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1/5. Detection of human immunodeficiency virus type 2 in brain tissue.

    infection due to human immunodeficiency virus (HIV) type 2 is believed to cause a clinical picture similar to that of hiv-1, although extensive data are not available. In 2 patients with West African exposure and neurologic symptoms, hiv-2 was detected in the central nervous system using dna and rna polymerase chain reaction, in situ hybridization, and immunohistology. In the first patient, the neurologic disease was most likely due to productive infection with hiv-2. In the second, a combination of neuropathologic abnormalities (including the presence of hiv-2) explained the clinical features. Thus hiv-2, like hiv-1, can be readily detected in brain tissue in patients with neurologic abnormalities, although the exact role of hiv-2 in pathogenesis of AIDS-associated neurologic disease requires further study.
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2/5. HTLV-I and chronic nervous diseases: present status and a look into the future.

    Three entities--multiple sclerosis, tropical spastic paraparesis, and human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM)--may represent manifestations of the same disease, with HTLV-I-like virus playing a role in their etiology. Tests for the presence of antibodies reacting with either HTLV-I-like virions or with p24 (gag) antigen, expression of HTLV-I antigen by cells of peripheral blood lymphocytes or cerebrospinal fluid, and viral sequences detected by in situ hybridization are essential to establish the role of HTLV-I-like virus in the disease. It is not yet known whether an incomplete form of the virus persists in the tissue following initial infection or whether the virus in question shares the gag protein with HTLV-I but carries the envelope of a different virus. It is recommended that investigative units comprising neurologists and laboratory workers be established as soon as possible to pursue vigorously the leads that may throw some light on the etiology of chronic neurological diseases such as multiple sclerosis.
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3/5. A first case of complete remission of beta-interferon sensitive adult T-cell leukemia.

    A case of complete remission of adult T-cell leukemia (ATL) induced by beta-interferon is reported. A 46-year-old male was diagnosed as ATL because of the increased number of ATL cells with deeply indented and lobulated nuclei in the peripheral blood, accompanied by elevated values of the lactic dehydrogenase, the alkaline phosphatase, and the calcium in the serum. The result of the cell surface marker analysis of peripheral blood lymphocytes was compatible with ATL and anti-ATL associated antibody (ATLA) was positive. The integration of proviral deoxyribonucleic acid (dna) of human T-cell leukemia virus type I(HTLV-I) was proved in the peripheral blood lymphocytes using Southern blot hybridization. Since an ordinal chemotherapy was not so effective for this patient, he was treated with 1.8 X 10(7) units of recombinant beta-interferon (beta-IFN) per day for 7 days as one course. After 5 courses of treatment, a markedly favorable response was recognized, and he achieved complete remission. A lower dose of beta-IFN (9 X 10(6) units per day for 3 days as one course, one or two courses per month) has been continued and he has still been in a complete remission state for 10 months. It is concluded that beta-IFN should be used to treat ATL.
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4/5. Molecular cloning of human T-cell lymphotrophic virus type I-like proviral genome from the peripheral lymphocyte dna of a patient with chronic neurologic disorders.

    Human T-cell lymphotropic virus type 1 (HTLV-I), the etiologic agent of human T-cell leukemia, has recently been shown to be associated with neurologic disorders such as tropical spastic paraparesis, HTLV-associated myelopathy, and possibly with multiple sclerosis. In this communication, we have examined one specific case of neurologic disorder that can be classified as multiple sclerosis or tropical spastic paraparesis. The patient suffering from chronic neurologic disorder was found to contain antibodies to HTLV-I envelope and gag proteins in his serum and cerebrospinal fluid. lymphocytes from peripheral blood and cerebrospinal fluid of the patient were shown to express viral rna sequences by in situ hybridization. Southern blot analysis of the patient lymphocyte dna revealed the presence of HTLV-I-related sequences. Blot-hybridization analysis of the rna from fresh peripheral lymphocytes stimulated with interleukin 2 revealed the presence of abundant amounts of genomic viral rna with little or no subgenomic rna. We have cloned the proviral genome from the dna of the peripheral lymphocytes and determined its restriction map. This analysis shows that this proviral genome is very similar if not identical to that of the prototype HTLV-I genome.
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5/5. Presence of HTLV-I proviral dna in patients with adult T-cell leukemia/lymphoma in taiwan.

    Human T-lymphotropic virus-I (HTLV-I) proviral dna was demonstrated in the leukemic cells of two newly identified cases of adult T-cell leukemia/lymphoma (ATL) in taiwan by the Southern blot hybridization method. Therefore, the ATL cases diagnosed clinicopathologically in taiwan were, for the first time, documented to be definitely related to HTLV-I.
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keywords = hybridization
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