American journal of infection control · 2009
Evidence of hepatitis C virus-specific interferon gamma-positive T cells in health care workers in an infectious disease department.
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Perrella Alessandro, Grattacaso Stella, d'Antonio Anna, Atripaldi Luigi, Sbreglia Costanza, Gnarini MariaRosaria, Conti Pio, Vecchiet Jacopo, Perrella Oreste
Аннотация
BACKGROUND: Few studies are available on possible hepatitis C virus (HCV)-specific T-cell immune response in health care workers (HCWs) involved in the care of patients with HCV infection. We aimed to investigate whether a HCV-specific interferon (IFN)-gamma T-cell response, known to be involved in infection resolution, was present in those HCWs involved in the management of patients with persistent HCV infection.
METHODS: Our study involved 30 subjects, classified as group A (20 consecutive patients, 16 males and 4 females, with histologically proven chronic hepatitis), or group B (10 HCWs, 7 males and 3 females, with at least 7 years of health care experience and HCV-RNA and anti-HCV negative). As a control group, we used 10 blood samples from healthy donors at a blood donor center (group C). HCV-RNA was measured by real-time polymerase chain reaction. Blood samples (at least 35 mL) were collected from all group A and group B subjects in our hospital. Specific IFN-gamma was stimulated with HCV pool peptides (core, 2 microg/mL), with influenza Mp peptides used as a positive control.
RESULTS: Levels of HCV-specific IFN-gamma-positive cells were higher in the HCWs (group B) compared with the infected patients (group A) and healthy blood donors (group C) (Mann-Whitney U test, P < .001).
CONCLUSION: A clinically silent persistent exposure to HCV, through some as-yet undetermined mechanism, may induce a virus-specific IFN-gamma-producing CD8(+) T-cell response in healthy aviremic HCWs. This finding suggests that possible unapparent parenteral routes may stimulate host defenses with no evidence of hepatitis.
METHODS: Our study involved 30 subjects, classified as group A (20 consecutive patients, 16 males and 4 females, with histologically proven chronic hepatitis), or group B (10 HCWs, 7 males and 3 females, with at least 7 years of health care experience and HCV-RNA and anti-HCV negative). As a control group, we used 10 blood samples from healthy donors at a blood donor center (group C). HCV-RNA was measured by real-time polymerase chain reaction. Blood samples (at least 35 mL) were collected from all group A and group B subjects in our hospital. Specific IFN-gamma was stimulated with HCV pool peptides (core, 2 microg/mL), with influenza Mp peptides used as a positive control.
RESULTS: Levels of HCV-specific IFN-gamma-positive cells were higher in the HCWs (group B) compared with the infected patients (group A) and healthy blood donors (group C) (Mann-Whitney U test, P < .001).
CONCLUSION: A clinically silent persistent exposure to HCV, through some as-yet undetermined mechanism, may induce a virus-specific IFN-gamma-producing CD8(+) T-cell response in healthy aviremic HCWs. This finding suggests that possible unapparent parenteral routes may stimulate host defenses with no evidence of hepatitis.