Introduction
Hepatitis C virus (HCV) is a single-stranded RNA virus that affects 130–150 million people worldwide as a chronic infection [1]. In HCV-infected patients, viral replication has been demonstrated not only in hepatocytes but also in cells of the immune system, such as B cells, monocytes, and CD4 + and CD8 + T lymphocytes [2]–[6]. In this laboratory, it was uncovered that primary T lymphocyte cultures, generated by ex vivo treatment of peripheral blood mononuclear cells (PBMC) from healthy individuals with a T cell-inducing mitogen phytoheamagglutin (PHA), are susceptible to wild-type (patient-derived) HCV and capable of supporting its replication at a level comparable to that of in vivo infected lymphoid cells [6], [7]. Furthermore, these cells were able to produce infectious virions that de novo infected lymphocytes [7]. It was also uncovered that patient-derived HCV is significantly more infectious to primary T cells than laboratory-derived clonal strains of HCV [8]. As well, HCV infection of T cells requires surface expression of CD5, and transfection of HCV non-susceptible T cell lines with CD5 renders these cells susceptible to infection [9].
IntroductionHepatitis C virus (HCV) is a single-stranded RNA virus that affects 130–150 million people worldwide as a chronic infection [1]. In HCV-infected patients, viral replication has been demonstrated not only in hepatocytes but also in cells of the immune system, such as B cells, monocytes, and CD4 + and CD8 + T lymphocytes [2]–[6]. In this laboratory, it was uncovered that primary T lymphocyte cultures, generated by ex vivo treatment of peripheral blood mononuclear cells (PBMC) from healthy individuals with a T cell-inducing mitogen phytoheamagglutin (PHA), are susceptible to wild-type (patient-derived) HCV and capable of supporting its replication at a level comparable to that of in vivo infected lymphoid cells [6], [7]. Furthermore, these cells were able to produce infectious virions that de novo infected lymphocytes [7]. It was also uncovered that patient-derived HCV is significantly more infectious to primary T cells than laboratory-derived clonal strains of HCV [8]. As well, HCV infection of T cells requires surface expression of CD5, and transfection of HCV non-susceptible T cell lines with CD5 renders these cells susceptible to infection [9].
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