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Hepatitis C virus within a malignant lymphoma lesion in the course of type
II mixed cryoglobulinemia
S De Vita, D Sansonno, R Dolcetti, G Ferraccioli, A Carbone, V Cornacchiulo, G Santini, M Crovatto, A Gloghini and F Dammacco
Department of Experimental Oncology 1, Centro di Riferimento Oncologico,
Aviano (PN), Italy.
Hepatitis C virus (HCV) has been implicated as the major etiologic factor
sustaining B-cell clonal expansion in type II mixed cryoglobulinemia (MC).
A putative pathogenetic role of HCV in the development of MC-associated
B-cell malignancies has also been speculated. We report for the first time
the localization of HCV within a parotid non-Hodgkin's lymphoma (NHL)
lesion in the course of HCV- related type II essential MC, an important
step to implicate any infectious agent in the lymphomagenesis. Plus and
minus strand HCV RNA was first demonstrated by polymerase chain reaction on
the whole RNA from the lesion. Further immunohistochemical studies
localized HCV c22 proteins in the residual ductal or acinar parotid
structures, which also abnormally expressed HLA-DR antigens. Weak c22
signals were inconstantly detected in cells strictly confined around the
residual epithelium, while all the remaining infiltrating cells in the
parotid lesion stained c-22-negative. Staining for c33 and c100 HCV
antigens was negative. In situ hybridization (ISH) studies again identified
the residual parotid epithelial cells as the site of HCV infection and
replication in the NHL lesion. Sialotropic viruses previously involved in
lymphoproliferation, ie, Epstein-Barr virus and human herpesvirus-6, were
absent in the same tissue lesion. According to the current models of B-cell
lymphomagenesis, a role of HCV as an exogenous antigenic stimulus should be
considered for NHL development in the present case, whereas malignant B
cells do not appear permissive of active HCV replication. Further efforts
would be worthwhile to clarify a role of HCV infection in the development
of some B-cell malignancies.
Volume 86,
Issue 5,
pp. 1887-1892,
09/01/1995
Copyright © 1995 by The American Society of Hematology
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