Papova Viruses

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Papova Viruses

• fackrel_at_Uwindsor.ca

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Papova Viruses

• Structure
• Classification
• Multiplication
• Clinical manifestations
• Epidemiology
• Diagnosis
• Control

Barons Web site
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Genome
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Genome Function
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Papova virus Replication
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Classification
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Pathogenesis

• Mechanisms not well understood.
• Human papillomavirus are associated with the
  development of malignant genital lesions
• types 16 and 18,.
• Cofactors are required for cancer development.

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Multiplication

• Viral DNA latent in basal cells of benign
  lesions.
• Replication occurs in differentiating cells.
• Capsid proteins and viral particles are found
  only in terminally differentiated epidermal
  cells.
• Viral DNA is integrated in cancer cells, which
  contain no replicating virus.

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• They induce tumors in laboratory rodents.

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Clinical manifestations

• Polyomaviruses exhibit asymptomatic persistent
  infections in humans.
• The JC type of polyomavirus causes progressive
  multifocal leukoencephalopathy in humans.

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Clinical manifestations

• Benign papillomatous lesions of skin and mucous
  membranes
• (common warts, plantar warts, flat warts,
  anogenital warts, epidermodysplasia
  verruciformis, and laryngeal papillomas).
• Cervical intraepithelial neoplasia and cervical
  cancer are associated with human papillomavirus
  infection.

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Epidemiology

• Infections occur during childhood,
• 70 to 80 of adults have antibodies.
• Route of transmission is unknown
• may be respiratory.
• No animal reservoirs.
• Some humans also possess antibodies to SV40, a
  simian virus.

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Transmission

• Papillomaviruses widely distributed
• Transmission by contact.
• Genital warts sexually transmitted.
• Laryngeal papillomas may acquired during birth
  from a mother with genital warts.

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Control

• Localized destructive methods
• application of caustic agents
• Most warts regress spontaneously
• Sterilize instruments
• after examination of patients
• Educate Public
• prevent sexual transmission..
• Interferon
• effective vs laryngeal papillomas, common warts,
  and anogenital warts.

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Diagnosis
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Host Defenses

• Infections are persistent
• induce humoral antibodies and cytotoxic T cells.
• Immunosuppressed
• Impaired cell-mediated immunity
• progressive multifocal leukoencephalopathy.
• Interferon
• weakly induced
• variable sensitivity
• transformation by polyomaviruses inhibited

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DONE!!!