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| HBV | WHV |
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Virology | | |
Classification | Family: Hepadnaviridae | Family: Hepadnaviridae |
Genus: Orthohepadnavirus | Genus: Orthohepadnavirus [91] |
Host | Human | Woodchuck (Marmota monax) |
Structure | 40–42 nm spherical; enveloped nucleocapsid; partially double-stranded DNA genome [22] | 42–45 nm spherical; enveloped nucleocapsid; partially double-stranded DNA genome [91, 104] |
Proteins | Surface glycoproteins (large-L, medium-M, small-S), core protein, “x” protein, “e” antigen, DNA polymerase with reverse-transcriptase activity [22, 105] | The corresponding proteins [91] |
Replication strategy | Replication of HBV DNA occurs by reverse transcription of an RNA intermediate within cytoplasmic nucleocapsids [22] | The same mechanism [97] |
Genetic diversity | 8 major genotypes [105] | 1 major genotype (minor sequence differences) [91] |
Integration into host chromosome | Yes [22] | Yes, often close to N-myc oncogene region [106] |
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Clinical course of infection | | |
Epidemic | 350 million people infected worldwide | Endemic in some woodchuck population in North America |
Vertical transmission | The most common: from mother to newborn | Neonatal woodchucks infected by WHV inoculum |
chronicity rate: 45%–90% [20, 105] | chronicity rate: 60%–75% [92] |
Horizontal transmission | Transmitted by body fluids, 90% of individuals recover [105] | Adult woodchucks infected by WHV inoculum, |
| 90%–95% of animals recover [92] |
Clinical features of chronic infection | Variable HBV DNA levels: copies/mL | WHV DNA levels: copies/mL |
Variable HBsAg levels | WHsAg: mean 100–300 ug/mL |
liver transaminases elevation [20, 22, 105] | liver transaminases elevation [92, 107] |
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Disease progression | | |
Liver cirrhosis | 2%–5% in HBeAg-positive patients (genotype dependent) [20] | Not common |
Hepatocellular carcinoma | 5-year cumulative HCC incidence in patients with cirrhosis: 16% (data in Asia) [20] | Nearly 100% of chronic infected animals have HCC after 3 years [92, 94, 95, 107] |
Efficacy of nucleos(t)ide analogues treatment | Effective: entecavir, tenofovir, telbivudine, adefovir, lamivudine [2–5] | Effective: clevudine, telbivudine, entecavir, emtricitabine, tenofovir, |
Less effective: tenofovir, adefovir, lamivudine [74, 108–118] |
Development of resistance mutations | Yes [6, 7, 105] | Lamivudine-resistant strains isolated [119] |
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