Flamand L, Zeman R A, Bryant J L, Lunardi-Iskandar Y, Gallo R C
Institute of Human Virology, University of Maryland Biotechnology Institute, University of Maryland, Baltimore 21201, USA.
J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Oct 1;13(2):194-7. doi: 10.1097/00042560-199610010-00011.
The recent detection of herpesvirus-like DNA sequences in Kaposi's sarcoma (KS) lesions has led to numerous speculations regarding the role of this new agent in KS pathogenesis. However, recent studies indicate a far wider distribution of such viral sequences, shadowing the potential etiologic role of this agent in KS. In this report we show that malignant KS cell lines do not harbor such viral sequences while B cells, CD14+ and CD34+ cells do, suggesting that if a KS malignancy originates from infection with HHV-8, the virus can be lost and is not necessary for maintenance of the neoplastic state. Alternatively, HHV-8 may be a "passenger" in KS.