HEPATITIS-B TODAY - CLINICAL AND DIAGNOSTIC OVERVIEW

被引:8
作者
KOFF, RS [1 ]
机构
[1] UNIV MASSACHUSETTS,SCH MED,WORCESTER,MA 01605
关键词
HEPATITIS-B; ACUTE; CHRONIC; SEROLOGY; SEQUELAE; TREATMENT;
D O I
10.1097/00006454-199305000-00035
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The hepatitis B virus is a member of an unusual family of noncytopathogenic, hepatotropic DNA viruses-the hepadnaviruses. The complete virus comprises a lipoprotein coat, the hepatitis B surface antigen, enveloping a nucleocapsid core that contains a small, circular DNA molecule. Four open reading frames have been identified on the hepatitis B virus DNA genome. They encode seven proteins, including a hepatitis B virus DNA polymerase molecule with reverse transcriptase activity. The replication of the virus resembles that of retroviruses and occurs predominantly but not exclusively in hepatocytes. Virus variants involving genomic mutations have been identified. Testing for hepatitis B surface antigen permits detection of many but not all acutely infected patients. Diagnosis of acute infection rests on the identification of IgM antibodies to the hepatitis B core antigen. Antibody to hepatitis B surface antigen appears in serum during the convalescent phase of hepatitis B virus infection. It is the neutralizing, protective antibody largely responsible for immunity to reinfection. In persistent infection hepatitis B surface antigen is present, antibody to hepatitis B core antigen is predominantly an IgG antibody, antibody to hepatitis B surface antigen is not detectable or is present in very low titers and viral replication may be active. Persistent infection leads to an asymptomatic carrier state, chronic hepatitis, cirrhosis and hepatocellular carcinoma. No specific treatment exists for acute hepatitis B virus infection. Current data indicate that approximately 50% of adults who have chronic infection achieve virologic, biochemical and histologic remission from treatment with alpha-2b interferon.
引用
收藏
页码:428 / 432
页数:5
相关论文
共 28 条
[1]  
BEASLEY RP, 1988, CANCER, V61, P1942, DOI 10.1002/1097-0142(19880515)61:10<1942::AID-CNCR2820611003>3.0.CO
[2]  
2-J
[3]   VACCINE-INDUCED ESCAPE MUTANT OF HEPATITIS-B VIRUS [J].
CARMAN, WF ;
ZANETTI, AR ;
KARAYIANNIS, P ;
WATERS, J ;
MANZILLO, G ;
TANZI, E ;
ZUCKERMAN, AJ ;
THOMAS, HC .
LANCET, 1990, 336 (8711) :325-329
[4]  
CARMAN WF, 1989, LANCET, V2, P588
[5]   LIVER-TRANSPLANTATION IN THE MANAGEMENT OF FULMINANT HEPATIC-FAILURE [J].
EMOND, JC ;
ARAN, PP ;
WHITINGTON, PF ;
BROELSCH, CE ;
BAKER, AL .
GASTROENTEROLOGY, 1989, 96 (06) :1583-1588
[6]   FREQUENT ACTIVATION OF N-MYC GENES BY HEPADNAVIRUS INSERTION IN WOODCHUCK LIVER-TUMORS [J].
FOUREL, G ;
TREPO, C ;
BOUGUELERET, L ;
HENGLEIN, B ;
PONZETTO, A ;
TIOLLAIS, P ;
BUENDIA, MA .
NATURE, 1990, 347 (6290) :294-298
[7]  
HART J, 1990, AM J SURG PATHOL, V14, P79
[8]   HEPATITIS-B VIRUS INTEGRATION SITE IN HEPATOCELLULAR-CARCINOMA AT CHROMOSOME 17-18 TRANSLOCATION [J].
HINO, O ;
SHOWS, TB ;
ROGLER, CE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (21) :8338-8342
[9]  
Hoofnagle J H, 1981, Semin Liver Dis, V1, P7, DOI 10.1055/s-2008-1063925
[10]   RANDOMIZED, CONTROLLED TRIAL OF RECOMBINANT HUMAN ALPHA-INTERFERON IN PATIENTS WITH CHRONIC HEPATITIS-B [J].
HOOFNAGLE, JH ;
PETERS, M ;
MULLEN, KD ;
JONES, DB ;
RUSTGI, V ;
DIBISCEGLIE, A ;
HALLAHAN, C ;
PARK, Y ;
MESCHIEVITZ, C ;
JONES, EA .
GASTROENTEROLOGY, 1988, 95 (05) :1318-1325