Human immunodeficiency virus-associated Hodgkin's disease derives from post-germinal center B cells

Antonino Carbone, Annunziata Gloghini, Luigi M. Larocca, Andrea Antinori, Brunangelo Falini, Umberto Tirelli, Riccardo Dalla-Favera, Gianluca Gaidano

Research output: Contribution to journalArticlepeer-review


Human immunodeficiency virus-associated Hodgkin's disease (HIV-HD) displays several peculiarities when compared with HD of the general population. These include overrepresentation of clinically aggressive histologic types and frequent infection of Reed-Sternberg (RS) cells by Epstein-Barr virus (EBV). Recently, we have reported that the histogenesis of HD of the general population may be assessed by monitoring the expression pattern of BCL-6, a transcription factor expressed in germinal center (GC) B cells, and of CD138/syndecan-1 (syn-1), a proteoglycan associated with post- GC, terminal B-cell differentiation. In this study, we have applied these two markers to the study of HIV-HD histogenesis and correlated their expression status to the virologic features of this disease. We have found that RS cells of all histologic categories of HIV-HD consistently display the BCL-6-/syn- 1+ phenotype and thus reflect post-GC B cells. Although BCL-6-/syn-1+ RS cells of HIV-HD express CD40, they are not surrounded by CD40 ligand-positive (CD40L+) reactive T lymphocytes, which, in HD of the general population, are thought to regulate the disease phenotype through CD40/CD40L interactions. Conversely, RS cells of virtually all HIV-HD express the EBV-encoded latent membrane protein 1 (LMP1), which, being functionally homologous to CD40, may contribute, at least in part, to the modulation of the HIV-HD phenotype.

Original languageEnglish
Pages (from-to)2319-2326
Number of pages8
Issue number7
Publication statusPublished - Apr 1 1999

ASJC Scopus subject areas

  • Hematology


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