Indirect immunofluorescence of certain human sera demonstrated an antigen(s) in the cytoplasm of 1-5% of the cells of a T-cell line, MT-1, from a patient with adult T-cell leukemia (ATh), which is endemic in southwestern Japan. The antigen was not detected in other human lymphoid cell lines, including six T-cell lines, seven B-cell lines, and four non-T non-B cell lines. The antigen did not show cross antigenicity with that of herpesviruses, including Epstein-Barr virus, herpes simplex virus, cytomegalovirus, varicella-zoster virus, herpesvirus saimiri, and Marek disease virus. The proportion of antigen-bearing cells was increased by a factor of =5 on culture in the presence of 5-iodo-2'-deoxyuridine. Antibodies against the antigen in MT-I cells were found in all 44 patients with ATL examined and in 32 of 40 patients with malignant T-cell lymphomas (most of them had diseases similar to ATL except that leukemic cells were not found in the peripheral blood). The antibodies were also detected in 26% of the healthy adults examined from ATL-endemic areas but in only a few of those examined from ATL-non-endemic areas. On electron microscopy, extracellular type C virus particles were detected in pelleted MT-I cells cultured in the presence of5-iodo-2'-deoxyuridine. Recently, a probably new disease entity, adult T-cell leukemia (ATL), was proposed by Takatsuki and his co-workers (1, 2). Since then, many patients having ATL have been reported. These patients have been reported from a restricted area of southwestern Japan (3-7). This malignant disease has also been called adult T-cell leukemia/lymphoma (ATLL) because of its leukemic lymphoma nature. Its characteristic clinical and hematological features are: (i) onset in adulthood; (ii) acute or chronic leukemia with rapid progression; (iii) resistance to treatment with current antileukemic agents; (iv) appearance in peripheral blood of pleomorphic leukemic cells that have markedly deformed nuclei and T-cell surface markers; (v) frequent accompaniment by lymphadenopathy, hepatosplenomegaly, and hypercalcemia; (vi) absence of mediastinal tumor; and (vii) frequent skin lesions such as erythroderma and nodule formation (1)(2)(3)(4)(5)8).While studying the viral etiology ofthis malignancy, we found an antigen associated with a long-term cultured ATL cell line that is reactive with the sera of all the ATL patients tested and also with the sera of >25% ofhealthy adults from ATL-endemic areas but not with sera from those from nonendemic areas. We also detected type C virus particles in this cell line by electron microscopy.MATERIALS AND METHODS Cells. The MT-1 cell line derived from the peripheral blood of a patient having ATL (9) Sera. Sera was obtained from adult patients who have ATL or various other diseases and from healthy adults from both ATL-endemic and ATL-non-endemic areas (Fig. 1) The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734...

The sequence of 5,037 amino acids composing the ryanodine receptor from rabbit skeletal muscle sarcoplasmic reticulum has been deduced by cloning and sequencing the complementary DNA. The predicted structure suggests that the calcium release channel activity resides in the C-terminal region of the receptor molecule, whereas the remaining portion constitutes the 'foot' structure spanning the junctional gap between the sarcoplasmic reticulum and the transverse tubule.

A nation-wide sero-epidemiologic survey of adult T-cell leukemia virus (ATLV), detected es anti-ATLA (ATLV-associated antigen), was made in Japan. Sera from adult donors in 15 different locations were screened for anti-ATLA. High incidences (6 to 37%) of antibody-positive donors were found in seven regions, one in northern Japan, and the others in southwestern regions. These areas are ATLV-endemic areas corresponding to ATL-endemic areas. Examination of sera from healthy donors aged 6 to 80 years in ATL-endemic areas showed an age-dependent increase of seropositive donors with a maximum of about 30% at 40 years of age. Anti-ATLA was found in all but two of 142 patients with ATL. Anti-ATLA-positive patients with ATL were mainly found in ATLV-endemic areas, and only a few in ATL-nonendemic areas. Six patients with cutaneous T-cell lymphoma in ATLV-nonendemic areas gave a negative reaction for anti-ATLA. The geometric mean titer of anti-ATLA of patients with ATL was higher than that of healthy donors.

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We have surveyed the incidence of adult T-cell leukemia/lymphoma (ATLL) in an endemic area of 290,464 inhabitants for 7 years. We now revise our previous results on the basis of additional findings and estimate the age- and sex-specific cumulative rate for HTLV-I carriers, the adoption of which is recommended by current cancer epidemiology as a new age-standardized incidence rate. An unequivocal age-dependent increase in seroprevalence was observed for both sexes with a characteristic predominance in females. The age-dependent seroconversion in females may be partly explained by additional infection from infected husbands to their wives but the reason for men remains obscure. The mean annual number of incident cases of ATLL was 11.4, giving 3.9 ATLL patients annually per 10(5) inhabitants, 6.1 per 10(5) inhabitants aged over 30, and 85.0 per 10(5) seropositives aged over 30. Crude annual incidence rate of ATLL among 10(5) male seropositives aged over 30 was 145.3 and that for females was 55.2 and 95% confidence intervals of ATLL incidence rates were 34.8 to 255.7 for males and 6.4 to 104.1 for females, respectively. Although the sex ratio of 80 ATLL patients was 1.35, males are more prone to the disease (46 male patients among 4,522 male seropositives aged over 30 vs 34 female patients among 8,801 female seropositives aged over 30; p less than 0.001) for unknown reason(s). Morbidity in male seropositives aged over 30 is 2.6 times as high as that of females. Decennial incidence rates in males in their fifties and sixties were significantly higher than those in females. The remarkable male preponderance in oncogenicity of HTLV-I may be due to the fact that men are more prone to the disease and the number of female carriers in the denominator used to calculate the incidence rate is larger than that of males. The whole life span (0-79) cumulative risk for males was 6.9% and significantly higher than that of females (2.95%).