The Evolution of Lymphadenopathy and Hypergammaglobulinemia Are Evidence for Early and Sustained Polyclonal B Lymphocyte Activation during Human Immunodeficiency Virus Infection

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Abstract
To examine whether polyclonal activation of B lymphocytes as measured by hypergammaglobulinemia contributes to lymphadenopathy in human immunodeficiency virus (DIY) infection, correlates of adenopathy were examined in 240 homosexual men. Lymph node size was measured in 12 sites semiannually over 4 years. Both adenopathy and hyperglobulinemia developed within 1 year after seroconversion and persisted at high levels. Adenopathy declined near diagnosis of AIDS whereas serum IgG decreased 8–16 months after diagnosis. Adenopathyattributable to HIV occurred in all palpable node groups. By logistic regression, HIV-positive men were best discriminated from HIV-negative men by size of posterior cervical nodes and the number of sites with enlarged nodes. In a repeated measures model of covariance, adenopathy in HIV-positive men was associated with more CD4+ cells (P <.002), elevated serum globulins (P <.01), and lower platelet counts (P < .05). Adenopathy declined over time (P < .001) and with diagnosis of AIDS or AIDS-related complex (P < .03). Thus, adenopathy and hypergammaglobulinemia are correlated and follow a similar course through various stages ofHIV infection, suggesting that both are caused by polyclonal B cell activation.

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