DESCARTES BEFORE THE HORSE - I CLONE, THEREFORE I AM - THE HEPATITIS-C VIRUS IN CURRENT PERSPECTIVE

被引:102
作者
ALTER, HJ [1 ]
机构
[1] NIH, DEPT TRANSFUS MED, BETHESDA, MD 20892 USA
关键词
HEPATITIS-C VIRUS; CLONING; MOLECULES; HEPATITIS ANTIBODIES; HEPATITIS; VIRAL; NON-A; NON-B; BLOOD TRANSFUSION;
D O I
10.7326/0003-4819-115-8-644
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In an unprecedented approach to viral discovery, the hepatitis C virus (HCV) was cloned before it was established by conventional methods of viral detection or by genomic characterization. Hepatitis C virus is a small (10-kb), single-stranded RNA virus with a genomic organization that places it in the family Flaviviridae. The virus is global in distribution, with a prevalence between 0.3% and 1.5%. The same agent causes parenterally acquired and sporadic non-A, non-B hepatitis. Nonparenteral modes of spread are poorly defined, but low-level sexual transmission is probable. There is a strong association between the presence of antibody to HCV (anti-HCV) and hepatocellular carcinoma; a causal role for HCV is suspected but has not been proved. Hepatitis C virus accounts for at least 85% of the cases of transfusion-associated hepatitis; an anti-HCV-reactive donor was retrospectively identified in nearly 90% of cases. Among donors confirmed by recombinant immunoblot assay (RIBA) to be anti-HCV positive, 80% to 90% are infectious. Hepatitis C virus RNA can be detected within 1 to 2 weeks of exposure and persists throughout the course of infection. Generally, the presence of anti-HCV cannot be confirmed until 9 to 20 weeks after exposure, creating a window period of seronegativity and potential infectivity. It is anticipated that the anti-HCV assay will reduce the number of cases of transfusion-associated hepatitis by 50% in the United States; a 70% reduction has been documented in Spain.
引用
收藏
页码:644 / 649
页数:6
相关论文
共 30 条
  • [1] DETECTION OF ANTIBODY TO HEPATITIS-C VIRUS IN PROSPECTIVELY FOLLOWED TRANSFUSION RECIPIENTS WITH ACUTE AND CHRONIC NON-A-HEPATITIS, NON-B-HEPATITIS
    ALTER, HJ
    PURCELL, RH
    SHIH, JW
    MELPOLDER, JC
    HOUGHTON, M
    CHOO, QL
    KUO, G
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (22) : 1494 - 1500
  • [2] THE HEPATITIS-C VIRUS AND ITS RELATIONSHIP TO THE CLINICAL SPECTRUM OF NANB HEPATITIS
    ALTER, HJ
    [J]. JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 1990, 5 : 78 - 94
  • [3] ALTER HJ, 1982, VIRAL HEPATITIS, P279
  • [4] ALTER HJ, 1991, IN PRESS 1990 INT S
  • [5] RISK-FACTORS FOR ACUTE NON-A, NON-B HEPATITIS IN THE UNITED-STATES AND ASSOCIATION WITH HEPATITIS-C VIRUS-INFECTION
    ALTER, MJ
    HADLER, SC
    JUDSON, FN
    MARES, A
    ALEXANDER, WJ
    HU, PY
    MILLER, JK
    MOYER, LA
    FIELDS, HA
    BRADLEY, DW
    MARGOLIS, HS
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1990, 264 (17): : 2231 - 2235
  • [6] IMPORTANCE OF HETEROSEXUAL ACTIVITY IN THE TRANSMISSION OF HEPATITIS-B AND NON-A, NON-B HEPATITIS
    ALTER, MJ
    COLEMAN, PJ
    ALEXANDER, WJ
    KRAMER, E
    MILLER, JK
    MANDEL, E
    HADLER, SC
    MARGOLIS, HS
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1989, 262 (09): : 1201 - 1205
  • [7] BLANCHETTE VS, 1991, IN PRESS BLOOD
  • [8] POST-TRANSFUSION NON-A, NON-B HEPATITIS - PHYSICOCHEMICAL PROPERTIES OF 2 DISTINCT AGENTS
    BRADLEY, DW
    MAYNARD, JE
    POPPER, H
    COOK, EH
    EBERT, JW
    MCCAUSTLAND, KA
    SCHABLE, CA
    FIELDS, HA
    [J]. JOURNAL OF INFECTIOUS DISEASES, 1983, 148 (02) : 254 - 265
  • [9] BRETTLER DB, 1990, BLOOD, V76, P254
  • [10] BRUIX J, 1989, LANCET, V2, P1004