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2022-01-01
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IMMUNOLOGIC EVIDENCE FOR LACK OF HETEROLOGOUS PROTECTION FOLLOWING RESOLUTION OF HCV IN PATIENTS WITH NON-GENOTYPE 1 INFECTION
HCV
Pacientes
Infecção não genotípica 1
Proteção heteróloga
Infection
Immunologic evidence
Heterologous protection
HCV
Autor
Schulze Zur Wiesch, Julian
Lauer, Georg M.
Timm, Joerg
Kuntzen, Thomas
Neukamm, Martin
Berical, Andrew
Jones, Andrea M.
Nolan, Brian E.
Longworth, Steve A.
Kasprowicz, Victoria
McMahon, Cory
Wurcel, Alysse
Lohse, Ansgar W.
Lewis-Ximenez, Lia L
Chung, Raymond T.
Kim, Arthur Y.
Allen, Todd M.
Walker, Bruce D.
Lauer, Georg M.
Timm, Joerg
Kuntzen, Thomas
Neukamm, Martin
Berical, Andrew
Jones, Andrea M.
Nolan, Brian E.
Longworth, Steve A.
Kasprowicz, Victoria
McMahon, Cory
Wurcel, Alysse
Lohse, Ansgar W.
Lewis-Ximenez, Lia L
Chung, Raymond T.
Kim, Arthur Y.
Allen, Todd M.
Walker, Bruce D.
Afiliación
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA / Heinrich Pette Institute for Experimental Virology. Hamburg, Germany.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
University of Essen. Institute of Virology. Essen, Germany.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Medizinische Klinik I, Universita tsklinikum Eppendorf. Hamburg, Germany.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Virologia. Rio de Janeiro, RJ. Brasil.
Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical Schoo. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA / Howard Hughes Medical Institute. Chevy Chase, MD, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
University of Essen. Institute of Virology. Essen, Germany.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Medizinische Klinik I, Universita tsklinikum Eppendorf. Hamburg, Germany.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Virologia. Rio de Janeiro, RJ. Brasil.
Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical Schoo. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA.
Partners AIDS Research Center. Infectious Disease Division. Massachusetts General Hospital and Harvard Medical School. Boston, MA, USA / Howard Hughes Medical Institute. Chevy Chase, MD, USA.
Resumen en ingles
Chronic hepatitis C virus (HCV) infection is typically characterized by a lack of virus-specific CD4(+) T-cell-proliferative responses, but strong responses have been described in a subset of persons with persistent viremia. One possible explanation for these responses is that they were primed by an earlier resolved infection and do not recognize the current circulating virus. We defined all targeted epitopes using overlapping peptides corresponding to a genotype 1a strain in 44 patients chronically infected with different HCV genotypes (GT). Surprisingly, more HCV-specific CD4(+) T-cell responses were detected in patients with chronic non-GT1 infection compared with patients with chronic GT1 infection (P = .017). Notably, we found serologic evidence of a previous exposure to GT1 in 4 patients with non-GT1 infection, and these persons also demonstrated significantly more responses than non-GT1 patients in whom genotype and HCV serotype were identical (P < .001). Comparison of recognition of GT1-specific peptides to peptides representing autologous virus revealed the absence of cross-recognition of the autologous circulating virus. These data indicate that persistent HCV infection can occur in the presence of an HCV-specific T-cell response primed against a heterologous HCV strain, and suggest that clearance of 1 GT does not necessarily protect against subsequent exposure to a second GT.
Palabras clave en portugues
Evidência imunológicaHCV
Pacientes
Infecção não genotípica 1
Proteção heteróloga
Palabras clave en ingles
Chronic hepatitis C virusInfection
Immunologic evidence
Heterologous protection
HCV
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