Non-enveloped capsid with a T=7d icosahedral symmetry, about 50 nm in diameter.
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Circular dsDNA about 5 kb in size, associated with cellular histones in a chromatin-like complex. Encodes for 5-9 proteins.
On rare non-specific recombination, the viral genome can be integrated in host chromosome. This inactivates the integrated virus but can give the host cell a replicative advantage sometimes leading to malignant tumours.


Transcription is nuclear, in two phases; early (replication), late (virion assembly/exit). 5-9 proteins are expressed from the two pre-MRNA by alternative splicing. All genes are transcribed by host RNA pol II.



  1. Attachement of the viral proteins to host receptors triggers lipid-mediated endocytosis of the virus into the host cell.
  2. Virion transits through endoplasmic reticulum where host protein disulfide isomerases rearrange its capsid structure
  3. Export of misfolded virion to the cytoplasm possibly through host ERAD pathway
  4. Loss of VP1 in the low-calcium conditions of the cytosol
  5. Import of genomic DNA into host nucleus.
  6. Transcription of early genes (LT and sT genes)
  7. Replication of the DNA genome in the nucleus.
  8. Transcription of late genes encoding for structural proteins (VP1, VP2 and VP3).
  9. Assembly of new virions in nuclear viral factories.
  10. Virions are released by lysis of the cell.

Host-virus interaction

Cell-cycle modulation

The large T antigen binds to host key cell cycle regulators retinoblastoma protein RB1/pRb and TP53 and induces the disassembly of host E2F1 transcription factors from RB1, thus promoting transcriptional activation of E2F1-regulated S-phase genes.