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Understanding Papova Viruses: Structure, Classification, and Clinical Manifestations

Learn about the structure, multiplication, and epidemiology of Papova viruses, including their clinical manifestations and control methods. Explore the genome, replication, and pathogenesis of these viruses.

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Understanding Papova Viruses: Structure, Classification, and Clinical Manifestations

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  1. Papova Viruses fackrel@Uwindsor.ca

  2. Papova Viruses • Structure • Classification • Multiplication • Clinical manifestations • Epidemiology • Diagnosis • Control Baron’s Web site

  3. Genome

  4. Genome Function

  5. Papova virus Replication

  6. Classification

  7. 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.

  8. 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.

  9. They induce tumors in laboratory rodents.

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

  11. 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.

  12. 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.

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

  14. 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.

  15. Diagnosis

  16. 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

  17. DONE!!!

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