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Epstein-Barr virus infections in hairy cell leukemia patients in the presence of complement-dependent neutralizing
Immune system status was characterized in patients with hairy cell leukemia (HCL) with respect to explaining their chronic or recurrent infections with Epstein-Barr virus. Measures of cellular immune responsiveness for a group of 11 HCL patients were, in general, decreased when expressed as the proportion of tested patients with values less than 2 S.D. below mean values for a group of 17 healthy adults: T-cell enumeration, seven of 13; mitogen responsiveness of phytohemagglutinin, 10 of 11; concanavalin A, 10 of 11; pokeweed mitogen, 10 of 11; B-cell responsiveness by anti-immunoglobulin immunobead stimulation, two of six; responsiveness to streptolysin O antigen, four of seven; mixed-lymphocyte reaction, six of seven; natural killer cell activity, six of eight. Specific immunity to Epstein-Barr virus was measured by complement-independent, antibody-mediated virus neutralization (mean index for HCL patients being 56% of control value) and complement-dependent virus neutralization (98% of control value). We concluded that, in spite of depressed levels of immune responses measured with general, cellular assays, functional levels of complement-dependent virus-neutralizing antibody were present in these HCL patients.
Immune system status was characterized in patients with hairy cell leukemia (HCL) with respect to explaining their chronic or recurrent infections with Epstein-Barr virus. Measures of cellular immune responsiveness for a group of 11 HCL patients were, in general, decreased when expressed as the proportion of tested patients with values less than 2 S.D. below mean values for a group of 17 healthy adults: T-cell enumeration, seven of 13; mitogen responsiveness of phytohemagglutinin, 10 of 11; concanavalin A, 10 of 11; pokeweed mitogen, 10 of 11; B-cell responsiveness by anti-immunoglobulin immunobead stimulation, two of six; responsiveness to streptolysin O antigen, four of seven; mixed-lymphocyte reaction, six of seven; natural killer cell activity, six of eight. Specific immunity to Epstein-Barr virus was measured by complement-independent, antibody-mediated virus neutralization (mean index for HCL patients being 56% of control value) and complement-dependent virus neutralization (98% of control value). We concluded that, in spite of depressed levels of immune responses measured with general, cellular assays, functional levels of complement-dependent virus-neutralizing antibody were present in these HCL patients.