Overexpression of STAT-1 by adenoviral gene transfer does not inhibit hepatitis B virus replication
OBJECTIVES: Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral activity against HBV in vitro.
METHODS: To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus expressing human STAT-1 (Adv-STAT-1). We analysed whether the overexpression of STAT-1 inhibits the replication of duck HBV and human HBV in vitro using Western blot analysis, the immunofluorescence of viral proteins and quantification of HBV-DNA copies, respectively.
RESULTS: In the duck model of HBV infection the overexpression of STAT-1 neither inhibited an established infection nor prevented the establishment of duck HBV replication when administered simultaneously with Adv-STAT-1. These observations were confirmed in an in-vitro model of human HBV infection using the human hepatoma cell line HepG2.2.15, which continuously replicates HBV.
CONCLUSION: These data demonstrate that the over-expression of STAT-1 alone is not sufficient to strengthen the biological response of interferon as an antiviral agent.
Medienart: |
Artikel |
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Erscheinungsjahr: |
2006 |
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Erschienen: |
2006 |
Enthalten in: |
Zur Gesamtaufnahme - volume:18 |
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Enthalten in: |
European journal of gastroenterology & hepatology - 18(2006), 2 vom: 21. Feb., Seite 167-74 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Siebler, Jürgen [VerfasserIn] |
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Themen: |
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Anmerkungen: |
Date Completed 31.07.2006 Date Revised 07.09.2019 published: Print Citation Status MEDLINE |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM15993883X |
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100 | 1 | |a Siebler, Jürgen |e verfasserin |4 aut | |
245 | 1 | 0 | |a Overexpression of STAT-1 by adenoviral gene transfer does not inhibit hepatitis B virus replication |
264 | 1 | |c 2006 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
338 | |a Band |b nc |2 rdacarrier | ||
500 | |a Date Completed 31.07.2006 | ||
500 | |a Date Revised 07.09.2019 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a OBJECTIVES: Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral activity against HBV in vitro | ||
520 | |a METHODS: To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus expressing human STAT-1 (Adv-STAT-1). We analysed whether the overexpression of STAT-1 inhibits the replication of duck HBV and human HBV in vitro using Western blot analysis, the immunofluorescence of viral proteins and quantification of HBV-DNA copies, respectively | ||
520 | |a RESULTS: In the duck model of HBV infection the overexpression of STAT-1 neither inhibited an established infection nor prevented the establishment of duck HBV replication when administered simultaneously with Adv-STAT-1. These observations were confirmed in an in-vitro model of human HBV infection using the human hepatoma cell line HepG2.2.15, which continuously replicates HBV | ||
520 | |a CONCLUSION: These data demonstrate that the over-expression of STAT-1 alone is not sufficient to strengthen the biological response of interferon as an antiviral agent | ||
650 | 4 | |a Journal Article | |
650 | 7 | |a DNA, Viral |2 NLM | |
650 | 7 | |a STAT1 Transcription Factor |2 NLM | |
700 | 1 | |a Protzer, Ulrike |e verfasserin |4 aut | |
700 | 1 | |a Wirtz, Stefan |e verfasserin |4 aut | |
700 | 1 | |a Schuchmann, Marcus |e verfasserin |4 aut | |
700 | 1 | |a Höhler, Thomas |e verfasserin |4 aut | |
700 | 1 | |a Galle, Peter R |e verfasserin |4 aut | |
700 | 1 | |a Neurath, Markus F |e verfasserin |4 aut | |
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