scholarly journals The Prevalence and Replication Capacity of a Tibetan Dominant HBV Strain, C/D Recombinant

2017 ◽  
Vol 2017 ◽  
pp. 1-10
Author(s):  
Lingyao Du ◽  
Menghan Liu ◽  
Miao Liu ◽  
Taoyou Zhou ◽  
Xing Cheng ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Sichuan Province ◽  
Replication Capacity ◽  
Viral Strain ◽  
Serum Samples ◽  
B Virus ◽  
Genotype C ◽  
Replication Intermediates ◽  
Recombinant Genome

This study aimed to estimate the distribution of hepatitis B virus (HBV) C/D recombinant in Han and Tibet patients with chronic hepatitis B (CHB) and then learn such strain’s replication capacity in vivo. A total of 331 serum samples were collected from Han outpatients from Sichuan Province and Tibetan outpatients from Tibet. Viral genotypes in these samples were identified. An HBV replicative plasmid of C/D recombinant was constructed with selected genome. Sequentially, HBV replicative mouse models were established and the replication capacity of the viral strain was studied in vivo. In the 314 Han patients, 66% (207) were infected by genotype B strain while 31% (96) were by genotype C strain. Only 1% (3) were by C/D recombinant. In the 17 Tibetan patients, 41% (7) were by genotype D and 35% (6) by C/D recombinant. A plasmid with 1.3 copies of C/D recombinant genome was constructed. And its replication intermediates were found at similar levels to that of genotype D strain. Thus, C/D recombinant, the dominant viral strain in Tibet, was rather rare in the genotype B predominated Han patients from Sichuan Province. And the C/D recombinant replicated at a similar level to viral strain of genotype D in vivo.

Duck hepatitis B virus polymerase gene mutants associated with resistance to lamivudine have a decreased replication capacity in vitro and in vivo

2001 ◽  
Vol 34 (1) ◽  
pp. 114-122 ◽  
Author(s):  
Béatrice Seignères ◽  
Stéphanie Aguesse-Germon ◽  
Christian Pichoud ◽  
Isabelle Vuillermoz ◽  
Catherine Jamard ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Replication Capacity ◽  
Polymerase Gene ◽  
Duck Hepatitis B Virus ◽  
Duck Hepatitis ◽  
B Virus

scholarly journals Hepatocyte Nuclear Factor 3β Inhibits Hepatitis B Virus Replication In Vivo

2002 ◽  
Vol 76 (24) ◽  
pp. 12974-12980 ◽  
Author(s):  
Krista E. Banks ◽  
Aimee L. Anderson ◽  
Hong Tang ◽  
Douglas E. Hughes ◽  
Robert H. Costa ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Transgenic Mice ◽  
Transgenic Mouse ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
B Virus ◽  
Chronic Hbv ◽  
Replication Intermediates

ABSTRACT Hepatitis B virus (HBV) transgenic mice expressing rat hepatocyte nuclear factor 3β (HNF3β) were generated by breeding HBV transgenic mice with transgenic mice that constitutively overexpress the rat HNF3β polypeptide in the liver. HBV 3.5-, 2.4- and 2.1-kb transcripts were reduced 2- to 4-fold in these mice relative to the HBV transgenic mouse controls. In contrast, the abundance of viral replication intermediates was profoundly reduced in HBV transgenic mice by overexpression of HNF3β. This results, in part, from the preferential reduction in the level of the pregenomic 3.5-kb RNA relative to the precore 3.5-kb RNA. Therefore, it is apparent that increased expression of HNF3β modestly reduces viral transcription and dramatically inhibits replication in vivo in the HBV transgenic mouse. This suggests that altering the activity of this transcription factor in vivo in chronic HBV carriers might be therapeutically beneficial.

scholarly journals Nuclear Covalently Closed Circular Viral Genomic DNA in the Liver of Hepatocyte Nuclear Factor 1α-Null Hepatitis B Virus Transgenic Mice

2001 ◽  
Vol 75 (6) ◽  
pp. 2900-2911 ◽  
Author(s):  
Anneke K. Raney ◽  
Carrie M. Eggers ◽  
Eric F. Kline ◽  
Luca G. Guidotti ◽  
Marco Pontoglio ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Transgenic Mice ◽  
Genomic Dna ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
B Virus ◽  
Hepatocyte Nuclear Factor 1Α ◽  
Replication Intermediates

ABSTRACT The role of hepatocyte nuclear factor 1α (HNF1α) in the regulation of hepatitis B virus (HBV) transcription and replication in vivo was investigated using a HNF1α-null HBV transgenic mouse model. HBV transcription was not measurably affected by the absence of the HNF1α transcription factor. However, intracellular viral replication intermediates were increased two- to fourfold in mice lacking functional HNF1α protein. The increase in encapsidated cytoplasmic replication intermediates in HNF1α-null HBV transgenic mice was associated with the appearance of nonencapsidated nuclear covalently closed circular (CCC) viral genomic DNA. Viral CCC DNA was not readily detected in HNF1α-expressing HBV transgenic mice. This indicates the synthesis of nuclear HBV CCC DNA, the proposed viral transcriptional template found in natural infection, is regulated either by subtle alterations in the levels of viral transcripts or by changes in the physiological state of the hepatocyte in this in vivo model of HBV replication.

In vitro and in vivo replication capacity of the precore region defective hepatitis B virus variants

1991 ◽  
Vol 13 ◽  
pp. S68-S73 ◽  
Author(s):  
S.P. Tong ◽  
B. Brotman ◽  
J.S. Li ◽  
L. Vitvitski ◽  
D. Pascal ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Replication Capacity ◽  
Precore Region ◽  
B Virus

scholarly journals In Vivo Regulation of Hepatitis B Virus Replication by Peroxisome Proliferators

1999 ◽  
Vol 73 (12) ◽  
pp. 10377-10386 ◽  
Author(s):  
Luca G. Guidotti ◽  
Carrie M. Eggers ◽  
Anneke K. Raney ◽  
Susan Y. Chi ◽  
Jeffrey M. Peters ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Transgenic Mice ◽  
Fold Increase ◽  
Nuclear Hormone Receptor ◽  
Peroxisome Proliferators ◽  
B Virus ◽  
Replication Intermediates ◽  
Transcription And Replication

ABSTRACT The role of the peroxisome proliferator-activated receptor α (PPARα) in regulating hepatitis B virus (HBV) transcription and replication in vivo was investigated in an HBV transgenic mouse model. Treatment of HBV transgenic mice with the peroxisome proliferators Wy-14,643 and clofibric acid resulted in a less than twofold increase in HBV transcription rates and steady-state levels of HBV RNAs in the livers of these mice. In male mice, this increase in transcription was associated with a 2- to 3-fold increase in replication intermediates, whereas in female mice it was associated with a 7- to 14-fold increase in replication intermediates. The observed increases in transcription and replication were dependent on PPARα. HBV transgenic mice lacking this nuclear hormone receptor showed similar levels of HBV transcripts and replication intermediates as untreated HBV transgenic mice expressing PPARα but failed to demonstrate alterations in either RNA or DNA synthesis in response to peroxisome proliferators. Therefore, it appears that very modest alterations in transcription can, under certain circumstances, result in relatively large increases in HBV replication in HBV transgenic mice.

scholarly journals Limited Effects of Fasting on Hepatitis B Virus (HBV) Biosynthesis in HBV Transgenic Mice

2008 ◽  
Vol 83 (4) ◽  
pp. 1682-1688 ◽  
Author(s):  
Lie Li ◽  
Claudia E. Oropeza ◽  
Klaus H. Kaestner ◽  
Alan McLachlan
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Nuclear Receptors ◽  
Natural Infection ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
B Virus ◽  
Hepatocyte Nuclear Factor 4Α ◽  
Replication Intermediates

ABSTRACT Nuclear receptors have a unique role in governing hepatitis B virus (HBV) transcription and replication. Hepatocyte nuclear factor 4α (HNF4α) and retinoid X receptor α (RXRα) plus peroxisome proliferator-activated receptor α (PPARα) have been shown to support viral biosynthesis in nonhepatoma cells in the absence of additional liver-enriched transcription factors. However, the in vivo importance of these nuclear receptors in HBV biosynthesis has been investigated only to a limited extent. Fasting has been shown to activate gluconeogenesis, in part, by activating PPARγ coactivator 1 α, which in turn leads to activation of HNF4α- and RXRα/PPARα-mediated transcription. As HBV pregenomic RNA synthesis is primarily believed to be regulated by HNF4α under normal physiological conditions, it was of interest to determine the effect of fasting on the levels of HBV RNA and DNA synthesis. Fasting was shown to rather modestly increase the levels of viral proteins, transcripts, and replication intermediates in the HBV transgenic mouse model of chronic viral infection, suggesting that caloric restriction may modulate viremia to some extent during natural infection.

Inhibition of hepatitis B virus replication in vivo by nucleoside analogues and siRNA

2015 ◽  
Vol 41 (08) ◽  
Author(s):  
C Klein ◽  
CT Bock ◽  
H Wedemeyer ◽  
T Wüstefeld ◽  
S Locarnini ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Virus Replication ◽  
Nucleoside Analogues ◽  
B Virus

A STUDY OF HEPATITIS B VIRUS GENOTYPES IN CHRONIC HEPATITIS B PATIENTS

2011 ◽  
pp. 25-29
Author(s):  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Clinical Laboratory ◽  
Laboratory Data ◽  
Hbv Dna ◽  
Hbv Genotypes ◽  
B Virus ◽  
Virus Genotypes ◽  
Genotype C

Aims: To measure the prevalence of HBV genotypes in chronic hepatitis B patients and their relation to HBeAg and HBV DNA level. Methods: 81 patients were enrolled in this study from January 2009 to December 2010. Clinical, laboratory data were collected during the patient’s hospitalization. Sera were quantitatively tested for HBeAg and HBV DNA. HBV genotyping was made by real-time PCR. Results: Among the 81 patients, 60.5% had genotype B, 26.7% had genotype C and 8.6% had mixed genotype B-C. Prevalence of symptoms (fatigue, anorexia, insomnia...) was higher in genotype C than in genotype B. Genotype C patients had positivity higher HBeAg than genotype B patients (56% vs. 38,8%, p <0.05). The rate of HBV DNA > 107 copies/mL was higher in genotype C group than in genotype B group (36% vs. 28,6%, p > 0.05). Conclusions: Most of the patients had genotypes B or C. Patients with genotype C had positive HBeAg and may be related to higher serological HBV DNA level than in genotype B.

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