Core and E antigen synthesis in rodent cells transformed with hepatitis B virus DNA is associated with greater than genome length viral messenger RNAs

Gough, Nicholas M.

doi:10.1016/s0022-2836(83)80274-5

Cited by 84 publications

(48 citation statements)

References 44 publications

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“…We could not detect 3' ends of RNA other than the HBsAg polyadenylation site by using probes labelled at other sites (data not shown) and thus we conclude that the HBsAg mRNA polyadenylation site is unique in HBV and that it is also used for the 3.8-kb transcript. This interpretation is consistent with data from other studies (Gough, 1983;Standring et al, 1984). In summary, a promoter, a splice acceptor site and a splice donor site strongly active in heterologous systems ( Figure 2E, signals a, c and d) could not be detected in the infected liver.…”

Section: Resultssupporting

confidence: 94%

“…In parallel we also analysed RNA produced from cell line L154. HBV (originally designated L/130.4/TK154, Gough and Murray, 1982), producing HBsAg, small quantitites of HBcAg/HBeAg and the corresponding transcripts (Gough and Murray, 1982;Gough, 1983). In the infected liver ( Figure IA, lanes liver) HBVspecific transcripts were identified in polyadenylated and non-polyadenylated RNA, whereas in cell line L154.HBV only polyadenylated HBV transcripts were detected.…”

Section: Resultsmentioning

confidence: 97%

“…In addition to the two transcripts detected in the infected liver, a minor transcript 4.2-4.5 kb in length was detected in cell line L154.HBV ( Figure IA, lane L154.HBV poly(A)+). Using highly sensitive assay conditions, Gough (1983) (Thomas, 1980) and hybridized with nick-translated plasmid pSHH2.1 (Cattaneo et Malpiece et al, 1983;Cattaneo et al, 1983a;Simonsen and Levinson, 1983). Nuclease digestion analysis was performed to discover if these signals were used in the infected liver (Berk and Sharp, 1978).…”

Section: Resultsmentioning

confidence: 99%

“…The other major transcript is larger than the 3.2-kb HBV genome, even after a correction for a poly(A) tail of 100-200 residues, and is present as a major RNA species only in the infected liver. It co-migrates with a minor transcript from cell line L154.HBV, where it has been correlated with low expression of HBcAg/HBeAg (Gough, 1983). Its abundance in the infected liver indicates that the 3.8-kb mRNA could also play a major role in the productive HBV replication cycle.…”

Section: Discussionmentioning

confidence: 99%

“…In sets of stable rodent cell lines into which HBV DNA had been introduced by transfection, the major HBsAg transcript and some minor HBV transcripts were identified Gough, 1983). In HBV-SV40 hybrids replicating to a high copy number in COS cells, spliced HBV RNAs were detected (Simonesen and Levinson, 1983;Cattaneo et al, 1983a).…”

Section: Introductionmentioning

confidence: 99%

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Hepatitis B virus transcription in the infected liver.

Cattaneo¹,

Will²,

Schaller³

1984

The EMBO Journal

166

110

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Hepatitis B virus (HBV) transcription was studied in the liver of an infected chimpanzee and compared with HBV transcription in heterologous systems. Besides the well characterized 2.3-kb surface antigen mRNA produced in most systems, a second major transcript was identified in the liver. This 3.8-kb transcript (-4300 bases) is slightly larger than the HBV genome and is probably involved both in core/e antigen synthesis and in HBV replication via reverse transcription. In addition, minor variants of the 2.3-kb surface antigen mRNA were characterzed as probably being involved in the expression of HBsAg-related minor proteins. Finally, several potential transcription signals, identified on the HBV genome using heterologous expression systems, were found to be poorly active if at all in the infected liver, thereby stressing the importance of HBV transcription studies performed with liver material.

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Section: Resultssupporting

confidence: 94%

Section: Resultsmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Hepatitis B virus transcription in the infected liver.

Cattaneo¹,

Will²,

Schaller³

1984

The EMBO Journal

166

110

View full text Add to dashboard Cite

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Hepatocellular Carcinoma: Molecular Aspects in Hepatitis B

Buendia¹,

Paterlini‐Bréchot²,

Tiollais³

et al. 2005

Viral Hepatitis

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Products of the “x” gene in hepatitis B and related viruses

Feitelson

1986

Hepatology

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The X region in hepatitis B virus DNA potentially encodes a polypeptide 154 amino acids in length. Two synthetic peptides spanning residues 100 to 115 (peptide 99) and 115 to 131 (peptide 100) in a hydrophilic domain within the carboxy terminal third of the proposed gene product were made and used to raise peptide antisera in rabbits. Such antisera specifically bound to X reactive determinants in liver-derived core antigen particles from humans (HBcAg), ducks (DHBcAg), ground squirrels (GSHcAg) and woodchucks (WHcAg) at each step of core antigen purification. This reactivity was blocked by addition of excess synthetic peptide, and neither sera were reactive with other purified antigens such as HBsAg. Individual polypeptides associated with these core particles were also reactive by Western blotting. These findings suggest that X reactive determinants are present in the core particles of hepatitis B virus and related viruses, and that one or more core-associated polypeptides may have both X and core antigenic determinants. The possible significance of these observations upon the genetic organization and expression of the X gene is discussed.

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Core and E antigen synthesis in rodent cells transformed with hepatitis B virus DNA is associated with greater than genome length viral messenger RNAs

Cited by 84 publications

References 44 publications

Hepatitis B virus transcription in the infected liver.

Hepatitis B virus transcription in the infected liver.

Hepatocellular Carcinoma: Molecular Aspects in Hepatitis B

Products of the “x” gene in hepatitis B and related viruses

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