The interaction between hepatitis C virus (HCV) and the host immune system is the focus of active research. HCV is a quasispecies RNA virus with a high rate of genetic variation, thus the virus may escape the host immune response through the continuous mutation of its relevant epitopes [1], [2]. Another feature associated to HCV infection is a defective humoral and cell-mediated immune response, which not only is inadequate to tackle the virus efficiently, but quite often promotes the development of autoimmune phenomena.
A new route to apoptosis in hepatitis C virus infection
Davide Gibellini
2001-01-01
Abstract
The interaction between hepatitis C virus (HCV) and the host immune system is the focus of active research. HCV is a quasispecies RNA virus with a high rate of genetic variation, thus the virus may escape the host immune response through the continuous mutation of its relevant epitopes [1], [2]. Another feature associated to HCV infection is a defective humoral and cell-mediated immune response, which not only is inadequate to tackle the virus efficiently, but quite often promotes the development of autoimmune phenomena.
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