Related Experiment Videos
Latent BK virus infection and Kaposi's sarcoma pathogenesis
P Monini1, A Rotola, L de Lellis
1Institute of Microbiology, University of Ferrara, Ferrara, Italy.
International Journal of Cancer
|June 11, 1996
Summary
BK virus (BKV) was consistently found in Kaposi
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Kaposi's sarcoma (KS) is a malignancy with complex etiology.
- The role of ubiquitous transforming viruses in KS pathogenesis is under investigation.
- Previous studies have explored viral associations with KS, but findings are often inconclusive.
Purpose of the Study:
- To investigate the presence and potential role of various transforming viruses in different forms of Kaposi's sarcoma (KS).
- To determine if specific viruses are consistently associated with KS lesions and derived cell lines.
- To explore the potential contribution of BK virus (BKV) transforming functions in KS development.
Main Methods:
- Polymerase chain reaction (PCR) analysis of skin lesions and cell lines from classic, endemic, and AIDS-related KS.
- Detection of DNA sequences for BK virus (BKV), JC virus (JCV), Simian virus 40 (SV40), Herpes simplex virus (HSV), and Human papillomavirus (HPV).
- Analysis of genital tissues and sperm for viral presence to assess transmission routes.
Main Results:
- BK virus (BKV) was detected in 100% of KS skin lesions and 75% of KS cell lines, with intact early regions.
- BKV was also prevalent in genital tissues and sperm (57-67%), suggesting a sexually transmitted role.
- JC virus (JCV), SV40, HSV, and HPV were detected at lower or inconsistent prevalences and were largely absent in KS cell lines, unlike BKV.
Conclusions:
- The constant association of BK virus (BKV) DNA with KS lesions and cell lines strongly suggests its involvement in KS pathogenesis.
- BKV's transforming functions may play a significant role in the development of Kaposi's sarcoma.
- Other tested viruses (JCV, SV40, HSV, HPV) show less consistent association with KS neoplastic cells.