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https://www.arca.fiocruz.br/handle/icict/16889
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ArtigoDireito Autoral
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- IOC - Artigos de Periódicos [12678]
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HEPATITIS C VIRUS (HCV) SEQUENCE VARIATION INDUCES AN HCV-SPECIFIC T-CELL PHENOTYPE ANALOGOUS TO SPONTANEOUS RESOLUTION
Autor(es)
Afiliação
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
Universitaet Freiburg. Medizinische Klinik. Freiburg, Germany.
Universitaet Freiburg. Medizinische Klinik. Freiburg, Germany.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Virologia. Rio de Janeiro, RJ. Brasil.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
Universitaet Freiburg. Medizinische Klinik. Freiburg, Germany.
Universitaet Freiburg. Medizinische Klinik. Freiburg, Germany.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Virologia. Rio de Janeiro, RJ. Brasil.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
Harvard Medical School. Massachusetts General Hospital. Boston, MA, USA / Massachusetts Institute of Technology. Ragon Institute of Massachusetts General Hospital. Boston, MA, USA.
University of Oxford. Nuffield Department of Medicine. Peter Medawar Building for Pathogen Research. Oxford, United Kingdom.
Harvard Medical School. Massachusetts General Hospital. Gastrointestinal Unit. Boston, MA, USA.
Resumo em Inglês
Hepatitis C virus (HCV)-specific CD8(+) T cells in persistent HCV infection are low in frequency and paradoxically show a phenotype associated with controlled infections, expressing the memory marker CD127. We addressed to what extent this phenotype is dependent on the presence of cognate antigen. We analyzed virus-specific responses in acute and chronic HCV infections and sequenced autologous virus. We show that CD127 expression is associated with decreased antigenic stimulation after either viral clearance or viral variation. Our data indicate that most CD8 T-cell responses in chronic HCV infection do not target the circulating virus and that the appearance of HCV-specific CD127(+) T cells is driven by viral variation.
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