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Hepatitis B virus - HBV

Virus Host Enzyme Edited Genes Phenotype Disease Details
Hepatitis B virus Human APOBEC3B NA Antiviral Hepatitis
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: G-to-A; C-to-U
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: NA
  • Correlation: Negative
  • Description: First, silencing endogenous APOBEC3B in an HBV infection system lead to upregulation of HBV replication. Second, APOBEC3B can inhibit replication of HBV isolates from genotypes (gt) A, B, C, and D as determined by employing transfection of plasmids expressing isolates from four different HBV genotypes. For HBV inhibition, APOBEC3B-mediated inhibition of replication primarily depends on the C-terminal active site of APOBEC3B. In addition, employing the HBV RNaseH-deficient D702A mutant and a polymerase-deficient YMHA mutant, we demonstrated that APOBEC3B can edit both the HBV minus- and plus-strand DNAs, but not the pregenomic RNA in core particles. Furthermore, we found by co-immunoprecipitation assays that APOBEC3B can interact with HBV core protein in an RNA-dependent manner. Our results provide evidence that APOBEC3B can interact with HBV core protein and edit HBV DNAs during reverse transcription.
  • PMID: 29129707
Hepatitis B virus Human APOBEC3A NA Antiviral Hepatitis
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: G-to-A; C-to-U
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: NA
  • Correlation: Negative
  • Description: Overexpressed APOBEC3A and APOBEC3G could be packaged in HBV capsids but did not change the amount or distribution of mutations. We found no deamination on pregenomic RNA (pgRNA), indicating that an intact genome is encapsidated and deaminated during or after reverse transcription. The deamination pattern suggests a model of rcDNA synthesis in which pgRNA and then newly synthesized minus-sense single-stranded DNA are protected from deaminase by interaction with the virus capsid; during plus-strand synthesis, when enough dsDNA has been synthesized to displace the remaining minus strand from the capsid surface, the single-stranded DNA becomes deaminase sensitive
  • PMID: 29491156
Hepatitis B virus Human APOBEC3G NA Antiviral Hepatitis
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: G-to-A; C-to-U
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: NA
  • Correlation: Negative
  • Description: Overexpressed APOBEC3A and APOBEC3G could be packaged in HBV capsids but did not change the amount or distribution of mutations. We found no deamination on pregenomic RNA (pgRNA), indicating that an intact genome is encapsidated and deaminated during or after reverse transcription. The deamination pattern suggests a model of rcDNA synthesis in which pgRNA and then newly synthesized minus-sense single-stranded DNA are protected from deaminase by interaction with the virus capsid; during plus-strand synthesis, when enough dsDNA has been synthesized to displace the remaining minus strand from the capsid surface, the single-stranded DNA becomes deaminase sensitive
  • PMID: 29491156
Hepatitis B virus Human ADAR1 NA Promote viral replication Hepatitis
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: A-to-I
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: NA
  • Correlation: Positive
  • Description: ADAR1 stimulates HBV replication
  • PMID: 31585913
Hepatitis B virus Human APOBEC3G, APOBEC3C and APOBEC3H NA Inhibit viral replication Hepatoma
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: G-to-A
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: Recoding
  • Correlation: Negative
  • Description: APOBEC3G, APOBEC3C and APOBEC3H, three members of this protein family present in human liver, for their ability to edit HBV genomes. Transfection of human HepG2 hepatoma cells with a plasmid encoding the APOBEC3C protein resulted in abundant GAA mutations in the majority of newly formed HBV genomes.
  • PMID: 18420796
Hepatitis B virus Human APOBEC3G, APOBEC3C and APOBEC3H NA Promote virus escape from the immune resistan Hepatoma
  • Edited Gene Alias: NA
  • Editing Site: NA
  • Editing Type: G-to-A
  • Amino Acid Change: NA
  • Editing Level: Present
  • Molecular Consequence: Recoding
  • Correlation: Negative
  • Description: The hepatitis B virus (HBV) infection is a major risk factor in the development of chronic hepatitis (CH) and hepatocellular carcinoma (HCC). Through G-to-A hypermutation, AID/APOBECs also edit HBV DNA and facilitate the mutation of HBV DNA, which may assist the virus to evolve and potentially escape from the immune responses.
  • PMID: 23341589;26398702