Longitudinal IgG recognition patterns of viral proteins were studied in 15 men who had seroconverted for lymphadenopathy associated virus/human T lymphotropic virus (LAV/HTLV-II). Antibodies to the major viral core protein p24, which is a cleavage product ofthe gag gene encoded precursorprotein pr55, appeared first. These were soon followed by antibodies to pr65 and more gradually by antibodies to the other gag gene encoded cleavage product p18, the env gene encoded transmembrane glycoprotein gp4l, the env gene encoded glycoproteins gp65 and gpllO, and the putative pol gene product p33.In 13 subjects who remained healthy the reactivity to the differept proteins increased or stabilised with time, while in two men who developed acquired immune deficiency syndrome (AIIDS) the reactivity, most noticeably to gag encoded proteins, diminished before or at the-onset of symptoms.

Peripheral-blood T cell subsets and functions were studied in 14 patients with malignancies treated with high-dose chemotherapy and radiotherapy followed by autologous bone-marrow transplantation (BMT). 8 CMV-positive patients (6 with latent infections and 2 with a primary infection) showed an inversion of the OKT4/OKT8 ratio caused by an increase in OKT8 + T cells and a decrease in OKT4 + T cells. This was accompanied by a pronounced increase in the percentage of HLA-DR+ T cells, and functionally by increased suppressor T cell activity and decreased helper T cell activity and T cell proliferation. These alterations in T cell subsets and functions were not observed in 6 patients who were kept CMV-negative by a deliberate transfusion policy. In the 6 patients helper T cell activity and T cell proliferation capacity recovered well after day 30. Differences between the two groups were most striking 60 days after BMT. This study suggests that CMV infection, whether primary or secondary, is a major cause of T cell alterations after (autologous) BMT.

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Two cases of transient biclonal gammopathy are described, one having an IgG kappa and an IgA kappa monoclonal component and another with IgG1 kappa and IgG4 kappa monoclonal components. In both of these cases the second monoclonal component gradually disappeared. Anti-idiotypic antibodies were made against the major monoclonal serum component; in the first case the idiotype of the IgG kappa clone was not found in the IgA kappa plasma cells (real biclonal gammopathy) whereas in the second case the idiotypes of the two clones were identical (apparent biclonal gammopathy). The evolution to monoclonal gammopathy is discussed with regard to the existence of common malignant precursor cells in biclonal gammopathy.

Plasmacellular hyperplasia in lymphoid tissue was found in 4 out of 9 patients 1-6 months after allogeneic bone marrow transplantation as treatment for leukaemia. In the plasma cell populations, 13-85% expressed a single immunoglobulin light and heavy chain isotype (monotypic Ig expression). DNA analysis, using a DNA probe specific for heavy chain JH gene segments and for light chains, did not reveal the presence of clonally restricted B lymphocytes. The patients' sera lacked homogeneous immunoglobulins. We conclude that plasmacellular hyperplasia found after allogeneic bone marrow transplantation represents a polyclonal B-cell expansion- with a restriction in Ig isotype.