IN HEPATOCYTES INFECTED WITH DUCK HEPATITIS-B VIRUS, THE TEMPLATE FOR VIRAL-RNA SYNTHESIS IS AMPLIFIED BY AN INTRACELLULAR PATHWAY

被引:185
作者
WU, TT
COATES, L
ALDRICH, CE
SUMMERS, J
MASON, WS
机构
[1] FOX CHASE CANC INST,INST CANC RES,7701 BURHOLME AVE,PHILADELPHIA,PA 19111
[2] UNIV NEW MEXICO,SCH MED,CTR CANC,ALBUQUERQUE,NM 87131
关键词
D O I
10.1016/0042-6822(90)90206-7
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
During the productive phase of chronic hepadnaviral infections, virion DNA synthesis occurs in the cytoplasm of the infected hepatocyte, but viral RNA is synthesized in the nucleus, apparently from a covalently closed, circular (CCC) viral DNA. J. Tuttleman, C. Pourcel, and 1. Summers (1986a, Cell 47, 451-460) have shown that the intracellular levels of CCC DNA can increase during initiation of infection of duck hepatocytes in vitro with duck hepatitis B virus and during long term culture of infected duck hepatocytes in vitro. This amplification of CCC DNA occurs through the reverse transcription pathway. To distinguish between an entirely intracellular process of amplification and amplification due to multiple infections by extracellular virus in the virus producing cultures, suramin was added to the infected cultures to block superinfection. We found that CCC DNA amplification occurred at least as efficiently in the presence of suramin as in its absence. First, there was a net increase in the total amount of CCC DNA in the cultures both in the presence and in the absence of suramin. Second, synthesis of CCC DNA in the presence and absence of suramin was observed by density labeling of this viral DNA by growth of the cultures in medium containing BUdR. Amplification was also demonstrable in the presence of neutralizing duck antibodies. These results support the hypothesis of Tuttleman et al. (1986a) that CCC DNA amplification in chronically infected cultures and, by inference, the mechanism of persistent infection involves primarily intracellular regulatory mechanisms. © 1990.
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页码:255 / 261
页数:7
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