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

Kumar, Rajesh; Pahal, Vikas; Singh, Jasbir

doi:10.1016/s0973-6883(11)60125-4

Cited by 5 publications

(7 citation statements)

References 32 publications

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“…Hepatitis B virus genotypes were determined by phylogenetic analysis of a 377 bp fragment of the HBV S gene as described previously . HDV genotypes were determined by phylogenetic analysis of the R0 region (400 bp) of the genome as described previously .…”

Section: Methodsmentioning

confidence: 99%

“…Hepatitis B virus genotypes were determined by phylogenetic analysis of a 377 bp fragment of the HBV S gene as described previously. 32 HDV genotypes were determined by phylogenetic analysis of the R0 region (400 bp) of the genome as described previously. 33 The ultra sensitive RT-PCR amplification of this region covering the 19 specific amino acids of the large delta protein discriminates between all eight known HDV genotypes.…”

Section: Hbv and Hdv Genotypingmentioning

confidence: 99%

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High prevalence and diversity of hepatitis B and hepatitis delta virus in Gabon

Groc

Abbate

Gal

et al. 2018

Journal of Viral Hepatitis

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Although central Africa is classified as having a high endemicity of hepatitis B virus (HBV) and hepatitis D virus (HDV) infection, there is paucity of prevalence studies. For the first time on a country-wide level in Central Africa, we show in Gabon an overall 7.4% prevalence of Hepatitis B surface antigen (HBsAg) and that more than 25% of the HBsAg-positive population are infected by HDV. Although HBV prevalence did not differ significantly between provinces, there is a north-south split in the distribution of HDV seroprevalence, with the highest rates (>66.0%) correlating with the presence of specific ethnic groups in the northeastern provinces. Genotyping revealed high genetic diversity of the HBV and HDV strains circulating in Gabon, including many restricted to this region of the globe. This work confirmed that high exposure to HBV and HDV infection reported in selected regions of Gabon holds true across the whole country.

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Section: Methodsmentioning

confidence: 99%

Section: Hbv and Hdv Genotypingmentioning

confidence: 99%

High prevalence and diversity of hepatitis B and hepatitis delta virus in Gabon

Groc

Abbate

Gal

et al. 2018

Journal of Viral Hepatitis

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“…The fragment was obtained by PCR and nested PCR using Taq DNA Core kit 25 (MP Biomedicals, France) and primers PS1F (5′-TCACAATACCGCAGAGTCT-3′) and PS1R (5′-AACAGCGGTATAAAGGGACT-3′) for the first round and PS2F (5′-GTGGTGGACTTCTCTCAATTTTC-3′) and PS2R (5′-CGGTATAAAGGGACTCACGAT-3′) for the second round of PCR. Amplifications were performed using the same conditions as described elsewhere ( 54 ). PCR products were sequenced bidirectionally using BigDye terminator technology.…”

Section: Methodsmentioning

confidence: 99%

High Prevalence and Diversity of Hepatitis Viruses in Suspected Cases of Yellow Fever in the Democratic Republic of Congo

et al. 2017

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The majority of patients with acute febrile jaundice (>95%) identified through a yellow fever surveillance program in the Democratic Republic of Congo (DRC) test negative for antibodies against yellow fever virus. However, no etiological investigation has ever been carried out on these patients. Here, we tested for hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV) viruses, all of which can cause acute febrile jaundice, in patients included in the yellow fever surveillance program in the DRC. On a total of 498 serum samples collected from suspected cases of yellow fever from January 2003 to January 2012, enzyme-linked immunosorbent assay (ELISA) techniques were used to screen for antibodies against HAV (IgM) and HEV (IgM) and for antigens and antibodies against HBV (HBsAg and anti-hepatitis B core protein [HBc] IgM, respectively), HCV, and HDV. Viral loads and genotypes were determined for HBV and HVD. Viral hepatitis serological markers were diagnosed in 218 (43.7%) patients. The seroprevalences were 16.7% for HAV, 24.6% for HBV, 2.3% for HCV, and 10.4% for HEV, and 26.1% of HBV-positive patients were also infected with HDV. Median viral loads were 4.19 × 105 IU/ml for HBV (range, 769 to 9.82 × 109 IU/ml) and 1.4 × 106 IU/ml for HDV (range, 3.1 × 102 to 2.9 × 108 IU/ml). Genotypes A, E, and D of HBV and genotype 1 of HDV were detected. These high hepatitis prevalence rates highlight the necessity to include screening for hepatitis viruses in the yellow fever surveillance program in the DRC.

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“…Xie et al [ 74 ] observed five different mutations in the preC/C region (1915, 2134, 2221, 2245 and 2288) and these mutations act as independent predictors of HCC survival. Various newly reported preC/C promoter mutations (1690A, 1695A/T/G, 1700A/C, 1703C, 1850A and 1915A/G) were observed in HBV-infected isolates of Punjab state (North India)[ 75 ].…”

Section: Hbv Precore Mutations and Relatedness With Genotype And Adva...mentioning

confidence: 99%

Review on hepatitis B virus precore/core promoter mutations and their correlation with genotypes and liver disease severity

Kumar¹

2022

WJH

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Of 350 million people worldwide are chronically infected with hepatitis B virus (HBV) and are at risk of developing cirrhosis and hepatocellular carcinoma (HCC) later in life. HBV is the most diverse DNA virus, and its genome is composed of four open reading frames: Presurface antigen/surface antigen gene (preS/S), precore/core gene (preC/C), polymerase gene (P), and the X gene (X). HBV produces quasispecies naturally or in response to antiviral agents because of the absence of proofreading activity amid reverse transcription and a high replication rate. The virus has 10 genotypes (A to J) with different geographical distributions. There are various HBV mutations in the HBV genome, including preC/C mutations, preS/S mutations, P gene mutations, and X gene mutations. The core promoter region plays a vital part in the replication, morphogenesis and pathogenesis of the virus. The precore region also plays a crucial role in viral replication. Both core promoter and precore mutations rescue the virus from host immune surveillance and result in the formation of mutated strains that may have altered pathogenicity. preC/C mutations are associated with liver disease progression. Precore mutations stop hepatitis B e antigen (HBeAg) production and basal core promoter mutations downregulate HBeAg production. Mutations in the basal core promoter are also associated with increased HBV replication and an increased incidence of advanced liver diseases such as cirrhosis and HCC. The emergence of antiviral-resistant mutations is the main reason for treatment failure. This review focuses mainly on preC/C promoter mutations and their correlation with genotypes and liver disease severity. Thorough perception and knowledge of HBV genetic variety and mutants could be vital to discover techniques for the prognosis and control of HBV infection.

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

Cited by 5 publications

References 32 publications

High prevalence and diversity of hepatitis B and hepatitis delta virus in Gabon

High prevalence and diversity of hepatitis B and hepatitis delta virus in Gabon

High Prevalence and Diversity of Hepatitis Viruses in Suspected Cases of Yellow Fever in the Democratic Republic of Congo

Review on hepatitis B virus precore/core promoter mutations and their correlation with genotypes and liver disease severity

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