Contribution of low level HBV replication to continuing inflammatory activity in patients with anti-HBe positive chronic hepatitis B virus infection.

Author:

Lok A S,Hadziyannis S J,Weller I V,Karvountzis M G,Monjardino J,Karayiannis P,Montano L,Thomas H C

Publisher

BMJ

Subject

Gastroenterology

Reference22 articles.

1. The detection of HBV-DNA in serum by molecular hybridisation: a more sensitive method for detection of complete HBV particles;Weller, I.V.D.; Fowler, M.J.F.; Monjardino, J.;J Med Virol,1982

2. Pattern of core and surface expression in liver tissue reflects state of specific immune response in hepatitis B;Gudat, F.; Bianchi, L.; Sonnabend, W.; Theil, G.; Aenishaenslin, W.; Stalder, G.A.,1975

3. patients are infected early in life, whereas the Oladapo J, Wiedmann KH. Immunological British patients acquire the infection in adulthood. It has been suggested that inflammatory liver disease is associated with viral replication.4 Although the majority (68%) of HBeAg positive patients had active liver lesions on biopsy, 57% of Greek and 38% of British patients who were anti-HBe positive also had chronic active hepatitis or active cirrhosis. Fourteen of these 23 anti-HBe mechanisms in chronic hepatitis B infection. Hepatology 1982; 2: 116S-21Sdleston ALWF, Williams R. Inadequate antibody response to HBV or suppressor T cell defect in development of active chronic hepatitis;Thomas, H.C.; Montano, L.; Goodall, A.; deKoning R;Lancet,1974

4. Cellular immunity and hepatitis-associated, Australia antigen liver disease;Dudley, F.J.; Fox, R.A.; Sherlock, S.;Lancet,1972

5. Seroconversion from hepatitis B e antigen to antibody in chronic type B hepatitis;Hoofnagle, J.; Dusheiko, G.M.; Seeff, L.B.;Ann Intern Med,1981

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