Reduced CC chemokine receptor (CCR) 1 and CCR5 surface expression on peripheral blood T lymphocytes from patients with chronic hepatitis C infection.

T cell recruitment to the infected liver is an essential step for the efficient elimination of hepatitis viruses. The surface expression of CC chemokine receptor (CCR) 1, CCR4, and CCR5 on peripheral blood T lymphocytes and their responsiveness to the chemokines macrophage inflammatory proteins (MIP)-1alpha, MIP-1beta, and RANTES (regulated on activation, normally T cell-expressed and secreted) was analyzed in patients with chronic hepatitis C and hepatitis B infection and compared with healthy subjects. Although CCR4 surface expression was not altered, hepatitis C virus (HCV)-infected patients had lower proportions of CD8 T cells with CCR1 and CCR5 surface expression (P<.

Risk of hepatitis C after immunoadsorption.

An episode of acute hepatitis in a patient with hemophilia during immunoadsorption therapy initially was misinterpreted as a reactivated hepatitis C virus (HCV) infection, but ultimately was shown to be an exogenous reinfection during cohort treatment with another HCV-positive patient. This incident illustrates that policies for the prevention of nosocomial transmission of blood-borne pathogens, especially in cohort treatment units, may need to be reassessed.

Frequency of the HIV-protective CC chemokine receptor 5-Delta32/Delta32 genotype is increased in hepatitis C.

Background & Aims: A homozygous 32-base pair deletion in the CCR5 gene (CCR5-Delta32) protects against human immunodeficiency virus infection (HIV). However, the role of this mutation in other infections, such as hepatitis C virus (HCV) infection, has not been defined.

Methods: We determined the frequency of the CCR5-Delta32 mutation by polymerase chain reaction in anti-HCV(+) (n = 153), anti-HIV(+) (n = 102), and anti-HCV(+)/HIV(+) (n = 130) white patients as well as in 102 healthy blood donors.

HCV-specific cytokine induction in monocytes of patients with different outcomes of hepatitis C.

Aim: Cytokine release by macrophages critically determines the type of immune response to an antigen. Therefore, we studied hepatitis C virus (HCV)-specific induction of interleukins-1 beta, -10, -12 (IL-1 beta, IL-10, IL-12), and tumor necrosis factor-alpha (TNF-alpha) in monocytes.

Methods: Intracellular cytokine expression was studied by flow cytometry in 23 patients with chronic hepatitis C, 14 anti-HCV seropositives without viremia and 11 controls after stimulation of peripheral blood mononuclear cells with recombinant core, NS3, NS4, NS5a and NS5b proteins.