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      Proteína Tax (HTLV-I), probable factor patogénico y marcador del síndrome sicca que se asocia a HAM/TSP Translated title: Viral Tax protein expression in salivary glands of patients infected with human t-cell lymphotropic virus type I and Sicca Syndrome

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          Human T-cell lymphotropic virus type I (HTLV-I) is a retrovirus that influences cellular metabolism modifying biological responses. This results in oncogenic, degenerative or inflammatory changes. The myelopathy associated to HTLV-I or tropical spastic paraparesia (HAM/TSP) is a mainly degenerative response to the virus infection. On the other hand, Sjögren syndrome has an inflammatory appearance. The immunohistochemical study of CD-4, CD-8 and CD45 lymphocytes, metalloproteinase MMP-9 and viral Tax protein in pathological samples of salivary glands may help to differentiate primary from viral Sicca syndrome. Aim: To perform an immunohistochemical study of salivary glands of patients with HAM/TSP and Sicca syndrome and control subjects. Material and Methods: Pathological samples of salivary glands from 53 patients with HAM/TSP and Sicca syndrome and 10 control subjects, were studied. Immunohistochemistry was performed using antibodies against CD-4, CD-8 and CD-45 lymphocytes, metalloproteinase MMP-9 and viral Tax protein. Results: Only in patients with HAM/TSP and Sicca syndrome, the presence of Tax protein was observed in CD-4 and CD-8 lymphocytes and in glandular acini. Conclusions: Patients infected with HTLV-I express Tax protein in salivary glands. This finding has diagnostic and pathogenic implications (Rev Méd Chile 2005; 133: 1183-90)

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          Adult T-cell leukemia: antigen in an ATL cell line and detection of antibodies to the antigen in human sera.

          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 (ATL), 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 approximately 5 on culture in the presence of 5-iodo-2'-deoxyuridine. Antibodies against the antigen in MT-1 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-1 cells cultured in the presence of 5-iodo-2'-deoxyuridine.
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            Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis.

            10 out of 17 (59%) patients with tropical spastic paraparesis (TSP) had antibodies to human T-lymphotropic virus-I (HTLV-I), as did 5 out of 5 TSP patients with systemic symptoms. Only 13 out of 303 (4%) controls, made up of blood donors, medical personnel, and other neurological patients, had such antibodies. These findings suggest either that HTLV-I is neurotropic or that the virus or a related one contributes to the pathogenesis of TSP.
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              Multiple viral strategies of HTLV-1 for dysregulation of cell growth control.

              The human T cell leukemia virus-1 (HTLV-1) is a retrovirus that causes adult T cell leukemia (ATL) and neurological disorder, the tropical spastic paraparesis (HAM/TSP). The pathogenesis apparently results from the pleiotropic function of Tax protein, which is a key regulator of viral replication. Tax exerts (a) trans-activation and -repression of transcription of different sets of cellular genes through binding to groups of transcription factors and coactivators, (b) dysregulation of cell cycle through binding to inhibitors of CDK4/6, and (c) inhibition of some tumor suppressor proteins. These effects on a wide variety of cellular targets seem to cooperate in promoting cell proliferation. This is an effective viral strategy to amplify its proviral genome through replication of infected cells; ultimately it results in cell transformation and leukemogenesis.
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                Author and article information

                Journal
                rmc
                Revista médica de Chile
                Rev. méd. Chile
                Sociedad Médica de Santiago (Santiago, , Chile )
                0034-9887
                October 2005
                : 133
                : 10
                : 1183-1190
                Affiliations
                [01] orgnameUniversidad de Chile orgdiv1Escuela de Medicina orgdiv2Departamento de Ciencias Neurológicas Chile lcartier@ 123456med.uchile.cl
                [02] orgnameInstituto de Salud Pública orgdiv1Sección de Virología Chile
                Article
                S0034-98872005001000007 S0034-9887(05)13301007
                10.4067/S0034-98872005001000007
                16341369
                fafcaa25-c05d-44ab-b9d8-21223e68f9cb

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 07 June 2005
                : 04 January 2005
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 29, Pages: 8
                Product

                SciELO Chile

                Categories
                ARTICULOS DE INVESTIGACION

                Tax,Sjögren syndrome,Human T-lymphotropic virus 1,Gene products

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