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Hepatitis B

GMJ News knowledge hub · last reviewed August 2026 · Georgian Medical Journal

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Hepatitis B virus (HBV) chronically infects 296 million people globally and kills approximately 820,000 people per year from cirrhosis and hepatocellular carcinoma — making it the most common serious chronic viral liver infection worldwide and a leading infectious cause of cancer death, yet a disease preventable by a safe, cheap, highly effective vaccine that has existed since 1982 (WHO). The central paradox of HBV: a vaccine-preventable infection with oral antiviral suppression (tenofovir, entecavir) available — yet WHO elimination targets for 2030 remain far off track, because 90% of infected infants (without birth-dose vaccination within 24 hours) develop chronic infection that silently progresses to cirrhosis over decades. The Caucasus region — including Georgia — has historically elevated HBV prevalence.

Key messages

296M chronically infected — 820K deaths/year
Hepatitis B virus (HBV) chronically infects 296 million people globally and kills approximately 820,000 per year from cirrhosis and hepatocellular carcinoma — making chronic HBV the most prevalent serious chronic viral liver infection and a leading infectious cause of cancer death (WHO).
90% of infected neonates develop chronic HBV
Perinatal HBV transmission from HBeAg-positive mothers results in chronic infection in approximately 90% of exposed neonates — versus only 5% of infected adults. This makes birth-dose vaccination (within 24 hours) and HBIG (hepatitis B immunoglobulin) the critical interventions.
Birth-dose vaccine prevents 85-95% of vertical transmission
The hepatitis B birth dose — given within 24 hours of birth — prevents 85-95% of vertical (mother-to-child) transmission, the dominant cause of chronic HBV globally. WHO recommends universal birth-dose HBV vaccination for all newborns worldwide.
Antiviral suppression — not cure
Tenofovir (TDF) and entecavir (ETV) effectively suppress HBV DNA to undetectable levels — reducing liver damage, cirrhosis progression and HCC risk. However, they rarely achieve HBsAg clearance (functional cure) — treatment is typically lifelong. Newer curative approaches are in clinical development.
HBV + alcohol + HCV = amplified cirrhosis risk
HBV coinfection with HCV, HDV (hepatitis D) or heavy alcohol use dramatically accelerates cirrhosis and HCC progression. HDV (the satellite virus that requires HBsAg to replicate) causes the most severe form of chronic viral hepatitis — affecting approximately 12 million HBsAg-positive people.
WHO 2030 elimination — off track
WHO targets 90% reduction in new HBV infections and 65% reduction in deaths by 2030. Progress is severely off track: only 10% of chronically infected people are diagnosed; only 22% of those eligible are on treatment. Finding the “missing millions” is the defining challenge.

Key statistics

296M
people chronically infected with HBV globally (WHO 2019)
WHO 2019
820K
HBV-related deaths/year (cirrhosis + HCC)
WHO
90%
of perinatally infected neonates develop chronic HBV
WHO
85-95%
perinatal transmission prevented by birth-dose + HBIG
WHO
10%
only 10% of chronically infected people are diagnosed (WHO)
WHO 2019
2030
WHO HBV elimination target — currently severely off track
WHO

HBsAg seroprevalence by WHO region — % of population chronically infected

Source: WHO. Africa and Western Pacific have highest HBV burden; Europe and Americas lowest.

Glossary of key terms

HBsAg (Hepatitis B surface antigen)
WHOThe outer envelope protein of HBV — the primary marker of HBV infection. Presence >6 months indicates chronic infection (CHB). Anti-HBs (antibody to HBsAg) indicates immunity — either from vaccination or past resolved infection. HBsAg clearance is the goal of curative therapy (functional cure).
HBeAg and HBV DNA
WHOHBeAg (hepatitis B e-antigen): a marker of high-level viral replication and infectivity. HBeAg-positive mothers have approximately 90% perinatal transmission rate. HBV DNA (viral load by PCR): quantifies viral replication; key marker for treatment eligibility and response monitoring.
Tenofovir (TDF) and Entecavir (ETV)
WHO EMLFirst-line antivirals for chronic HBV on WHO Essential Medicines List. Both are oral, well-tolerated, with high barrier to resistance. Tenofovir alafenamide (TAF): newer formulation with fewer renal and bone side effects. These drugs suppress HBV DNA to undetectable levels but rarely cure HBV (HBsAg rarely clears). Lifelong treatment typically required.
HDV (Hepatitis D virus)
WHOA defective RNA virus that requires HBsAg to replicate — only affects people with HBV infection (coinfection or superinfection). HDV coinfection causes the most severe form of chronic viral hepatitis — accelerating cirrhosis and HCC. Approximately 12 million HBsAg-positive people are HDV-coinfected. Bulevirtide (HBV/HDV entry inhibitor) — first approved HDV treatment (EMA 2020).
HBV 1982 vaccine
WHOThe hepatitis B vaccine (recombinant HBsAg) has been available since 1982 — a safe, highly effective 3-dose series. Routine childhood immunisation has dramatically reduced HBV prevalence in high-coverage countries. Birth dose: must be given within 24 hours of birth to prevent perinatal transmission. WHO recommends universal birth-dose vaccination.
Functional cure vs virological cure
ResearchFunctional cure: HBsAg loss + anti-HBs seroconversion (sustained after treatment cessation) — occurs in <10%/year with current antivirals. Virological cure: elimination of cccDNA (covalently closed circular DNA — the HBV persistence reservoir in hepatocyte nuclei) — the true cure target, requiring agents that eliminate cccDNA or permanently silence it. Multiple curative approaches (siRNA, capsid assembly modulators, PD-1 immune checkpoint inhibitors) are in Phase 2-3 trials.

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Related health topics

Viral hepatitis (overview)Hepatitis CHepatitis DLiver cancer (HCC)Liver diseaseHBV vaccination

About this hub. Produced by the GMJ News Editorial Team as a public-good service. Every statistic is linked to its primary source. Documents are preserved in the GMJ Repository with full attribution. Georgian Medical Journal · Contact the editorial team
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