Hepatitis B virus precore mutants in serum and liver of Southern African Blacks with hepatocellular carcinoma

Kramvis, Anna; Kew, Michael C.; Bukofzer, Stan

doi:10.1016/s0168-8278(98)80212-2

Cited by 73 publications

(71 citation statements)

References 41 publications

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“…30,31 However, we observe this mutation in genotype D. So, our observation is not in accordance with the observation of Kramvis et al 30 and Kimbi et al 31 1888 A mutation has a stabilizing effect on encapsidation signal 30 and it also possibly affects reverse …”

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confidence: 70%

Prevalence of Genotype D and Precore/Core Promoter Mutations in Hepatitis B Virus-infected Population of North India

Kumar¹,

Pahal²,

Singh³

2011

Journal of Clinical and Experimental Hepatology

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Hepatitis B virus (HBV) isolates (21) from Punjab (North India) were studied for genotype distribution and precore/core promoter mutations. Assays of alanine aminotransaminase (ALT) and HBeAg were performed in all isolates. Genotypes were determined in all the samples by restriction fragment length polymorphism and the precore/core promoter mutations were studied by amplification and by direct sequencing of precore/core promoter region. Sixty-two percent of the isolates had higher ALT levels and 57% of the isolates were HBeAg negative. It was observed that 90% of the isolates were HBV D genotype (subgenotype D1 and D2) and 10% of the isolates were HBV A genotype (subgenotype A1). Amplification and sequencing of the precore/core promoter region showed

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confidence: 70%

Prevalence of Genotype D and Precore/Core Promoter Mutations in Hepatitis B Virus-infected Population of North India

Kumar¹,

Pahal²,

Singh³

2011

Journal of Clinical and Experimental Hepatology

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“…The precore region in Southern African isolates of HBV, studied previously in the same sera, 8,9 showed significantly less nucleotide and amino acid divergence than did the BCP. This was true in both ASCs and patients with HCC.…”

Section: Discussionmentioning

confidence: 64%

High Prevalence of 1762T 1764A Mutations in the Basic Core Promoter of Hepatitis B Virus Isolated From Black Africans With Hepatocellular Carcinoma Compared With Asymptomatic Carriers

1999

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The purpose of this study was to identify mutations in the basic core promoter and enhancer II region of the hepatitis B virus (HBV) that might cause the HBV e antigen (HBeAg)-negative phenotype and contribute to hepatocarcinogenesis in black African carriers of the virus. The basic core promoter/enhancer II overlaps with the X gene. HBV DNA from serum of 47 asymptomatic carriers and 50 patients with hepatocellular carcinoma and from 28 tumor and 10 nontumor liver tissues was amplified and sequenced directly. That part of the enhancer II region not overlapping the basic core promoter was completely conserved in all samples. Missense mutations at nucleotides 1809 and 1812 in the basic core promoter were found in 80% of all sequences and may represent wild-type sequence in Southern African isolates. Nucleotide and amino acid divergences were higher in the basic core promoter of hepatocellular carcinoma patients when compared with asymptomatic carriers (P F .0001). This applied particularly to the paired 1762 adenine to thymine (1762 T ) and 1764 guanine to adenine (1764 A ) missense mutations, the prevalence of which was 66% in patients with hepatocellular carcinoma compared with 11% in asymptomatic carriers (P F .0001). Black Africans who are symptomless carriers of the hepatitis B virus (HBV) usually seroconvert from HBV e antigen (HBeAg) positivity to negativity after a relatively short time. 1 The carrier state is established in the first few years of life, 2 and by early adulthood between 1% and 14% only of black carriers remain HBeAg positive compared with 40% or more among ethnic Chinese, another population in which the virus is endemic. 1-4 Why black African carriers seroconvert earlier is not known. Nucleotide sequencing of the precore region of HBV isolates from a number of countries has shown the 1896 stop codon mutation to be a frequent cause of the HBeAgnegative phenotype, 5,6 with other nonsense or frame-shift mutations accounting for a small proportion (reviewed in Miyakawa et al. 7 ). However, these mutations are seldom present in black African carriers in Southern Africa 8,9 and our focus has shifted to the X open reading frame.The X open reading frame encodes the X protein that has transactivating activity (reviewed in Koike and Takada 10 ) and contains the basic core promoter (BCP)/enhancer II complex. The BCP, mapping between nucleotides 1742 and 1849, controls the transcription of both precore messenger RNA (mRNA), which codes for the protein that is the precursor of the e antigen, and pregenomic RNA (pgRNA), which controls HBV replication. 11 A pair of mutations in the BCP that is associated with a reduced level of HBeAg expression was first described in Japanese patients [12][13][14] : an adenine (A) to thymine (T) transversion at position 1762 together with a guanine (G) to A transition at 1764 in the second AT-rich region of the BCP are often present in patients with chronic hepatitis B [15][16][17][18][19][20] and fulminant hepatitis B, [14][15][16][21][22][23] and less often in asymptoma...

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“…Concentrated [5] 0 -Biotin-TCA GGG CCT CAC CAC CTA CTT CAT CCA CGT TCA CTC AGG GCC TCA CCA CCT [3] 0 and 23mer - [5] 0 -Biotin-GTA CGG CTG TCA TCA CTT AGA CC [3] 0 DNA oligonucleotides and derivatization of the 40 nm NeutrAvidin nanoparticles were described in reference [27]. For the 40 nm DNA derivatized nanoparticle and 200 nm nanoparticle experiments, 0.5 mL of the stock solution was added to 299 mL of the appropriate buffer.…”

Section: Buffers and Conductivity Measurementsmentioning

confidence: 99%

“…The separation and detection of low numbers of bacteria and virus; drug delivery nanoparticles, high molecular weight (hmw) DNA biomarkers, antibodies and other entities from blood and other complex biological samples remains a significant challenge [1][2][3][4][5][6]. For many research and clinical applications, sample preparation is used to enrich a specific analyte before detection is carried out.…”

Section: Introductionmentioning

confidence: 99%

An AC electrokinetic method for enhanced detection of DNA nanoparticles

Krishnan

Heller

2009

Journal of Biophotonics

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Journal of BIOPHOTONICSIn biomedical research and diagnostics it is a challenge to isolate and detect low levels of nanoparticles and nanoscale biomarkers in blood and other biological samples. While highly sensitive epifluorescent microscope systems are available for ultra low level detection, the isolation of the specific entities from large sample volumes is often the bigger limitation. AC electrokinetic techniques like dielectrophoresis (DEP) offer an attractive mechanism for specifically concentrating nanoparticles into microscopic locations. Unfortunately, DEP requires significant sample dilution thus making the technology unsuitable for biological applications. Using a microelectrode array device, special conditions have been found for the separation of hmw-DNA and nanoparticles under high conductance (ionic strength) conditions. At AC frequencies in the 3000-10 000 Hz range, 10 mm microspheres and human T lymphocytes can be isolated into the DEP low field regions, while hmw-DNA and nanoparticles can be concentrated into microscopic high field regions for subsequent detection using an epifluorescent system.Final separation and detection of 150 ng/mL OliGreen fluorescent stained high molecular weight (hmw) DNA in 1 Â TBE buffer (109 mS/m). The DEP field was applied at 10 000 Hz and 10 volts pk-pk for 5 minutes to group of nine microelectrodes. The green fluorescent image (Ex 505 nm, Em 520 nm) shows fluorescence from the OliGreen stained hmw DNA concentrated on the 80-micron diameter microelectrodes with the far right column of unactivated microelectrodes showing no concentration of hmw-DNA.

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Hepatitis B virus precore mutants in serum and liver of Southern African Blacks with hepatocellular carcinoma

Cited by 73 publications

References 41 publications

Prevalence of Genotype D and Precore/Core Promoter Mutations in Hepatitis B Virus-infected Population of North India

Prevalence of Genotype D and Precore/Core Promoter Mutations in Hepatitis B Virus-infected Population of North India

High Prevalence of 1762T 1764A Mutations in the Basic Core Promoter of Hepatitis B Virus Isolated From Black Africans With Hepatocellular Carcinoma Compared With Asymptomatic Carriers

An AC electrokinetic method for enhanced detection of DNA nanoparticles

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