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A VH clonal deficit in human immunodeficiency virus-positive individuals
reflects a B-cell maturational arrest [published erratum appears in Blood
1991 Oct 1;78(7):1899]
L Berberian, Y Valles-Ayoub, N Sun, O Martinez-Maza and J Braun
Department of Pathology, UCLA School of Medicine 90024-1732.
A major feature of human immunodeficiency virus (HIV) infection is
disordered B-cell function, which paradoxically includes both pathologic
overactivity (elevated serum antibodies, lymphadenopathy, and increased
risk for lymphoma) and underactivity (impaired antibody immunity,
particularly to bacterial polysaccharide antigens). B-cell immune
dysfunction contributes significantly to HIV-related morbidity and also
represents an obstacle to eventual definitive treatment by anti-HIV
immunization. Our laboratory has recently identified in normal B-cell
populations certain VH gene subfamilies with a developmentally regulated
pattern of utilization. In particular, B cells bearing rearranged VH3L were
rare in the germinal center but uniformly abundant in the blood and
lymphoid mantle zone. We used this index gene subfamily as a clonal
criterion for the pattern of B-cell development in lymphocytes of
HIV-positive individuals. In a series of 19 HIV- positive subjects, a
striking deficit of VH3L B cells was observed; in contrast, none of the 16
normal subjects showed this abnormality. Other VH subfamilies (VH1N, VH4/6,
and VH5N) were unaffected in the HIV- positive patients. This VH3L clonal
deficit and other recent phenotype and histopathologic findings suggest
that the general B-cell dysfunction in HIV is due to a discreet
maturational arrest at the germinal center stage.
Volume 78,
Issue 1,
pp. 175-179,
07/01/1991
Copyright © 1991 by The American Society of Hematology
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