A panel of conventional and monoclonal antibodies was used to examine the immunohistological characteristics of malignant epithelial cells and infiltrating lymphocytes in frozen sections of nasopharyngeal carcinoma (NPC) biopsies from 10 Tunisian patients. Three main categories of cells were identified. (1) Tumour cells which were positive for Epstein-Barr nuclear antigen, HLA-ABC and keratin determinants. In most samples, the tumour cells also expressed variable amounts of HLA-DR antigens. The presence of HLA-DR antigens has not been previously reported in NPC and may be a contributory factor in effecting the transfer of Epstein-Barr virus to the epithelial cells. (2) Infiltrating lymphocytes which were mainly composed of T inducer (T4+) and T suppressor/cytotoxic (T8+) cells although one sample contained predominantly immature T cells expressing the HTA-I+ cortical thymocyte phenotype. Few B cells or natural killer cells were demonstrated. (3) Large HTA-I+ dendritic cells which were invariably present within the tumour masses. These were morphologically and phenotypically similar to antigen presenting Langerhans cells which are usually located in the skin but also found in other epithelial sites. These cells may be a residual population from the normal nasopharynx or represent part of a specific immunological response to the presence of Epstein-Barr virus in the epithelial cells.

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Epstein-Barr virus (EBV) is a B lymphotrophic human herpes virus which is the causative agent of Infectious Mononucleosis (IM) (Henle et al., 1968) and is aetiologically associated with Burkitt's lymphoma (Epstein & Achong, 1979) and nasopharyngeal carcinoma (Epstein, 1978). In most individuals infection occurs subclinically during childhood (Evans et al., 1968) and leads to the production of antibodies to virus-determined antigens which thereafter persist for life (Hewetson et al., 1973). Following either IM or sub-clinical infection EB virus persists in the body, and can be found in saliva (Golden et al., 1973) and in lymphoid tissue (Nilsson et al., 1971). This persistent infection with EBV is probably, at least in part, controlled by EBV-specific memory T cells which have been demonstrated in the peripheral blood of seropositive individuals (Moss et al., 1978). These T cells are activated in cultures of EB virusinfected peripheral blood mononuclear cells to produce cytotoxic cells which then cause regression of proliferating foci of the EB virus-infected B cells within the culture (Rickinson et al., 1979) in an HLA-restricted manner (Rickinson et al., 1980).In the present study we have used the fluorescence activated cell sorter (FACS) to separate peripheral blood cells stained with monoclonal antibodies into subsets with specific activities. These subsets have then been assayed for their capacity to cause regression of autologous EBV-infected B cell targets. Materials and methodsMedium RPMI 1640 medium containing 2mM glutamine, 100 IU penicillin and 100 IU streptomycin was used throughout. 5 mM HEPES buffer and 2% calf serum were added for all cell preparation procedures, and 20% v/v foetal calf serum (FCS) was added for all culture procedures. DonorsNormal healthy adults who were seropositive for antibodies to EB virus were selected as leucocyte donors.Cell preparation Whole blood was diluted with an equal volume of medium and centrifuged on a Ficoll-hypaque gradient. The peripheral blood mononuclear cells (PBMC) were harvested from the interface band and washed twice in medium. E rosettes were formed using AET-treated sheep red cells by the method of Kaplan & Clark (1974) and the E rosette-positive population (E+) was separated from the E rosette-negative population (E-) on a percoll gradient (Callard & Smith, 1981). The E-cells were harvested from the interface band and the E+ cells were recovered from the pellet by lysis of the red cells with 0.83% ammonium chloride. Both cell populations were washed twice in medium before use.(C) The

By November 7, 1983, 24 cases of AIDS in the United Kingdom had been reported to the Communicable Disease Surveillance Centre. At the same time an increasing number of homosexual men with unexplained lymphadenopathy syndrome (LAS) have been seen in our department. Between December 1982 and July 1983, 14 homosexual men with LAS and 11 healthy homosexual men were studied. Patients with LAS had a high number of lifetime episodes of sexually transmitted diseases, a history of recent sexual activity in the United States (9 of 14), sexual contact with British AIDS patients or other persons with LAS (7 of 14), and hypergammaglobulinemia. Low T-helper/T-suppressor ratios (less than 0.8), due mainly to a decrease in T-helper cells, were found in both groups. Lymph node biopsies showed follicular hyperplasia and hypocellular pattern. All 25 patients studied had antibodies to Epstein-Barr virus capsid antigen (anti-VCA) and 11 had antibodies to early antigen (anti-EA); 13 of 17 were excreting the virus; and two showed no Epstein-Barr-virus-specific regression. Peripheral blood immunoglobulin-producing B-cells from six patients with hypergammaglobulinemia were negative for the Epstein-Barr virus nuclear antigen (EBNA). Five lymph node biopsies showed no EBNA-positive cells. Epstein-Barr virus reactivation is common in the patients with LAS and healthy homosexual men in London, but would not seem to be the cause of the polyclonal B-cell activation or lymphadenopathy.

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