Analysis of fitness differences of hepatitis B virus genotypes D and F using a cotransfection assay

Sevic, Ina; Elizalde, Mercedes; Ledesma, María Mora González López; Flichman, Diego Martín; Campos, Rodolfo Héctor

doi:10.1007/s00705-018-4090-5

Cited by 4 publications

(3 citation statements)

References 18 publications

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“…These subgenotypes, native from Latin America, present epidemiological as well as biological differences. It has been reported that sgtF1b possess a higher replication capacity and a major fitness compared to sgtF4 [20,21]. In addition, sgtF1b, the most prevalent in acute and HBeAg positive chronic infections in Argentina, has a delayed HBeAg seroconversion in comparison with genotypes/subgenotype A, F4 and D and, most importantly, it has been associated with a more severe course of chronic infection and HCC progression [18,19,22,24].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown differences at the molecular and clinical level between these two sgts. In transfection and co-transfection assays, sgtF1b showed a higher replication capacity and a major fitness compared to sgtF4 [20,21]. In addition, individuals infected with sgtF1b seroconvert to anti-HBe later in life than those infected with sgtF4 [18].…”

Section: Introductionmentioning

confidence: 99%

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Hepatitis B Virus X Gene Differentially Modulates Subgenotype F1b and F4 Replication

Elizalde

Speroni

Campos

et al. 2019

Viruses

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Hepatitis B virus (HBV) is classified into ten genotypes and numerous subgenotypes (sgt). In particular, sgt F1b and sgt F4, native of Latin America, have been associated with differences in clinical and virological characteristics. Hepatitis B virus X protein (HBx) is a multifunctional regulatory protein associated with the modulation of viral transcription and replication. In this work, we analyzed the role of the X gene and the encoded X protein in sgtF1b and sgtF4 replication. Transfection with HBx deficient genomes revealed remarkable differences in the replicative capacity of sgtF1b and sgtF4 mutants. The silencing of HBx increased sgtF1b X(-) transcription and replication by more than 2.5 fold compared to the wild type variant, while it decreased sgtF4 X(-) transcription and replication by more than 3 fold. Trans-complementation of HBx restore sgtF1b and sgtF4 wild type transcription and replication levels. In addition, transfection with chimeric variants, carrying wild type (F1b/XF4 and F4/XF1b) or mutated (F1b/X(-)F4 and F4/X(-)F1b) X gene of one sgt in the backbone of the other sgt, showed that the nucleotide sequence of the X gene, that includes regulatory elements that modulate pgRNA transcription, was responsible for the disparity observed between sgtF1b X(-) and sgtF4 X(-). These results showed that sgtF1b and sgtF4 X gene play a central role in regulating HBV transcription and replication, which eventually lead to a common purpose, to reach wild type replication levels of sgtF1b and sgtF4 viruses.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus X Gene Differentially Modulates Subgenotype F1b and F4 Replication

Elizalde

Speroni

Campos

et al. 2019

Viruses

Self Cite

View full text Add to dashboard Cite

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“…The viral genome has four overlapping open reading frames encoding the HBV core protein (HBc), the envelope protein, viral polymerase, reverse transcriptase, and regulatory HBX which is regarded as an oncoprotein. Studies have shown that HBeAg status is an indicator of viral replication fitness and disease prognosis 3 , and HBV-DNA levels have a predictive value for estimating hepatocellular carcinoma (HCC) risk and disease prognosis 4 . HBV is characterized by a narrow host range.…”

Section: Introductionmentioning

confidence: 99%

HBV promotes its replication by up-regulating RAD51C gene expression

Peng,

Ma,

et al. 2024

Sci Rep

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Chronic hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC), pegylated-interferon-α(PEG-IFNα) and long-term nucleos(t)ide analogs (NUCs) are mainly drugs used to treat HBV infection, but the effectiveness is unsatisfactory in different populations, the exploration of novel therapeutic approaches is necessary. RAD51C is associated with DNA damage repair and plays an important role in the development and progression of tumors. Early cDNA microarray results showed that RAD51C expression was significantly increased in HBV-infected HCC cells, however, the relationship between HBV infection and abnormal expression of RAD51C has not been reported. Therefore, we conducted RT-PCR, western blot, Co-immunoprecipitation(Co-IP), and immunofluorescence(IF) to detect HBV-RAD51C interaction in RAD51C overexpression or interfering HCC cells. Our results showed that RAD51C and HBV X protein(HBX) produced a direct interaction in the nucleus, the HBV infection of HCC cells promoted RAD51C expression, and the increased expression of RAD51C promoted HBV replication. This indicated that RAD51C is closely related to the occurrence and development of HCC caused by HBV infection, and may bring a breakthrough in the the prevention and treatment study of HCC.

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Mutation pattern and methylation susceptibility of Hepatitis B virus American genotypes

Jaspe

Loureiro

Chemin

et al. 2020

Clinics and Research in Hepatology and Gastroenterology

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Analysis of fitness differences of hepatitis B virus genotypes D and F using a cotransfection assay

Cited by 4 publications

References 18 publications

Hepatitis B Virus X Gene Differentially Modulates Subgenotype F1b and F4 Replication

Hepatitis B Virus X Gene Differentially Modulates Subgenotype F1b and F4 Replication

HBV promotes its replication by up-regulating RAD51C gene expression

Mutation pattern and methylation susceptibility of Hepatitis B virus American genotypes

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