Acute hepatitis B of genotype H resulting in persistent infection

Yamada, Noriko; Shigefuku, Ryuta; Sugiyama, Ryuichi; Kobayashi, Minoru; Ikeda, Hiroki; Takahashi, Hideaki; Okuse, Chiaki; Suzuki, Michihiro; Itoh, Fumio; Yotsuyanagi, Hiroshi; Yasuda, Kiyomi; Moriya, Kyoji; Koike, Kazuhiko; Wakita, Takaji; Kato, Takanobu

doi:10.3748/wjg.v20.i11.3044

Cited by 9 publications

(12 citation statements)

References 27 publications

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“…This reinforces that the spread to Asia may have probably occurred due to trips of HBV‐H infected people from North America to Asia. Interestingly there are reports of some Japanese patients positive for HBV‐H, who had no history of international travel abroad, 10 also suggesting the local spreading of the lineage HBV‐H II after its introduction in the country. Furthermore, HBV‐H was also already detected in other countries, such as Brazil 13 and Turkey, 14 in the last decades.…”

Section: Discussionmentioning

confidence: 99%

Evolutionary history of hepatitis B virus genotype H

Wolf

Pereira

Simon

et al. 2020

Journal of Medical Virology

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Hepatitis B virus genotype H (HBV‐H) molecular evolution was studied by comparing all published whole‐genome sequences. Bayesian coalescent analysis was performed to estimate phylogenetic relationships, time to the most recent common ancestor (tMRCA), and viral population dynamics along the time. Phylogenetic tree demonstrated two main clades or lineages: HBV‐H I (with sequences from Central and North America) and HBV‐H II (with sequences from North and South America, and Asia). HBV‐H II had more genome sequences (n = 26; 83.9%), including one specific subclade with all sequences outside of the Americas. Overall HBV‐H tMRCA dated back to 1933 (95% highest posterior density interval [HPD 95%]: 1875–1957) with a very probable origin in Mexico and posterior dissemination to other American and Asian countries. The temporal analysis demonstrated that HBV‐H I spread only in Mexico and the neighbor country of Nicaragua probably in the 1960s to the 1970s (1968; HPD 95%: 1908–1981), while HBV‐II disseminated to other American and Asian countries around one decade later (1977; HPD 95%: 1925–1985). The phylogeographic analysis reinforced the Mexican origin of this genotype. The whole HBV‐H population increased from the 1980s to the 2000s. In conclusion, HBV‐H has two main lineages with a common origin in Mexico approximately nine decades ago.

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Section: Discussionmentioning

confidence: 99%

Evolutionary history of hepatitis B virus genotype H

Wolf

Pereira

Simon

et al. 2020

Journal of Medical Virology

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“…1 using the QIAamp Blood Mini Kit (Qiagen K.K., Tokyo, Japan). The entire genome of HBV was amplified by PCR using primers as described 14. Amplified fragments were sequenced directly with an automated DNA sequencer (3500 Genetic Analyzer; Applied Biosystems, Foster City, CA).…”

Section: Methodsmentioning

confidence: 99%

Resistance mutations of hepatitis B virus in entecavir‐refractory patients

Yamada

Sugiyama

Nitta

et al. 2017

Hepatology Communications

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The emergence of resistance mutations in the reverse transcriptase gene of hepatitis B virus (HBV) is associated with treatment failure. Entecavir (ETV) is one of the most potent anti‐HBV reagents; it has a very low resistance rate and is used as the first‐line treatment for chronic hepatitis B. In this study, we isolated HBVs in 4 ETV‐refractory patients (2 with viral breakthrough, 1 with partial virological response, and 1 with flare‐up) and assessed ETV resistance using replication‐competent 1.38‐fold HBV genome‐length molecular clones. The full genome sequences of infected HBVs in ETV‐refractory patients were determined. The HBV molecular clones were generated with the patient‐derived sequences. After transfection of these molecular clones into HepG2 cells, viral replications and ETV susceptibilities were evaluated by measuring the amount of intracellular core‐particle‐associated HBV DNA using Southern blotting and real‐time polymerase chain reaction. Among these cases, ETV‐resistant variants were detected in 2 patients with viral breakthrough and responsible amino acid mutations in reverse transcriptase were successfully identified in these variants. No ETV‐resistant mutation was detected in the other cases. The identified ETV‐resistant mutations did not confer resistance to tenofovir disoproxil fumarate. Conclusion: The HBV replication model with patient‐derived sequences is useful for assessing replication efficiency, susceptibility to anti‐HBV reagents, and responsible resistance mutations and can aid in choosing the appropriate treatment strategy for treatment‐failure cases of chronic hepatitis B. (Hepatology Communications 2017;1:110‐121)

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“…Therefore, HBV has diverse genetic variability and is classified into at least eight genotypes: A to H. Some differences in clinical features and outcomes have been reported among these genotypes. ( 3‐8 ) HBV comprises four open reading frames (ORFs) coding for hepatitis B surface antigen (HBsAg), hepatitis B e (HBe) antigen/hepatitis B core (HBc) antigen (HBe/c), hepatitis B polymerase (HBp), and HBV X protein (HBx). HBsAg consists of three species: small (S‐), middle (M‐), and large (L‐) hepatitis B surface (HBs) proteins.…”

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confidence: 99%

N‐Terminal PreS1 Sequence Regulates Efficient Infection of Cell‐Culture–Generated Hepatitis B Virus

et al. 2020

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Background and Aims An efficient cell‐culture system for hepatitis B virus (HBV) is indispensable for research on viral characteristics and antiviral reagents. Currently, for the HBV infection assay in cell culture, viruses derived from HBV genome‐integrated cell lines of HepG2.2.15 or HepAD‐38 are commonly used. However, these viruses are not suitable for the evaluation of polymorphism‐dependent viral characteristics or resistant mutations against antiviral reagents. HBV obtained by the transient transfection of the ordinary HBV molecular clone has limited infection efficiencies in cell culture. Approach and Results We found that an 11‐amino‐acid deletion (d11) in the preS1 region enhances the infectivity of cell‐culture–generated HBV (HBVcc) to sodium taurocholate cotransporting polypeptide–transduced HepG2 (HepG2/NTCP) cells. Infection of HBVcc derived from a d11‐introduced genotype C strain (GTC‐d11) was ~10‐fold more efficient than infection of wild‐type GTC (GTC‐wt), and the number of infected cells was comparable between GTC‐d11‐ and HepG2.2.15‐derived viruses when inoculated with the same genome equivalents. A time‐dependent increase in pregenomic RNA and efficient synthesis of covalently closed circular DNA were detected after infection with the GTC‐d11 virus. The involvement of d11 in the HBV large surface protein in the enhanced infectivity was confirmed by an HBV reporter virus and hepatitis D virus infection system. The binding step of the GTC‐d11 virus onto the cell surface was responsible for this efficient infection. Conclusions This system provides a powerful tool for studying the infection and propagation of HBV in cell culture and also for developing the antiviral strategy against HBV infection.

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Acute hepatitis B of genotype H resulting in persistent infection

Cited by 9 publications

References 27 publications

Evolutionary history of hepatitis B virus genotype H

Evolutionary history of hepatitis B virus genotype H

Resistance mutations of hepatitis B virus in entecavir‐refractory patients

N‐Terminal PreS1 Sequence Regulates Efficient Infection of Cell‐Culture–Generated Hepatitis B Virus

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