دورية أكاديمية

Strongyloidiasis and Infective Dermatitis Alter Human T Lymphotropic Virus-1 Clonality in vivo

التفاصيل البيبلوغرافية
العنوان: Strongyloidiasis and Infective Dermatitis Alter Human T Lymphotropic Virus-1 Clonality in vivo
المؤلفون: Gillet, Nicolas A., Cook, Lucy, Laydon, Daniel J., Hlela, Carol, Verdonck, Kristien, Alvarez, Carolina, Gotuzzo, Eduardo, Clark, Daniel, Farré, Lourdes, Bittencourt, Achiléa, Asquith, Becca, Taylor, Graham P., Bangham, Charles R.M.
بيانات النشر: Public Library of Science
سنة النشر: 2013
المجموعة: Repositorio - UPCH (Universidad Peruana Cayetano Heredia)
مصطلحات موضوعية: Animals, Humans, major clinical study, Middle Aged, Adult, controlled study, polymerase chain reaction, Human T-lymphotropic virus 1, Strongyloides, Strongyloides stercoralis, strongyloidiasis, Risk Factors, follow up, Coinfection, cell proliferation, dermatitis, HTLV-I Infections, Human T cell leukemia virus 1, peripheral blood mononuclear cell, clonal variation, in vivo study, skin defect, T-Lymphocytes, virus load, cerebrospinal fluid, Vermes, epigenetics, genetic similarity, Leukemia-Lymphoma, Adult T-Cell
الوصف: Human T-lymphotropic Virus-1 (HTLV-1) is a retrovirus that persists lifelong by driving clonal proliferation of infected T-cells. HTLV-1 causes a neuroinflammatory disease and adult T-cell leukemia/lymphoma. Strongyloidiasis, a gastrointestinal infection by the helminth Strongyloides stercoralis, and Infective Dermatitis associated with HTLV-1 (IDH), appear to be risk factors for the development of HTLV-1 related diseases. We used high-throughput sequencing to map and quantify the insertion sites of the provirus in order to monitor the clonality of the HTLV-1-infected T-cell population (i.e. the number of distinct clones and abundance of each clone). A newly developed biodiversity estimator called “DivE” was used to estimate the total number of clones in the blood. We found that the major determinant of proviral load in all subjects without leukemia/lymphoma was the total number of HTLV-1-infected clones. Nevertheless, the significantly higher proviral load in patients with strongyloidiasis or IDH was due to an increase in the mean clone abundance, not to an increase in the number of infected clones. These patients appear to be less capable of restricting clone abundance than those with HTLV-1 alone. In patients co-infected with Strongyloides there was an increased degree of oligoclonal expansion and a higher rate of turnover (i.e. appearance and disappearance) of HTLV-1-infected clones. In Strongyloides co-infected patients and those with IDH, proliferation of the most abundant HTLV-1+ T-cell clones is independent of the genomic environment of the provirus, in sharp contrast to patients with HTLV-1 infection alone. This implies that new selection forces are driving oligoclonal proliferation in Strongyloides co-infection and IDH. We conclude that strongyloidiasis and IDH increase the risk of development of HTLV-1-associated diseases by increasing the rate of infection of new clones and the abundance of existing HTLV-1+ clones.
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1553-7374
العلاقة: urn:issn:1553-7374; https://hdl.handle.net/20.500.12866/10709Test; PLoS Pathogens; https://doi.org/10.1371/journal.ppat.1003263Test
DOI: 10.1371/journal.ppat.1003263
الإتاحة: https://doi.org/20.500.12866/10709Test
https://doi.org/10.1371/journal.ppat.1003263Test
https://hdl.handle.net/20.500.12866/10709Test
حقوق: info:eu-repo/semantics/restrictedAccess ; https://creativecommons.org/licenses/by-nc-nd/4.0/deed.esTest
رقم الانضمام: edsbas.B561C1DD
قاعدة البيانات: BASE
الوصف
تدمد:15537374
DOI:10.1371/journal.ppat.1003263