Co-Infection with Hepatitis B Virus Genotype D and Other Genotypes in Western Japan

Michitaka, Kojiro; Horiike, Norio; Yan, Chen‐Hua; Dương, Trần Như; Matsuura, Kazuaki; Terada, Yoshio; Hiasa, Yoichi; Akbar, Fazle; Onji, Morikazu

doi:10.1159/000084604

Cited by 5 publications

(4 citation statements)

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“…Infection with mixed genotypes are common in geographical regions where two or more than two genotypes cohabitates. Several studies from different parts of the world reported presence of mixed genotypes in their HBV infected population [Kato et al, ; Michitaka et al, ; Toan et al, ] including from Indian subcontinent [Arankalle et al, ; Chattopadhyay et al, ]. Probable consequences associated with mixed HBV genotypes are: (i) high viral replication rate; (ii) increased disease severity; and (iii) diagnostic challenges and it can also lead to recombinant HBV molecular forms [Tran et al, , ; Valsamakis, ; Yin et al, ; Andernach et al, ; Zhong et al, ].…”

Section: Introductionmentioning

confidence: 99%

Analysis of hepatitis B virus genotype changes in patients with chronic hepatitis B infection on tenofovir therapy

et al. 2016

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Antiviral therapy for chronic hepatitis B (CHB) is often required for prolonged periods. We investigated the instance of one HBV genotype switching to another during tenofovir therapy. Of the 67 patients, genotype A was present in 6 (8.9%), D in 43 (65.6%), C in 1 (1.5%), and mixed in 17 (23.8%) patients. Genotype changes were detected in 51 (76.1%) patients on therapy during a follow-up of 192 (range 52-312) weeks. Inter-genotype changes were seen in 17 (33.3%) and intra-genotype in 28 (55%) and both inter- and intra-genotype in 6 of 51 (11.7%) patients. The distribution of genotypes in patients achieving complete virological response was genotype D, 32/43 (74.4%); genotype A, 6/6 (100%); and mixed genotypes, 13/17 (76.47%). The cumulative time of genotype switch among genotype A was 12 months (range 6-18), in genotype D, 12 months (range 6-48), and mixed genotype, 18 months (range 6-24). The type of inter-genotype switch most frequently detected among genotype A1 was from A1 to D1 5/6 (83.3%), followed by mixed to genotype D3 7/13 (54%) and among intra-genotype changes, from D1 to D3 in 14/20 (70%). Pretreatment HBV genotype was the only factor predicting inter-genotype switches with genotype A or mixed genotypes more likely to undergo inter-genotype switches as compared to genotype D patients (OR 66.6 [13.6-327.0, P < 0.001]). Compared to genotype D, genotype A, and mixed genotypes are more inclined to switch while on tenofovir therapy. Genotypes tend to switch and select to a particular type possibly due to constant antiviral drug pressure. J. Med. Virol. 88:1364-1375, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Introductionmentioning

confidence: 99%

Analysis of hepatitis B virus genotype changes in patients with chronic hepatitis B infection on tenofovir therapy

et al. 2016

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“…Many clinical and biological characteristics including transmission, seroconversion and frequency of mutations are completely dependant on HBV genotype (Table 1 ). These different genotypes generally have restricted geographic distributions, with HBV genotype A is found in North America and Africa, genotype B and C are dominant in Asia, and genotype D present in Mediterranean countries and Europe [6-9] as well as some districts in western Japan [10]. Numerous subgenotypes that differ in nucleotide sequence by 4-8% have also been identified, and in some cases these too have a geographical limited distribution.…”

Section: Introductionmentioning

confidence: 99%

Effects of Hepatitis B Virus Mutations on its Replication and Liver Disease Severity

Hakami¹,

Ali²,

Khalid³

2013

TOVJ

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Hepatitis B virus (HBV), nowadays, is one of the major human pathogens worldwide. Approximately, 400 million people worldwide have chronic HBV infection. Only 5% of persons infected during adulthood develop chronic infection. The reverse is true for those infected at birth or in early childhood, i.e. more than 90% of these persons progress to chronic infection. Currently, eight different genotypes o f HBV have been identified, differing in nucleotide sequence by greater than 8%. In addition, numerous subgenotypes have a l s o been recognized based on the nucleotide sequence variability of 4- 8%. It has invariably been found that these genotypes and mutations play a pivotal role in the liver disease aggravation and virus replication. The precore mutations (G1896A) and the double mutation (T1762/A1764) in the basal core promoter are important mutations that alter expression of the hepatitis B e antigen (HBeAg). The HBeAg is important for establishing viral persistence. The precore G1896A mutation abrogates the expression of HBeAg. Numerous other mutations alter the disease severity and progression. It is predictive that the infected patient has high risk of hepatocellular carcinoma if the genotype C is incriminated or if HBV possesses basal core promoter double mutation. Association of the remaining genotypes have been noted but with less degree than genotype C. Phenotypic assays of the different HBV protein markers with different molecular techniques illustrate the replication efficiency of the virus in cell lines. This review will discuss various mutations into their association with liver disease severity and progression as well as virus replication.

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“…Superinfection denotes an infection with a second strain that occurs after the initial infection and after its immune response (Smith et al, 2005). Despite several studies on the natural progression of dual infections, their clinical implications are largely unknown (Hannoun et al, 2002;Kao et al, 2001;Michitaka et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Genotyping hepatitis B virus dual infections using population-based sequence data

Beggel

Neumann-Fraune

Döring

et al. 2012

Journal of General Virology

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The hepatitis B virus (HBV) is classified into distinct genotypes A-H that are characterized by different progression of hepatitis B and sensitivity to interferon treatment. Previous computational genotyping methods are not robust enough regarding HBV dual infections with different genotypes. The correct classification of HBV sequences into the present genotypes is impaired due to multiple ambiguous sequence positions. We present a computational model that is able to identify and genotype inter-and intragenotype dual infections using population-based sequencing data. Model verification on synthetic data showed 100 % accuracy for intergenotype dual infections and 36.4 % sensitivity in intragenotype dual infections. Screening patient sera (n5241) revealed eight putative cases of intergenotype dual infection (one A-D, six A-G and one D-G) and four putative cases of intragenotype dual infection (one A-A, two D-D and one E-E). Clonal experiments from the original patient material confirmed three out of three of our predictions. The method has been integrated into geno2pheno [hbv] , an established web-service in clinical use for analysing HBV sequence data. It offers exact and detailed identification of HBV genotypes in patients with dual infections that helps to optimize antiviral therapy regimens. geno2pheno [hbv] is available under http://www.genafor.org/g2p_hbv/index.php. INTRODUCTIONWorldwide an approximate number of 350 million people are chronically infected with the hepatitis B virus (HBV) with mortality rates of about 600 000 per year. The 3.2 kilobase genome has been classified into eight well characterized genotypes A-H based on a nucleotide variation threshold of 8 % over the entire genome (Arauz-Ruiz et al., 2002;Naumann et al., 1993;Norder et al., 1994Norder et al., , 2004Okamoto et al., 1988;Stuyver et al., 2000). Several authors suggested two additional putative genotypes, namely I (Olinger et al., 2008;Huy et al., 2008;Thuy et al., 2010) and J (Tatematsu et al., 2009). HBV genotypes have been found to influence the rate of chronicity (Ogawa et al., 2002;Suzuki et al., 2005;Zhang et al., 2008), the course of the disease (Chan et al., 2004;Kao et al., 2000a;Livingston et al., 2007; Sánchez-Tapias et al., 2002;Thakur et al., 2002;Yuen et al., 2004) and the response to interferon treatment. Genotypes A and B show a significantly better response to interferon compared with genotypes D and C, respectively (Janssen et al., 2005;Kao et al., 2000b;Wai et al., 2002). Therefore, the German guidelines for the management of HBV infection recommend genotyping before therapy (Cornberg et al., 2008). Nevertheless, treatment with nucleos(t)ide analogues does not appear to be strongly influenced by genotype (Raimondi et al., 2010;Wiegand et al., 2008) and thus the major international guidelines do not recommend the determination of the HBV genotype before the start of treatment (European Association For The Study Of The Liver, 2012;Liaw et al., 2008;Lok & McMahon, 2009). Several methods have been developed for the de...

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Co-Infection with Hepatitis B Virus Genotype D and Other Genotypes in Western Japan

Cited by 5 publications

References 71 publications

Analysis of hepatitis B virus genotype changes in patients with chronic hepatitis B infection on tenofovir therapy

Analysis of hepatitis B virus genotype changes in patients with chronic hepatitis B infection on tenofovir therapy

Effects of Hepatitis B Virus Mutations on its Replication and Liver Disease Severity

Genotyping hepatitis B virus dual infections using population-based sequence data

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