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Mechanisms downstream of reverse transcription reduce serum levels of HBV DNA but not of HBsAg in chronic hepatitis B virus infection

Artikel i vetenskaplig tidskrift
Författare Simon B. Larsson
Sebastian Malmström
Charles Hannoun
Gunnar Norkrans
Magnus Lindh
Publicerad i Virology Journal
Volym 12
Sidor Article Number: 213
ISSN 1743-422X
Publiceringsår 2015
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor Article Number: 213
Språk en
Länkar dx.doi.org/10.1186/s12985-015-0447-...
Ämnesord HBV DNA, HBsAg, cccDNA, Replication, pgRNA, SURFACE-ANTIGEN LEVELS, NATURAL-HISTORY, ANTIVIRAL THERAPY, REPLICATION, PERSPECTIVE, CONVERSION, CLEARANCE, DISEASE, VIREMIA, CELLS, Virology
Ämneskategorier Virologi

Sammanfattning

Background: Hepatitis B virus (HBV) DNA in serum of chronically infected patients declines by 3-4 log(10) units at loss of HBe antigen (HBeAg) from serum. The mechanisms behind this decline, and the much smaller decline of surface antigen (HBsAg) levels, are still not well known. The aim of this study was to get a better understanding of this process by analysing both serum and intrahepatic markers of HBV replication. Methods: Levels of HBV DNA and HBsAg in serum, and covalently closed circular DNA (cccDNA), pregenomic RNA (pgRNA) and S-RNA and total intrahepatic HBV DNA (ihDNA) in liver biopsies from 84 chronically infected patients (16 positive and 68 negative for HBeAg) were analysed. Results: Lower HBV DNA levels within HBeAg-positive stage reflected lower levels of cccDNA and pgRNA with strong correlation. In HBeAg-negative patients, ihDNA levels were greater and HBV DNA levels in serum lower than expected from pgRNA levels. A lower HBV DNA/HBsAg ratio corresponded with lower pgRNA/cccDNA (p < 0.01) and higher S-RNA/cccDNA (p < 0.0001) ratios, suggesting that in HBeAg-negative patients transcription of pgRNA, but not of S-RNA, becomes suppressed. Conclusions: The marked reduction of HBV DNA in serum after loss of HBeAg appears to be due to combined reduction of cccDNA, pgRNA and yet unidentified mechanisms downstream of reverse transcription. Such mechanisms include faster clearance of circulating virus or blocked secretion of virions, the latter supported by the observed relative increase of ihDNA in HBeAg-negative patients. The smaller reduction of S-RNA than of pgRNA partly explains why HBsAg remain high in the HBeAg-negative stage, supporting the possibility of HBsAg synthesis from integrated HBV DNA.

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Denna text är utskriven från följande webbsida:
http://www.gu.se/forskning/publikation/?publicationId=229980
Utskriftsdatum: 2019-09-16