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Pathogenesis of AIDS-associated Kaposi's sarcoma

B Ensoli1, G Barillari, R C Gallo

  • 1Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Insights

Kaposi's sarcoma (KS) pathogenesis is being uncovered using new models. HIV-Tat protein may play a key role in the development and progression of this mesenchymal tumor in infected individuals.

Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Kaposi's sarcoma (KS) is a mesenchymal tumor with complex origins, frequently affecting individuals with HIV.
  • Epidemic KS lesions exhibit mixed cellularity, spindle cell proliferation, and new blood vessel formation.
  • Spindle cells, the presumed tumor cells, originate from mesenchymal cells and share traits with endothelial and smooth muscle cells.

Purpose of the Study:

  • To investigate the pathogenesis of Kaposi's sarcoma using established in vitro and in vivo models.
  • To explore the role of specific cytokines and the HIV Tat protein in KS development and progression.

Main Methods:

  • Utilized AIDS-KS cell cultures for in vitro studies.
  • Employed a transgenic mouse model for in vivo investigations.
  • Assessed autocrine and paracrine growth activities of AIDS-KS cells.
  • Examined the effect of exogenous Tat protein on KS cell proliferation.

Main Results:

  • AIDS-KS cells exhibit autocrine and paracrine growth activities, producing specific cytokines that may explain lesion histology.
  • Inoculation of cultured AIDS-KS cells into nude mice induced KS-like lesions, suggesting KS is an inducible disease.
  • Tat-transgenic mice developed KS-like lesions, and Tat protein induced proliferation of AIDS-KS cells.

Conclusions:

  • Kaposi's sarcoma is an inducible disease, with significant implications for understanding its development in HIV-infected individuals.
  • The HIV Tat protein is strongly implicated as a factor in the development or progression of Kaposi's sarcoma.
  • Further research into KS pathogenesis can benefit from the established cell culture and transgenic mouse models.

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