Virus-specific T-helper cells are considered critical for the control of chronic viral infections. Successful treatment of acute HIV-1 infection leads to augmentation of these responses, but whether this enhances immune control has not been determined. We administered one or two supervised treatment interruptions to eight subjects with treated acute infection, with the plan to restart therapy if viral load exceeded 5,000 copies of HIV-1 RNA per millilitre of plasma (the level at which therapy has been typically recommended) for three consecutive weeks, or 50,000 RNA copies per ml at one time. Here we show that, despite rebound in viraemia, all subjects were able to achieve at least a transient steady state off therapy with viral load below 5,000 RNA copies per ml. At present, five out of eight subjects remain off therapy with viral loads of less than 500 RNA copies per ml plasma after a median 6.5 months (range 5-8.7 months). We observed increased virus-specific cytotoxic T lymphocytes and maintained T-helper-cell responses in all. Our data indicate that functional immune responses can be augmented in a chronic viral infection, and provide rationale for immunotherapy in HIV-1 infection.
Background. The frequency and clinical significance of bcl‐2 rearrangement in de novo B‐cell diffuse large cell lymphoma is largely unknown. Methods. Using Southern blot hybridization and multiple DNA probes, the status of the protooncogene bcl‐2 was investigated in frozen tissue samples from 45 carefully selected cases of de novo diffuse large cell lymphoma of B‐cell origin. Results were correlated with the presenting clinical and immunophenotypic features and with the subsequent clinical course. Results. Rearrangements of bcl‐2 were identified in nine tumor specimens (20%). The bcl‐2‐positive cases more often presented as early‐stage, nonmucosal associated extranodal tumors (P = 0.06) and were more often HLA‐DR negative (P = 0.07). Five‐year failure‐free survival was poor among the bcl‐2‐positive cases (11% versus 48%). Overall survival was no different, however, because relapses in bcl‐2‐positive cases tended to be responsive to further therapy. Conclusions. Analysis of bcl‐2 rearrangements in de novo diffuse large cell lymphoma may identify a subset of patients with unusual clinical features. Cancer 1993; 72:231–6.
Although monoclonal B-cell populations can be identified both by surface-marker analysis and by immunoglobulin-gene rearrangements, this has not been possible with T cells. We have employed cDNA probes that are specific for the entire beta chain of the T-cell receptor, and for its constant and variable regions, to investigate gene rearrangements in T-cell chronic lymphocytic leukemia and related disorders. In three malignant proliferations of helper (T4-positive) T cells, rearrangements of the beta-chain constant-region gene were readily demonstrated. A patient from the Caribbean who had adult T-cell lymphoma and antibody to human T-cell lymphotrophic virus Type I (HTLV-I), a patient with virus-negative chronic lymphocytic leukemia, and a patient with cutaneous T-cell lymphoma (Sézary variant) made up the T4-positive group. Three additional patients with chronic T8 (cytotoxic-suppressor) lymphocytosis and neutropenia were studied; in two; rearrangements were found. In all five patients with constant-region rearrangements, deletions of variable-region restriction fragments were observed as well. The presence of rearrangements of a T-cell receptor gene provides presumptive evidence for the clonal nature of T-cell proliferation and for its neoplastic character.
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