[Transmission of ATLV (HTLV-I) through blood transfusion].
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Biomedical subjects
Publications and source records attributed to K Okochi.
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Cell-associated transmission of adult T-cell leukemia virus (ATLV/HTLV-I) suggested early in a follow-up study on recipients of blood has been supported with the latest results of an extended follow-up. Approximately 10(8) lymphocytes of blood donors carrying the antibodies against ATLV seemed to be necessary for the infection through blood transfusion. The infection transmitted by transfusion is now almost completely prevented by eliminating blood units that have been derived from blood donors having antibodies to ATLV/HTLV-I.
An outbreak of erythema infectiosum ("fifth disease") was studied in Fukuoka, Japan, in 1980-1981. Human parvovirus (HPV) antigen was not detected in any patients, but anti-HPV, measured by countercurrent immunoelectrophoresis, was found in 33 of 34 affected children and in 21 (15%) of 141 children of the same ages without the disease. Immunoglobulin M class anti-HPV was present in all 25 children with erythema infectiosum tested. In a survey of hospital patients, the prevalence of anti-HPV detected by CIE was 12% in the cohort 5 to 9 years of age, 19% in the cohort 10 to 14 years, and 32 to 55% in the cohorts greater than or equal to 30 years. The antibody reactions in the cases of erythema infectiosum, which were already well established at the onset of disease, indicate that HPV was the cause of the outbreak.
Analysis of HLA antigens and case control study were performed in 50 patients with Behcet's disease. Frequency of HLA-Bw51 was significantly increased in the patients (52.0%) as compared to that in the control subjects (16.0%). In case control study, the incidence of tonsillitis, and use of public bath and a privy were more frequently seen in the patients than in the controls. The patients were frequently exposed to agricultural chemicals before onset of the disease. Daily ingestion of vegetable salad and milk was less frequent in the patients than in the controls. Heterogeneity of Behcet's disease and results of multivariate analysis for selected variables were discussed.
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Human T-cell leukemia virus producer cell line MT-2 was labeled with [32P]phosphoric acid, and its cell extracts were immunoprecipitated with mouse monoclonal antibodies (GIN-7, and KK-1) and rabbit sera (anti-p24, and anti-gp68). Analysis of the immunocomplexes on sodium dodecyl sulfate-polyacrylamide gell electrophoresis revealed that p53, p28, and p19 of adult T-cell leukemia-associated antigens were phosphorylated in vivo. Immunocomplexes of MT-2 cell extract with monoclonal antibody KK-1 were incubated with [gamma-32P]ATP in vitro and it was revealed that the phosphokinase activity was associated with p28. The phosphokinase activity of p28 was specific to the serine residue but was not to the tyrosine residue.
Serum from healthy human subjects and serum from animals demonstrated a splitting of the H2M2 isoenzyme fraction of lactate dehydrogenase (LDH) into two subbands on polyacrylamide gel electrophoresis. These subbands were designated H2M2-a and H2M2-b, based on their relative electrophoretic mobilities, with the H2M2-a band being more anodal. The doublet of the H2M2 band was also demonstrated in human erythrocytes and in the hybridization mixture from porcine LDH, indicating the production of two forms of H2M2 isoenzyme in tissues. Supportive evidence for the presence of two H2M2 subforms was obtained by ion-exchange chromatography of the hybridization mixture. The recombination experiments of LDH-binding IgA with both normal human serum and LDH M subunit variant serum indicated the difference of molecular structure between the two subforms. On the basis of the results obtained in this study, a theoretical model of the probable molecular structure of LDH isoenzymes is proposed which could account for both the occurrence of two subforms of H2M2 and their selective binding to LDH-linking IgA.
A nation-wide survey of carriers of adult T-cell leukemia virus (ATLV) detected as anti-ATLA (ATLV-associated antigens) in volunteer blood donors was made in Japan. A total of 200 sera from donors between 40 and 64 years of age, collected in each of 64 blood centers located in eight districts, were tested for anti-ATLA by an indirect immunofluorescence test. The highest rate (8%) of seropositive donors was found in Kyushu and lower rates of 0.3 to 1.2% in other districts. However, the positive rate varied considerably in different localities even within districts with a high or low seropositive incidence. Further studies of all the donors (16 to 64 years old) in eight centers in Kyushu demonstrated two facts: (1) that the frequency of seropositive donors increased with age, and (2) that four centers in this district showed distinctly high incidences of seropositive donors, while the other four centers showed low incidences. The seropositive rate among all donors was estimated to be about 3% in Kyushu and 0.08 to 0.3% in all other districts.
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HLA-A, B, C, and DR antigens were studied in Japanese patients with adult T-cell leukemia. No associations were found in comparisons with normal healthy controls.
Possible transmission of adult T cell leukemia virus (ATLV) by blood transfusion was studied retrospectively. Of 41 recipients of whole blood or blood components containing cells from donors having antibodies to antigen that is associated with ATLV (anti-ATLA), 26 (63.4%) produced anti-ATLA. However, no anti-ATLA was detected in all 14 recipients of fresh-frozen plasma prepared from anti-ATLA-positive donors. None of 252 recipients of blood with cell components from anti-ATLA-negative donors produced anti-ATLA. The development of anti-ATLA in the recipients may correspond to antibody production after establishment of primary infection with ATLV that is associated with cells in blood from anti-ATLA-positive donors who are ATLV carriers.
In a follow-up of blood recipients, antibodies against adult T-cell leukemia antigen (anti-ATLA) were found in those who had received blood preparations containing cells. Detection of lymphocytes carrying viral antigen of ATLV (human T-cell leukemia virus type I (HTLV-I) ) in seroconverted recipients and the appearance of the viral antigen in cord blood lymphocytes co-cultured with a T-cell clone of a seroconverted recipient strongly suggested that the virus was transmitted through blood transfusion. Screening of blood donors by testing their antibodies against the virus is necessary to prevent future transmission through transfusion, and should be done even if such transmission does not result in the development of adult T-cell leukemia.
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Human cytotoxic T cells (Tc) specific for autologous adult T cell leukemia virus- (ATLV) bearing cells were induced in vitro. Peripheral blood leukocytes (PBL) from healthy donors were stimulated repeatedly with autologous ATLV-bearing T cells. In two out of four seropositive donors and one out of two seronegative donors, the responder cells showed cytotoxicity for autologous ATLV-bearing cells, but not for autologous PBL, autologous cloned T cell lines, Epstein Barr virus-transformed autologous lymphoblastoid B cell line (LCL) cells, or various ATLV-negative cell line cells. The effector cells induced were cytotoxic T cells possessing Leu-1 and Leu-2a antigens that were able to proliferate continuously in vitro with periodic restimulation by appropriate cells and supplementation with partially purified T cell growth factor (TCGF). Of three Tc lines tested, one exhibited significant cytotoxicity against allogeneic ATLV-bearing cells that shared HLA-A2 antigen with the effector cells, possibly indicating HLA-restriction of ATLV-specific Tc. HLA-restriction was also suggested by cold target inhibition of cytotoxicity. Interestingly, Tc from this individual could also kill fresh adult T cell leukemia cells that were not expressing the ATLV surface antigens. These results, together with the target specificities of other Tc lines, suggest the possibility of at least two distinct target antigens recognized by ATLV-specific Tc, with one of these antigens differing from the ones detected by serologic methods.
We report the presence of complexes between aspartate aminotransferase (AST, EC 2.6.1.1) and immunoglobulin (Ig) in the serum of a patient suffering from lung cancer with metastasis to the liver. After fractionation of the serum by gel filtration, AST-Ig complexes (AST-IgA, AST-IgG) were demonstrated by counterimmunoelectrophoresis. Dissociating the complexes and recombining them with purified isoenzyme fractions, s-AST (cytoplasmic) and m-AST (mitochondrial), revealed that only s-AST binds to IgG, whereas IgA binds to both s-AST and m-AST. Although the association of AST with IgG has been reported, to our knowledge this is the first finding of both AST-IgA and AST-IgG complexes in a patient's serum. Serum AST-IgG complexes have been demonstrated in both healthy and diseased individuals; in the latter category, as reported here and by others, the liver is implicated.
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