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...

Sixteen isolates of simian retrovirus closely related to human immunodeficiency virus (HIV) were obtained from healthy African green monkeys (AGM) (Cercopithecus aethiops). The first isolate was obtained from a monkey seropositive for HIV, and the others were isolated from monkeys harboring antibodies to the first isolate. These simian retroviruses were referred to as simian immunodeficiency virus from AGM, SIV[AGM], due to their cross-reactivities with HIV structural proteins. These SIV[AGM] isolates were found by Western blotting analysis to have virus-specific proteins of 120, 66, 55, 32-40, 24 and 17 kDa, which were all similar in size to the analogous proteins of HIV. Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV. The transmembrane glycoproteins of these 3 SIV[AGM] isolates showed size heterogeneity, being 32, 35 and 40 kDa. This virus had particles that were morphologically similar to those of HIV, and had Mg2+-dependent reverse transcriptase. Furthermore, the SIV[AGM] showed tropism and cytopathic effects on CD4-positive human cell lines. In a sero-epidemiological survey of SIV[AGM] in various non-human primates, 2 other African monkey species, the mandrill and de Brazza's monkey, were also found to have antibodies to SIV[AGM]. These HIV-related simian retroviruses will be important in determining the origin and transmission of HIV group viruses, and may provide useful animal models for studies on the infection and pathogenesis of HIV and AIDS.

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Receptor-mediated internalization and degradation of IL-2 were investigated in cell lines carrying human T cell leukemia/lymphoma (lymphotrophic) virus type I (HTLV-I) and PHA-treated normal PBL. The HTLV-I-carrying cell lines ILT-Yan and TL-Mor, and the PBL expressed both high- and low-affinity IL-2-R. However, another HTLV-I-carrying T cell line, MT-1, expressed mainly low-affinity receptors. Greater than 50% of the IL-2 bound to high-affinity receptors was internalized within 10 min when these cells were incubated at 37 degrees C. The internalized IL-2 was rapidly degraded and the products were excreted into the culture fluid. The t1/2 of IL-2 degradation in these cells was estimated as 60-80 min at 37 degrees C. The internalization and degradation of IL-2 were both temperature dependent. Light-microscopic autoradiography with 3H-labeled IL-2 confirmed the internalization of IL-2, and suggested that some IL-2 might be carried to the nucleus.

Myristoylation of human immunodeficiency virus (HIV)Gag protein is essential for virus particle budding. Two reactions are involved; activation of free myristate to myristoyl-CoA and transfer of the myristoyl residue to the Gag N-terminal glycine. We have investigated the effects of triacsin C, an inhibitor of long chain acyl-CoA synthetase, on release of HIV Gag virus-like particle (VLP) produced using the recombinant baculovirus system. First, inhibition of acyl-CoA formation by triacsin C was confirmed using the membrane fractions of insect Sf9 cells as an enzyme source. Second, when HIV Gag protein was expressed in the presence of triacsin C (0 -48 M), Gag myristoylation was inhibited in a dosedependent manner. Budding of Gag VLP, however, did not follow similar inhibition kinetics but appeared unaffected up to 24 M, yet was completely abolished at 48 M when the myristoylation of Gag protein was also completely inhibited. The "all-or-none" inhibition of Gag VLP budding suggests that although inhibition of acyl-CoA synthetase blocks the production of myristoylated Gag protein, only complete inhibition of Gag myristoylation prevents VLP budding. Thus, relatively few myristoylated Gag molecules are sufficient for plasma membrane targeting and VLP budding.