A collaborative study of sera from men in New York City with AIDS and at risk for AIDS, by investigators in Omaha, Cambridge and Kyoto, has failed to identify antibodies to human T cell leukemia virus I (HTLV-I).
Cell-mediated immunity in hypophysectomized (HYX) and non-hypophysectomized (NHYX) rats was assessed by measuring lymph node weight and lymph node cellular proliferation responses to cutaneous application of the skin sensitizer dinitrochlorobenzene (DNCB). Differences were found in the lymph node weight assay, with the responses of the HYX rats being significantly lower than the responses of the NHYX rats. There were, however, no significant differences as measured by the lymph node cellular proliferation assay. An explanation for these contradictory results was sought by examining dose-responsiveness to DNCB. It was found that, over a range of doses of DNCB, HYX rats showed a linear dose-response relationship in terms of both lymph node weight and lymph node cellular proliferation. No dose-responsiveness was observed in NHYX rats. Since HYX rats required a greater degree of antigenic stimulation to achieve a response level equivalent to that of NHYX rats, it may be concluded that HYX rats are immunodeficient at lower antigen levels.
Male homosexuals at risk for developing AIDS frequently exhibit chronic lymphadenomegaly (LAD). They are at high risk for developing malignant B cell lymphomas. A study of Epstein-Barr virus (EBV) revealed marked abnormalities in these patients. One hundred percent of the patients were seropositive. The patients with most severe acquired immune deficiency disorders manifested a decreased number of circulating B cells with EBV receptors and decreased lymphocyte transformation. Patients often showed defective memory T cell cytotoxic responses to autologous EBV infection in vitro. Three of five lymph node specimens contain significant EBV genome copies to suggest a significant etiologic role. In addition, a Burkitt-like lymphoma carried EBV genome. Although all of the men were seropositive for EBV, reactivation patterns were not as common as anticipated. Given the presence of EBV genome in the lymph nodes of the patients who lack anti-early antigen (EA) antibodies indicative of reactivation, we suggest that reliance on serology to indicate EBV involvement is insufficient for assessing the patient. The detection of a t(8;14) transposition in the monoclonal mu kappa Burkitt-like lymphoma containing EBV genome supports the view that cytogenetic transposition is a mechanism in lymphomagenesis.
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