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STRONGYLOIDIASIS AND INFECTIVE DERMATITIS ALTER HUMAN T LYMPHOTROPIC VIRUS-1 CLONALITY IN VIVO.
Infecções por HTLV-I/complicações
Vírus 1 Linfotrópico T Humano/fisiologia
Strongyloides stercoralis
Estrongiloidíase/complicações
Linfócitos T/virologia
Carga Viral
Adulto
Animais
Coinfecção
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/genética
Humanos
Leucemia-Linfoma de Células T do Adulto/virologia
Meia-Idade
Provirus/fisiologia
Fatores de Risco
Estrongiloidíase/parasitologia
Autor
Afiliación
Wright-Fleming Institute. Imperial College London. London, United Kingdom / University of Liège (ULg). Molecular and Cellular Epigenetics. Interdisciplinary Cluster for Applied Genoproteomics (GIGA). Liège, Belgium
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru / Institute of Tropical Medicine. Antwerp, Belgium
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Laboratório de Patologia Experimental. Salvador, BA, Brasil
Federal University of Bahia. Complexo Hospitalar Universitário Prof. Edgard Santos. Department of Pathology. Salvador, BA, Brasil
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Section of Infectious Diseases. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru / Institute of Tropical Medicine. Antwerp, Belgium
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Universidad Peruana Cayetano Heredia. Instituto de Medicina Tropical Alexander von Humboldt. Lima, Peru / Hospital Nacional Cayetano Heredia. Lima, Peru
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Laboratório de Patologia Experimental. Salvador, BA, Brasil
Federal University of Bahia. Complexo Hospitalar Universitário Prof. Edgard Santos. Department of Pathology. Salvador, BA, Brasil
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Section of Infectious Diseases. Imperial College London. London, United Kingdom
Wright-Fleming Institute. Imperial College London. London, United Kingdom
Resumen en ingles
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-1â º 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-1â º clones.
DeCS
Dermatite/complicaçõesInfecções por HTLV-I/complicações
Vírus 1 Linfotrópico T Humano/fisiologia
Strongyloides stercoralis
Estrongiloidíase/complicações
Linfócitos T/virologia
Carga Viral
Adulto
Animais
Coinfecção
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/genética
Humanos
Leucemia-Linfoma de Células T do Adulto/virologia
Meia-Idade
Provirus/fisiologia
Fatores de Risco
Estrongiloidíase/parasitologia
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