Papilloma and polyoma viruses
Also known as: papillomaviruses and polyomaviruses
Papillomaviruses and polyomaviruses are small, nonenveloped viruses with circular double-stranded DNA genomes that replicate in the host cell nucleus. Papillomaviruses cause warts and cervical cancer, while polyomaviruses such as JC and BK cause disease mainly in immunocompromised patients.
Both families share an unusual structural profile: nonenveloped icosahedral capsids enclosing circular double-stranded DNA, replicated in the nucleus using host machinery. The circular genome distinguishes them from most other DNA viruses, and the absence of an envelope makes them environmentally stable and resistant to detergents and drying. Historically grouped together as papovaviruses, they are now recognized as separate families.
Human papillomavirus (HPV) infects squamous epithelium, producing lesions that range from benign to malignant depending on the serotype. Types 1, 2, and 4 cause common and plantar warts; types 6 and 11 cause anogenital condyloma acuminatum and laryngeal papillomatosis; and types 16 and 18 are the high-risk oncogenic types responsible for most cervical cancer, along with many anal, vulvar, and oropharyngeal cancers. The oncogenic mechanism is well defined: viral protein E6 promotes degradation of the tumor suppressor p53, while E7 inactivates Rb, together releasing the cell cycle from its normal checkpoints. Cytology shows koilocytes — squamous cells with perinuclear halos. The multivalent HPV vaccine targets the major high-risk and wart-causing types.
The medically important human polyomaviruses are JC virus and BK virus, both of which infect most people asymptomatically in childhood and then persist latently. Reactivation occurs in immunosuppression. JC virus causes progressive multifocal leukoencephalopathy (PML), a demyelinating brain disease seen in advanced HIV infection and in patients on certain immunomodulatory therapies. BK virus reactivates most often after renal transplantation, causing nephropathy and hemorrhagic cystitis. A common mnemonic pairs JC with the brain ("junky cerebrum") and BK with the kidney and bladder ("bad kidney").
USMLE Step 1 tests these viruses in virology, expecting you to recall the shared naked, circular double-stranded DNA structure, match HPV serotypes to their lesions, explain E6 and E7 action on p53 and Rb, and associate JC with PML and BK with post-transplant renal disease.
Key takeaways
- Both families are nonenveloped viruses with circular double-stranded DNA genomes that replicate in the nucleus.
- HPV types 6 and 11 cause genital warts, while types 16 and 18 are the main oncogenic types.
- HPV E6 degrades p53 and E7 inactivates Rb, disabling cell cycle control and driving carcinogenesis.
- JC virus reactivation causes progressive multifocal leukoencephalopathy in immunocompromised patients.
- BK virus reactivation causes nephropathy and hemorrhagic cystitis, most notably after renal transplantation.