© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 9, 729-736,
May 3, 2000
© 2000 Oxford University Press
Monoclonality or Oligoclonality of Human Herpesvirus 8 Terminal Repeat Sequences in Kaposi's Sarcoma and Other Diseases
Affiliations of authors: J.-G. Judde, V. Lacoste, A. Gessain (Unité d'Oncologie Virale, Département des Rétrovirus), C. Buchrieser (Unité de Génomique des Microorganismes Pathogènes, Département de Biologie Moléculaire), Institut Pasteur, Paris, France; J. Brière, Département d'Anatomopathologie, Hôpital Laënnec, Paris; E. Kassa-Kelembho, J. Morvan, Institut Pasteur de Bangui, Central African Republic; E. Clyti, P. Couppié, Département de Dermatologie, Cayenne Hospital, French Guyana; M. Tulliez, Département d'Anatomopathologie, Hôpital Cochin, Paris.
Correspondence to: Jean-Gabriel Judde, Ph.D., Unité d'Oncologie Virale, Département des Rétrovirus, Institut Pasteur, 28, rue du Docteur Roux, 75724 Paris cedex 15, France (e-mail: jgjudde{at}pasteur.fr).
Background: Infection with human herpesvirus 8 (HHV8), also termed Kaposi's sarcoma (KS)-associated herpesvirus, is associated with all forms of KS, with primary effusion lymphoma (PEL), and with some forms of multicentric Castleman's disease (MCD), but the pathogenic role of HHV8 in these tumors and the clonal nature of KS are still unclear. The purpose of this study was to examine whether the number of terminal repeats (TRs) contained in the fused TR region of HHV8 could be used as a marker of clonality in HHV8-associated tumors. Methods: Pulsed-field gel electrophoresis (PFGE) and multiple-probe Southern blot analysis of the HHV8 TR region were performed on high-molecular-weight DNA obtained from tumoral KS, PEL, and MCD lesions. Results: These analysis showed that the fused TR region contains a large but variable number of TR units (ranging from 16 to 75) and that the viral genome is present as extrachromosomal circular DNA in these tumors in vivo, with occasional ladders of heterogeneous linear termini reflecting lytic replication. All PEL tumors and PEL-derived cell lines as well as some KS tumors contained monoclonal or oligoclonal fused TR fragments; however, the TR region appeared polyclonal in MCD tumors and in a few KS lesions. Conclusion: Several KS and PEL lesions are monoclonal expansions of a single infected cell, suggesting that HHV8 infection precedes tumor growth and thus supporting an etiologic role of latent HHV8 in these proliferations. Our finding that nodular KS lesions display all possible patterns of clonality supports the model according to which KS begins as a polyclonal disease with subsequent evolution to a monoclonal process.
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