Human T cell lymphocyte lines, established from lymphoid tissues from patients with adult T cell malignancies infected with the human T cell lymphoma virus (HTLV), were used in co-culture experiments to infect newborn cord blood lymphocytes (CBL). The infected and non-infected CBL cell lines were typed for HLA alloantigen determinants and tested for cell surface antigens using selected monoclonal antibodies. Infected cord blood lymphocytes showed inappropriate expression of alloantigenic determinants of the HLA-A and -B alleles. The monoclonal antibody 4D12, detecting an antigen common to the HLA-B5 cross-reactive group, was reactive with all infected cultures; this determinant appeared de novo in CBL cells lacking B5 cross-reactive group antigens in the uninfected state, and it increased in density in the infected cultures where the HLA-B5 cross-reactive alloantigens were present in uninfected CBL. HLA-DR was expressed in low levels or not detected on non-infected cultured cord blood lymphocytes and was present on all infected cells. OKT4 positive cells predominated in infected cultures, whereas OKT8 positive cells decreased in number or were absent. The TCGF receptor also increased both in density and in percent positive cells in all infected cell lines. The results suggest that HTLV may be tropic for a subset of T cells expressing mature T cell markers and that viral infections directly affect expression of cell surface antigens controlled by the human major histocompatibility complex (MHC).
The prevalence of antibodies to Treponema pallidum and Borrelia burgdorferi was investigated in Jamaicans with tropical spastic paraparesis (TSP). A significantly higher prevalence of reactive serologic tests for syphilis (STS) was found in TSP patients (35.0%) when compared with controls (14.5%; P < .001). Venereal Disease Research Laboratory (VDRL) test titers less than 1:8 were obtained in 88.4% of reactive sera from patients and in all reactive sera of controls. The biologic false-positive rate was also significantly higher in TSP patients (P < .05). A higher frequency of a reactive STS was observed in TSP patients (P < .01) and controls (P < .001) more than 40 years of age. The prevalence of reactive serologic tests for syphilis in TSP patients younger than 40 years was also higher than in controls in this age group (P < .1). The prevalence of positive immunofluorescent antibody tests and enzyme immunoassay for antibodies to B burgdorferi was similar in sera of TSP patients (12.5%) and healthy controls (10%). However, none of the sera was positive by Western immunoblot. Leptospiral antibodies were not present in any serum tested. This study's data do not support an etiologic role for treponemal disease in tropical spastic paraparesis, but rather suggest that the high prevalence of reactive STS in Jamaicans is multifactorial.
Cell lines were established from the peripheral blood of two patients with adult T cell leukemia. In contrast to our previous experience, where all such lines expressed T cell markers, these two cell lines expressed B cell antigens and Ig light chains (kappa on CF-2, lambda on HS). Human T cell lymphoma proviral (HTLV) sequences were demonstrated in both cell lines. Since only a portion of the cells in culture expressed Ig light chains, experiments were carried out to exclude the possibility that the cultures were not a mixture of B and T or non-B cells. Cells that expressed kappa- or lambda-light chains were separated by cell sorting from kappa- or lambda-negative cells and replaced in culture. Light chain negative cells reexpressed light chains after time in culture. After 5-azacytidine treatment of the cell lines, all cells expressed Ig light chains. These studies show that the human retrovirus HTLV, which has been demonstrated to be associated with certain T cell malignancies, can infect B cells or B cell precursors.
Abstract The primary interaction of HIV-1 with the target cell involves the viral large envelope protein (gp120) and the cellular CD4 molecule. mAb reacting with portions of CD4 have been shown to block HIV-1 attachment and infection. In one of the early reports describing HIV-1 cell interaction, some mAb reacting with MHC class II Ag were also found to block infection. To investigate further a possible role for MHC class II in HIV-1 binding, a cultured T lymphocyte cell line (H-9) that expresses MHC class II molecules and PHA-stimulated PBL was exposed for various time periods to concentrated viral particles and individual HIV-1 proteins. A decrease in the ability to detect the CD4a epitope and HLA-DR was observed after the cells were exposed to virus for 15, 30, and 60 min whereas HLA-DP and HLA-DQ Ag increased or remained unchanged. After 120 min of virus exposure, the CD4a epitope remained diminished whereas HLA-DR was detected at levels found on cells not exposed to virus. mAb detecting the CD4a epitope and HLA-DR, as well as alloantisera detecting the specific HLA-DR Ag on the target cell, blocked HIV-1 binding. When immunopurified gp120 was added to PHA-stimulated and unstimulated PBL, the CD4a epitope decreased in the same manner as was observed with whole virus preparations. In contrast to exposure to the intact virus, HLA-DR expression appeared to increase. Other viral proteins, p17, p24, and a portion of the small envelope protein, gp41, had no effect on the ability to detect cell surface Ag. Thus, although CD4 is the primary receptor for HIV-1 binding, HLA-DR appears to be involved in the binding site, probably by virtue of its close proximity to the CD4 molecule on the cell surface.
