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Cancer-causing viruses Persistence (latency) Immune evasion

Cancer-causing viruses Persistence (latency) Immune evasion. Papovaviridae. dsDNA, non-enveloped, cubic symmetry, 55nm. Small, non-enveloped icosahedral viruses containing a closed circular ds genome of ~ 8kpb and encode ~ 10 genes

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Cancer-causing viruses Persistence (latency) Immune evasion

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  1. Cancer-causing viruses Persistence (latency) Immune evasion

  2. Papovaviridae dsDNA, non-enveloped, cubic symmetry, 55nm • Small, non-enveloped icosahedral viruses containing a closed circular ds genome of ~ 8kpb and encode ~ 10 genes • Papillomaviruses infect epithelial cells (epitheliotropic) inducing a benign proliferation recognised as a wart. • In some cases lesions induced by papillomaviruses may progress to form carcinomas. • Strictly species specific • Tissue specific • Site specific

  3. Structure

  4. Structure • The capsid has 72 capsomeres made up of two structural proteins • Genome is divided into: • An early region that encodes functions necessary for replication and contains the genes associated with neoplastic transformation. • • A late region transcribed after DNA replication that encodes the two capsid proteins

  5. Papillomavirus Replication • In a typical infection of squamous epithelium, a basal cell becomes infected following a minor abrasion. • Viral replication occurs in the nucleus and proceeds in step with the differentiation of the epithelium. • In many virus infections viral functions suppress cellular DNA synthesis but in papillomavirus infections, expression of the early genes results in a proliferative stimulus to cells so that they undergo additional cell divisions leading to a papilloma or wart. • DNA synthesis follows early gene expression. • New virus particles are assembled in the nucleus and free virus is shed with the dead cells that slough off from the surface of the wart.

  6. Virion assembly L1, L2 E4, Viral DNA replication E1, E2, E5, E6, E7 Papillomavirus Replication

  7. BPV-2 Papillomaviruses & disease Papillomavirus is heterogeneous Human Papillomavirus – HPV >100 types Bovine Papillomavirus – BPV >19 types Cottontail Rabbit Papillomavirus – CRPV Canine Oral Papillomavirus - COPV Equine Papillomavirus – EqPV European Elk Papillomavirus – EEPV Rabbit Oral Papillomavirus - ROPV Etc. etc

  8. BPV-1 causes teat frond papillomas. These are associated with a florid fibroblastic proliferation in the dermis although the virus only infects epithelial cells. • BPV-2 Is the agent of common cutaneous warts. • BPV-1 and 2 are the exception to the rule that papilloma viruses are species specific. The genomes of both these viruses have been found in sarcoids of horses and donkeys and in pre-cancerous lesions on the ears of sheep. • BPV-2 has also been found in bladder cancers of cattle. Consumption of bracken fern appears to be a necessary co-factor for the development of these cancers. Bracken fern has been shown to contain both immunosuppressants and mutagens • BPV-4 is the cause of alimentary papillomas found in the palate, oesophagus and entrance to the rumen. Bovine Papillomaviruses

  9. BPV GI cancer Bladder cancer Bracken fern BPV and Cancer in Cattle

  10. Papillomavirus Is A Cancer Virus • BPV-2 is involved in bovine urinary bladder cancer • BPV-4 is involved in bovine upper GI tract cancer • BPV-1 is involved in bovine penile cancer and equine sarcoid • HPV-16 (and others) is involved in ano-genital cancer

  11. BPV and Sarcoids in Horses Fibroblastic tumour of viral etiology: BPV-1 (BPV-2) Location: head/ears, limbs, abdomen, sites of trauma/healed wounds Type: occult (flat), nodular, verrucous (warty), fibroblastic, mixed, malignant

  12. Prevention and Control • Papillomaviruses are either transmitted by individual-to-individual contact or, as they are relatively resistant, they may be transmitted by abrasions from contaminated fomites. • Warts often regress under the influence of T-cell mediated immunity. Consequently, the identification of early pre-cancerous lesions offers an opportunity to attempt therapeutic as opposed to prophylactic (preventative) vaccination. • Papillomaviruses cannot be grown in tissue culture and in the past crude autogenous vaccines were prepared from wart material. In the last few years, the genes for the early and late proteins of papillomaviruses have been cloned and expressed in bacteria. Very promising results have been obtained by using the late proteins to prevent infection or to induce regressions in pre-existing papillomas. These results have obvious implications for the treatment of the pre-neoplastic stages of cervical carcinoma in women.

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