INFLUENCE OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION ON CELL-MEDIATED-IMMUNITY IN CHRONIC-D HEPATITIS
被引:17
作者:
BUTI, M
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
BUTI, M
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ESTEBAN, R
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
ESTEBAN, R
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ESPANOL, MT
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
ESPANOL, MT
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MALAGELADA, A
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
MALAGELADA, A
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JARDI, R
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
JARDI, R
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RODRIGUEZFRIAS, F
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
RODRIGUEZFRIAS, F
[1
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ROGET, M
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
ROGET, M
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GUARDIA, J
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UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAINUNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
GUARDIA, J
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机构:
[1] UNIV AUTONOMA BARCELONA,HOSP GEN VALL DHEBRON,IMMUNOL SECT,E-08035 BARCELONA,SPAIN
To determine whether the abnormalities of cell-mediated immunity described in chronic D hepatitis are associated with hepatitis D virus (HDV) infection or concomitant human immunodeficiency virus (HIV) infection, serologic and tissue hepatitis B virus (HBV) and HDV markers and T lymphocyte subsets were studied in serum samples from 38 patients with chronic D hepatitis, 26 of whom had HIV infection. Patients with chronic D hepatitis and HIV infection had significantly lower peripheral blood T4:T8 ratios resulting from a significant increase in T8+ (suppressor/cytotoxic) cells, while numbers of T lymphocyte subsets were normal in cases with chronic D hepatitis only. HIV+ patients showed an increase in HBV replication (identified by hepatitis B core antigen in liver and hepatitis B e antigen and HBV DNA in serum) and in HDV replication (tissue D antigen and HDV RNA) without evidence of more active liver disease. Probably the immunologic disturbances detected in chronic D hepatitis are secondary to HIV infection, do not contribute to the pathogenesis of liver injury, and are associated with increased viral B and D replication.