rise in serum creatinine occurs
  • After treatment for acute rejection
• Urine cytology: Detection of "decoy cells" (virus-laden cells shed from tubules or urinary tract epithelium) 3
• Threshold for concern: BKV plasma NAT persistently greater than 10,000 copies/ml 3

JC Virus

• CSF testing: Detection of JCV DNA in cerebrospinal fluid by NAAT has largely replaced brain biopsy for PML diagnosis 3
• Brain biopsy: May reveal characteristic pathologic changes with in situ hybridization for JC virus 3

Management

BK Virus Nephropathy

• Reduction of immunosuppressive medications when BKV plasma NAT is persistently greater than 10,000 copies/ml 3
• Cidofovir: May be effective when combined with reduced immunosuppression, though renal toxicity is a significant complication 3, 2

JC Virus (PML)

• Reduction or cessation of immunosuppressive medication is the primary management strategy 3
• No FDA-approved specific antiviral therapy is available

Prevention in Transplant Recipients

• Screening protocols for BKV in kidney transplant recipients are recommended 3
• Early detection allows for preemptive reduction in immunosuppression before nephropathy develops

Special Considerations

Kidney Transplant Recipients

• BK virus is a significant cause of allograft nephropathy
• Regular screening with quantitative plasma NAT is recommended 3

Inflammatory Bowel Disease Patients

• Screening for JC virus (human polyoma virus-2) before initiating vedolizumab therapy is not recommended 3
• Only one case of PML has been reported with vedolizumab in a patient with co-existing HIV infection 3

Emerging Research

• Polyomaviruses have been implicated in various neoplastic disorders and autoimmune conditions 1
• The role of MCV in the pathogenesis of Merkel cell carcinoma is under active investigation 3

Polyomaviruses represent an important class of pathogens that primarily cause disease in immunocompromised hosts. Early detection through appropriate screening protocols and management through immunosuppression reduction remain the cornerstones of treatment for polyomavirus-associated diseases.