Hepatitis B — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV) — a partially double-stranded DNA hepadnavirus. It is a major global health problem: approximately 296 million people are chronically infected worldwide, with 1.5 million new infections annually, and approximately 820,000 deaths per year from HBV-related cirrhosis and hepatocellular carcinoma (HCC). HBV infection can be acute (most adults clear the virus spontaneously) or chronic (failure to clear HBsAg after 6 months — defined by persistent HBsAg positivity). The risk of developing chronic infection is inversely related to age at acquisition: 90% of perinatally infected infants develop chronic infection compared with fewer than 5% of adults. The global burden of chronic HBV is concentrated in sub-Saharan Africa and East Asia. HBV is completely preventable by the hepatitis B vaccine — a 3-dose recombinant vaccine series providing over 95% protection. Screening of all pregnant women for HBsAg is recommended — infants of HBsAg-positive mothers should receive HBIG and vaccination at birth.

HBV transmission occurs through contact with infected blood, sexual secretions, or other body fluids. Routes of transmission: perinatal (mother-to-child at birth — the most important route globally, particularly in high-endemic regions); sexual transmission (unprotected intercourse — particularly men who have sex with men, multiple partners); percutaneous exposure (sharing needles among people who inject drugs — PWID; needlestick injuries in healthcare workers; unsterile tattooing, piercing, or acupuncture); and horizontal transmission in early childhood in endemic regions (sharing razors, toothbrushes, household contact). HBV is NOT transmitted by casual contact (hugging, sharing utensils, food, water, breastfeeding if the infant has been vaccinated). Risk factors for acquisition: birth in a high-prevalence country (sub-Saharan Africa, China, Southeast Asia), PWID, men who have sex with men, sex workers, household or sexual contacts of HBsAg-positive individuals, healthcare workers, prisoners, and people on renal dialysis (high nosocomial exposure). Risk factors for progression to chronic liver disease: male sex, age at infection (perinatally-acquired is highest risk for chronicity), alcohol excess (dramatically accelerates fibrosis), coinfection with HIV or hepatitis C (HCV), and metabolic liver disease (NAFLD/MASLD).

Acute hepatitis B: 70% of adults with acute HBV infection are asymptomatic or have mild non-specific illness. Symptomatic acute infection (30% of adults): prodrome (fatigue, malaise, nausea, vomiting, right upper quadrant pain, anorexia, arthralgia, low-grade fever), followed after 1-2 weeks by jaundice (yellowing of skin and sclera), dark urine (bilirubinuria), and pale stools (acholic stools). Acute fulminant hepatitis B: rare but life-threatening — coagulopathy, hepatic encephalopathy (confusion, asterixis — liver flap), and acute liver failure requiring urgent liver transplant assessment. Chronic hepatitis B: most patients are asymptomatic for decades. Symptoms of advanced liver disease: fatigue, right upper quadrant discomfort, and eventually features of cirrhosis — jaundice, ascites (abdominal distension from fluid), peripheral oedema, spider naevi, palmar erythema, caput medusae, gynaecomastia (in men), and splenomegaly. Hepatocellular carcinoma (HCC): may present as sudden deterioration, right upper quadrant pain, weight loss, or hepatic mass discovered on surveillance ultrasound. Extrahepatic manifestations (immune complex-mediated): polyarteritis nodosa, membranous glomerulonephritis, and serum sickness-like prodrome.

Hepatitis B is diagnosed through serological markers: HBsAg (hepatitis B surface antigen): the primary marker of HBV infection — positive in acute and chronic infection; persists beyond 6 months in chronic hepatitis B. Anti-HBs (antibody to HBsAg): indicates immunity from vaccination (anti-HBs only) or cleared infection (anti-HBc and anti-HBs). Anti-HBc IgM: present in acute HBV infection and flares of chronic HBV. Anti-HBc IgG (total anti-HBc): present in past and current infection — does not indicate immunity. HBeAg and anti-HBe: HBeAg indicates high viral replication and infectivity; anti-HBe indicates lower replication (HBeAg-negative chronic HBV with anti-HBe can still have active disease). HBV DNA (viral load, quantitative PCR): the most sensitive marker of viral replication — used to guide and monitor treatment. Liver function tests: ALT, AST, bilirubin, albumin, INR (prothrombin time) — elevated ALT indicates hepatic inflammation. Liver fibrosis assessment: non-invasive — FIB-4 score, APRI score, liver elastography (FibroScan — measures liver stiffness in kPa); liver biopsy for cases where non-invasive assessment is inconclusive. HCC surveillance: 6-monthly liver ultrasound (plus or minus AFP — alpha-fetoprotein) for all patients with cirrhosis and for HBsAg-positive patients over 40 years with ongoing viral replication or family history of HCC.

Acute hepatitis B: supportive care for most patients — rest, adequate hydration, avoid hepatotoxic substances (alcohol, NSAIDs, paracetamol at high dose). Antiviral treatment is not routinely given for acute HBV (as 95% of adults clear spontaneously); it is considered for acute liver failure or severely ill patients. Chronic hepatitis B treatment: the goal is to suppress HBV DNA to undetectable levels, normalise ALT, prevent fibrosis progression, and reduce HCC risk. Treatment is not required for all patients — the decision is based on HBV DNA level, ALT, HBeAg status, fibrosis stage, and age. Antiviral treatment indications (simplified): HBV DNA above 2,000 IU/mL with elevated ALT or significant fibrosis (F2 or above). First-line nucleos(t)ide analogues (NAs): tenofovir disoproxil fumarate (TDF — 300mg daily), tenofovir alafenamide (TAF — 25mg daily, lower bone/renal toxicity), or entecavir (0.5mg daily) — all highly effective with high barrier to resistance; generally required long-term (often lifelong). Pegylated interferon-alpha-2a (PEG-IFN): 48-week finite course; induces immune-mediated viral suppression; suitable for a minority of patients (HBeAg-positive, high ALT, genotype A/B); side effects include flu-like symptoms, depression, and neutropenia; aims for HBsAg loss and sustained response off-treatment. HBsAg loss (functional cure) occurs in fewer than 5% on NA therapy and 5-10% on PEG-IFN. New agents in development: capsid assembly modulators, RNA interference (siRNA/ASO) therapies — ongoing clinical trials aim to improve HBsAg clearance rates. HIV coinfection: tenofovir-containing antiretroviral regimens with activity against HBV.

Chronic HBV infection causes progressive liver damage with risk of severe complications, particularly in patients with high viral replication, coinfections, or cofactors such as alcohol use. Cirrhosis develops in approximately 15–40% of chronically infected patients over 20–30 years; once cirrhosis is established, the 5-year probability of hepatic decompensation is 15–20% and 5-year mortality without liver transplantation is 65–85%. Hepatocellular carcinoma (HCC) is the most feared complication — HBV is responsible for approximately 50% of global HCC cases, and uniquely can cause HCC even without preceding cirrhosis, particularly in individuals with ongoing viral replication and certain HBV genotypes. The annual incidence of HCC in HBsAg-positive cirrhotic patients is 2–3%, justifying 6-monthly surveillance ultrasound. Portal hypertension from cirrhosis causes life-threatening variceal haemorrhage (oesophageal or gastric varices — presenting as haematemesis or melaena), ascites (abdominal fluid accumulation requiring diuretics or paracentesis), spontaneous bacterial peritonitis (bacterial infection of ascitic fluid — a medical emergency requiring urgent antibiotics), hepatorenal syndrome (functional renal failure from severe circulatory dysfunction), and hepatic encephalopathy (ammonia-driven confusion, asterixis, and coma). Acute liver failure from acute HBV superinfection or HBV reactivation during immunosuppressive therapy can develop rapidly, with jaundice, coagulopathy, and encephalopathy requiring urgent liver transplant assessment. Extrahepatic manifestations of chronic HBV include polyarteritis nodosa (medium-vessel vasculitis from immune complex deposition) and membranous glomerulonephritis causing nephrotic syndrome.

Hepatitis B vaccine: the most effective prevention. Recombinant HBsAg vaccine series (3 doses at 0, 1, and 6 months — alternative accelerated schedule 0, 1, and 2 months with a booster at 12 months) provides over 95% protective immunity (anti-HBs above 10 mIU/mL). WHO recommends universal infant vaccination starting within 24 hours of birth (critical for preventing perinatal transmission). Catch-up vaccination for adults in high-risk groups: sexual partners of HBsAg-positive individuals, PWID, men who have sex with men, healthcare workers, travellers to endemic countries. Perinatal transmission prevention: all pregnant women screened for HBsAg; infants of HBsAg-positive mothers receive hepatitis B immunoglobulin (HBIG — passive immunity) and HBV vaccine within 12 hours of birth; antiviral treatment (tenofovir) for mothers with HBV DNA above 200,000 IU/mL in third trimester. Harm reduction for PWID: needle exchange programmes, supervised injection facilities, and opiate substitution therapy. Safe sex practices: condoms reduce sexual transmission. Blood safety: universal screening of blood donations, single-use needles. Healthcare: standard precautions, post-exposure prophylaxis (HBIG + vaccine) within 48 hours for unvaccinated healthcare workers after needlestick injury. People with chronic HBV: avoid alcohol (accelerates fibrosis), maintain healthy weight (MASLD coexistence worsens outcomes), avoid raw shellfish (Vibrio vulnificus infection risk), and inform sexual partners and household contacts who should be vaccinated.

Get tested for hepatitis B if you were born in a high-prevalence country, have had unprotected sex with multiple partners, use or have used injectable drugs, or have a household member or sexual partner with chronic HBV. Seek immediate medical attention for: jaundice (yellow skin or eyes), severe abdominal pain, vomiting blood, confusion or extreme fatigue — these may indicate acute liver failure or decompensated cirrhosis. See a hepatologist or gastroenterologist urgently if newly diagnosed with HBsAg positive test or HBV DNA detected — specialist staging of liver disease and treatment planning is required. If you have cirrhosis from HBV, ensure 6-monthly liver ultrasound for hepatocellular carcinoma surveillance — early HCC is treatable with curative intent. Healthcare workers experiencing a needlestick injury from a source of unknown or known HBV status should seek occupational health review within 48 hours for post-exposure prophylaxis.