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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2319-2326
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, and
Gianluca Gaidano
From the Divisions of Pathology and Medical Oncology and the AIDS
Program, Centro di Riferimento Oncologico, Istituto Nazionale Tumori,
Istituto di Ricovero e Cura a Carattere Scientifico
(IRCCS), Aviano; Institutes of Pathology and Infectious
Diseases, Università Cattolica del Sacro Cuore, Roma; Institute
of Hematology, University of Perugia, Perugia; the Division of Internal
Medicine, the Department of Medical Sciences, Amedeo Avogadro
University of Eastern Piedmont, Novara, Italy; and the Division of
Oncology, the Department of Pathology, College of Physicians and
Surgeons, Columbia University, New York, NY.
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.
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