Many viruses enter lympho-reticular cells during pathogenesis and thereby induce immunosuppression, which is of practical importance in that it may be related to overall virulence. Immunosuppression may result from a selective infection, as viruses often show an affinity for different lymphocyte subpopulations: Epstein-Barr virus, for example, infects only a small percentage of B cells. We reported previously that herpes simplex virus (HSV) type 1 suppressed the induction of an antibody response to diphtheria toxoid in cultures of human tonsil cells, and that this seemed to result from the infection of a small percentage of T lymphocytes. However, as fully infectious virus was used in these experiments, it had probably spread from cell to cell in the course of the culture, so complicating the interpretation of the results. Accordingly, we have now reinvestigated the mechanism of immunosuppression using temperature-sensitivity (ts) mutants which fail to complete their growth cycle in the conditions selected for antibody synthesis. In this study, mutants tsB, tsD and tsF, derived from HSV type 1 strain 17, and ts 9, derived from HSV type 2 HG 52, were used. The results suggest that the immunosuppression is due to the selective infection by the viruses of helper T cells.

SUMMARY Evidence for retroviral infection in general and human immunodeficiency virus (HIV) infection in particular was sought in freshly isolated peripheral blood T cells, B cells, and monocyte-macrophages from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and also in T cell and B cell lines established from the same source. Similar cells isolated from rheumatoid synovial membrane were also examined. The strategy used for the detection of virus was cocultivation with susceptible cell lines looking for syncytia formation, reverse transcriptase production, and nucleic acid hybridisation with HIV cDNA probes. No evidence for infection was obtained.

The blood mononuclear cells from forty-six patients with infectious mononucleosis were separated into populations of normal and atypical cells by velocity sedimentation. Both populations were characterized in terms of surface markers and response to standard mitogens. The atypical cells were of both T-and Blymphocyte origin. Some reactivity of the normal against the freshly isolated atypical cells was detected by mixed lymphocyte reactions and 51Cr release, but this was less marked than that obtained against autochthonous lymphoblastoid cell lines. Both normal and atypical lymphocytes were stimulated by and were cytotoxic for lymphoblastoid cell-line cells. It is concluded that the atypical cells consist of two populations, a major one which is part of the host reaction to EB virus-infected cells, and a minor one which is the target for immunological responses and may represent cells transformed by virus.

Nineteen T-cell clones from seven patients with RA were obtained by cloning infiltrating lymphocytes from needle synovial biopsies. Southern blot analysis of the T-cell receptor (TCR) beta-chain genes in these clones revealed that there were no T-cell clones with an identical rearrangement of the TCR beta gene. These results do not support the idea that the infiltrating T-lymphocytes in RA are of monoclonal or oligoclonal origin.