Viral Hepatitis (Hepatitis A, B, C, D, E)

Meet the patient

A 28-year-old man presents with a week of anorexia, nausea, dark urine, and now yellow eyes. He mentions he has lost his taste for cigarettes. On examination he is icteric with a tender liver edge and palpable spleen. His ALT is over 1000 and his INR is normal.^[1]

The loss of taste for cigarettes is the classic exam pearl for acute viral hepatitis, and the next move is serology to name the virus — because the answer changes everything. Two questions now run: which virus, and is this acute or chronic? Hold those two and the algorithm unfolds.^[1]

Vowels enteric, consonants blood-borne — the organising rule

One mnemonic sorts the whole topic, and it is the expected opener. The vowels — A and E — are enteric (faecal-oral, water-borne); the consonants — B, C, D — are blood-borne (parenteral, sexual, vertical).^[1]

^{[1] [1]}

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Etymology for viva gold: hepatitis is Greek hepar, "liver", plus -itis, "inflammation". The viruses were named in order of discovery — A and B in the 1960s (the Australia antigen, HBsAg, was Baruch Blumberg's Nobel-winning find), C in 1989 (the mysterious "non-A non-B" agent finally identified by molecular cloning before the virus itself was ever seen), D the delta agent, and E the enteric non-A non-B.^[1]

Chronicity by age — the single highest-yield table

The chronicity rates of HBV by age of acquisition are the most frequently tested numbers in viral hepatology, and they explain the entire global epidemiology.^[1]

• Perinatal acquisition — 90 percent become chronic.
• Children under 5 years — 25 to 50 percent.
• Immunocompetent adults — under 5 percent (over 95 percent clear the virus).^[1]

Set that against the others: HCV chronicity is 75 to 85 percent regardless of age; HDV superinfection becomes chronic in 80 to 90 percent; HAV and HEV are never chronic in the immunocompetent. This single set of numbers is the reason universal HBV birth-dose vaccination is the cornerstone of the WHO elimination strategy — the neonatal immune system is too immature to clear the virus, so preventing the perinatal transmission prevents the chronic disease.^[1][4]

HBV serology — the most-tested table in hepatology

The HBV serology panel uses six markers to define the phase and natural history of infection, and reproducing the patterns is a guaranteed exam question. Know each marker, then know the patterns.^[1][4]

^[1]

The classic serological patterns — memorise verbatim:^[1]

^[1]

The window period is bridged by IgM anti-HBc — the single most-tested serological fact. When HBsAg has disappeared (typically 4 to 6 months after acute infection) and anti-HBs has not yet appeared, IgM anti-HBc is the only marker that proves acute HBV. Everyone forgets the window; examiners love it.^[1][4]

HCV — the two-step algorithm and the trap beneath it

HCV testing is a two-step algorithm, and the trap is assuming a positive antibody means active infection.^[2]

1. anti-HCV antibody — the screening test; positive indicates past or current infection (it cannot distinguish). It becomes positive 4 to 10 weeks after exposure and never declines.
2. HCV RNA (PCR) — confirmatory; positive means active infection and quantifies the viral load for treatment and sustained-virological-response monitoring.^[1]

A positive antibody with a negative HCV RNA means resolved infection — either spontaneous clearance or prior cure. Reach for the RNA before you reach for the DAAs. There is no reliable IgM anti-HCV, so acute HCV is diagnosed by a documented seroconversion (negative then positive antibody) or HCV RNA positivity within 6 months of a defined exposure.^[2][3]

Genotyping (1 through 6) was once essential to choose the regimen; with pan-genotypic DAAs it is now less critical, but still recommended for difficult cases such as genotype 3 with cirrhosis. The global distribution is approximately genotype 1 (46 percent), genotype 3 (22 percent), and genotypes 2 and 4 (about 10 percent each).^[2][7]

Why HBV is not curable and HCV is — cccDNA versus no DNA stage

The reason HBV needs lifelong suppression and HCV is curable in weeks is a single virological difference: HBV makes a DNA minichromosome, HCV does not.^[1]

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HBV is a DNA virus that forms a stable minichromosome. The partially double-stranded DNA genome is delivered to the nucleus and repaired into covalently closed circular DNA (cccDNA), a stable minichromosome that serves as the transcription template. Nucleos(t)ide analogues block new reverse transcription but do not eliminate the cccDNA, which persists as the reservoir for viral rebound when therapy stops. Functional cure (HBsAg loss) occurs in only 1 to 3 percent of patients per year on treatment.^[1][5]

HCV is a positive-sense single-stranded RNA virus with no DNA intermediate, no integration into the host genome, and no long-lived reservoir. DAAs target the essential viral enzymes — NS3/4A protease, NS5A, and NS5B RNA-dependent RNA polymerase — and over 8 to 12 weeks eliminate the virus entirely. Sustained virological response at 12 weeks (SVR12) — HCV RNA undetectable 12 weeks after therapy ends — is virologically equivalent to cure.^[2][3][6]

Why HBV (and not HCV) causes hepatocellular carcinoma without cirrhosis. HBV DNA integrates into the host genome (a near-universal event in HBV-related HCC), causing chromosomal instability and insertional mutagenesis; the HBx protein transactivates growth pathways and sequesters p53; and chronic inflammation drives oxidative damage. HCV, with no DNA intermediate and no integration, causes HCC almost exclusively through established cirrhosis. This is why HCC surveillance is offered to high-risk chronic HBV patients even without cirrhosis, but to HCV patients only once cirrhotic.^[1]

EASL 2017 replaced the older descriptive labels with five numbered phases of chronic HBV — the viva answer is to name them in order:^[11]

1. HBeAg-positive chronic infection (phase I).
2. HBeAg-positive chronic hepatitis (phase II).
3. HBeAg-negative chronic infection (phase III).
4. HBeAg-negative chronic hepatitis (phase IV).
5. HBsAg-negative phase (phase V).

All patients with chronic HBV infection are at increased risk of progression to cirrhosis and hepatocellular carcinoma, depending on host and viral factors — the phase decides who is treated.^[11]

Acute hepatitis — the four phases

Acute hepatitis from any of the five viruses runs a stereotyped four-phase course, and naming the phases in order is a viva staple.^[8]

1. Incubation (asymptomatic, viraemic) — HAV 15 to 50 days (median 28); HBV 30 to 180 days (median 75); HCV 2 weeks to 6 months (median 50); HDV as for HBV; HEV 2 to 9 weeks (median 40).
2. Prodromal or pre-icteric (1 to 2 weeks) — anorexia (often the first symptom), nausea, vomiting, fatigue, low-grade fever, right-upper-quadrant discomfort, arthralgia, and the classic distaste for cigarettes. A serum-sickness-like prodrome (arthralgia, urticarial rash, fever) occurs in HBV — immune-complex mediated.
3. Icteric (1 to 6 weeks) — dark urine first (bilirubinuria, the first objective sign), then pale stools, then jaundice (scleral then cutaneous), with pruritus and tender hepatomegaly.
4. Convalescent (weeks to months) — symptoms resolve; fatigue may persist for months. ALT and bilirubin normalise.^[1]

Atypical acute presentations to name: anicteric hepatitis (commonest in children, easily missed); relapsing hepatitis (biphasic, common with HAV); cholestatic hepatitis (deep prolonged jaundice, especially HAV in older adults); fulminant hepatitis (acute liver failure); and aplastic anaemia (rare, classically after HAV in young men).^[1]

Chronic hepatitis — the silent disease, and its extrahepatic signatures

Chronic HBV and HCV are usually asymptomatic for decades, detected incidentally on liver tests, on screening (blood donation, antenatal, pre-immunosuppression), or at presentation with cirrhosis or HCC. Vague fatigue is the commonest reported symptom. This silence is the whole problem — and why screening matters.^[1][2]

The extrahepatic manifestations are favourite exam topics and may precede the liver diagnosis. Each carries a teaching hook.^[1]

HBV extrahepatic (immune-complex mediated):^[1][4]

• Serum-sickness-like prodrome — arthralgia or arthritis, urticarial rash, fever (10 to 30 percent of acute HBV).
• Polyarteritis nodosa (PAN) — medium-vessel vasculitis, mononeuritis multiplex, mesenteric ischaemia, hypertension; HBV accounts for 10 to 30 percent of PAN.
• Membranous glomerulonephritis and membranoproliferative GN (especially in children).
• Gianotti-Crosti syndrome — papular acrodermatitis of childhood, a symmetrical papular rash on cheeks, buttocks, and extensor surfaces.^[1]

HCV extrahepatic (the extrahepatic HCV syndrome):^[2][3]

• Mixed cryoglobulinaemia (Type II) — palpable purpura, arthralgia, weakness, glomerulonephritis, peripheral neuropathy.
• Membranoproliferative glomerulonephritis.
• Porphyria cutanea tarda — photosensitive bullae on sun-exposed skin.
• Lichen planus — oral Wickham striae, pruritic polygonal purple papules on the wrists.
• Non-Hodgkin lymphoma (especially marginal-zone and diffuse large B-cell).
• Type 2 diabetes (HCV-induced insulin resistance) and sicca syndrome.^[1]

Not every hepatitis is viral — the differential

An acute hepatitis picture (ALT over 10 times the upper limit of normal, with or without jaundice) is not always viral, and the recurring miss is drug-induced liver injury.^[8][9]

• Drug-induced liver injury (DILI) — paracetamol (zone-3 necrosis, ALT over 1000, an overdose history); anti-tuberculous drugs (isoniazid, rifampicin, pyrazinamide); amoxicillin-clavulanate; statins; antiepileptics; herbal and ayurvedic supplements; anabolic steroids. Distinguished by a detailed drug history, the AST/ALT pattern, eosinophilia, and negative viral serology.
• Ischaemic hepatitis ("shock liver") — AST and ALT both over 1000 with a clear episode of hypotension, shock, or sepsis, halving in 24 to 48 hours.
• Alcoholic hepatitis — AST and ALT typically under 300, with AST over ALT (ratio over 2), markedly raised gamma-GT, and macrocytosis.
• Autoimmune hepatitis — high IgG, positive ANA, anti-smooth-muscle antibody, or anti-LKM1, female predominance.
• Wilson disease — young patient, Coombs-negative haemolytic anaemia, low caeruloplasmin, Kayser-Fleischer rings, ALP markedly low.
• Biliary obstruction — ALP and gamma-GT disproportionately high, pain, fever, dilated ducts on ultrasound.^[1]

Distinguishing the five hepatotropic viruses from one another is done entirely by serology — the clinical picture alone is rarely sufficient, though the exposure history, incubation period, and chronicity risk provide strong clues.^[1]

Management — suppress HBV, cure HCV, support the rest

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The definitive therapies for chronic HBV and HCV are entirely different in goal: HBV is lifelong viral suppression, HCV is short-course cure. HAV and HEV are managed supportively.^[1]

Hepatitis A and E are managed supportively — and the job that matters is recognising progression to acute liver failure: the clinical pattern is rapid-onset elevation of aminotransferases with altered mentation and disturbed coagulation, with no pre-existing liver disease to explain it. Liver transplantation — used in nearly 30 percent of patients with acute liver failure — remains the life-saving treatment, so early transplant-centre referral decides outcome.^[8]

Chronic hepatitis B — lifelong suppression

First-line oral nucleos(t)ide analogues — EASL: the treatment of choice is long-term administration of a potent nucleos(t)ide analogue with a high barrier to resistance, i.e. entecavir, tenofovir disoproxil, or tenofovir alafenamide:^[11]

• Tenofovir disoproxil fumarate (TDF) 300 mg orally once daily — in the pivotal 48-week trial it beat adefovir dipivoxil on viral suppression (93 versus 63 percent in HBeAg-negative disease; 76 versus 13 percent in HBeAg-positive disease), and no tenofovir resistance substitutions had developed at week 48 (Marcellin 2008, NEJM).^[5][15]
• Tenofovir alafenamide (TAF) 25 mg orally once daily — a prodrug with improved renal and bone safety; preferred in renal impairment and osteoporosis.
• Entecavir 0.5 mg orally once daily — in the phase 3 HBeAg-positive trial, 0.5 mg daily beat lamivudine 100 mg daily on histologic improvement (72 versus 62 percent) and undetectable HBV DNA (67 versus 36 percent), with no viral resistance to entecavir detected at week 48 (Chang 2006, NEJM).^[16]

Pegylated interferon-alpha-2a 180 microgram subcutaneously once weekly for 48 weeks is reserved for selected young patients with HBeAg-positive disease, high ALT, low HBV DNA, and genotype A or B who want finite therapy — it achieves HBeAg seroconversion in 30 percent and HBsAg loss in 3 to 7 percent. It is contraindicated in decompensated cirrhosis, pregnancy, autoimmune disease, and severe depression.^[1][4]

The EASL 2017 treatment indications:^[11]

• Typical indication — HBV DNA over 2,000 IU/mL plus elevated ALT, and/or at least moderate histological lesions on liver biopsy.
• Cirrhosis — all cirrhotic patients with detectable HBV DNA should be treated.
• Additional indications — prevention of mother-to-child transmission in pregnant women with high viremia, and prevention of HBV reactivation in patients requiring immunosuppression or chemotherapy.^[11][15]

Chronic hepatitis C — the curative DAA revolution

Modern HCV therapy uses pan-genotypic direct-acting antivirals for 8 to 12 weeks, achieving SVR over 95 percent across genotypes, including in cirrhosis and HIV co-infection. Interferon is obsolete.^[2][3][6]

^{[12] [18] [13] [14]}

Ledipasvir/sofosbuvir (Harvoni) for 12 weeks remains an option for genotype 1, 4, 5, and 6 (Afdhal 2014, ION-1).^[6]

Before starting DAAs, two checks are non-negotiable: HBV serology (HBV reactivation is a boxed warning — give prophylactic tenofovir or entecavir if HBsAg positive), and a pregnancy test plus drug-interaction check (amiodarone is contraindicated with sofosbuvir because of bradyarrhythmia; ribavirin, where used, is teratogenic and needs 6 months of contraception after).^[2][3]

After SVR (cure), fibrosis regresses over years and portal hypertension falls — but HCC surveillance continues if cirrhosis was present at SVR (6-monthly ultrasound plus AFP). Re-infection risk remains in people who inject drugs; offer harm reduction.^[2]

Prevention — the most powerful intervention, and the preventable death

Vaccination is the cornerstone of prevention for HAV and HBV, and screening before immunosuppression prevents the single most preventable death in the topic.^[1]

HBV reactivation on immunosuppression — prevent it

Every patient starting immunosuppression must be screened for HBV (HBsAg, anti-HBc, anti-HBs). This is the recurring fatal, entirely preventable miss.^[1]

• HBsAg-positive patient starting a high-risk regimen (rituximab, ofatumumab, anti-CD20, high-dose corticosteroids over 4 weeks, anthracyclines, haematopoietic stem cell transplant): prophylactic tenofovir or entecavir for the entire duration of immunosuppression plus 12 to 18 months afterwards. Do not wait for reactivation.
• HBsAg-negative, anti-HBc-positive (past infection) on a high-risk regimen: prophylactic antiviral for rituximab; monitor closely otherwise.
• If reactivation occurs (DNA rise over 2 log, or an ALT flare): start tenofovir or entecavir immediately; stop or reduce immunosuppression if possible.^[1]

Vaccines and vertical-transmission prevention

Hepatitis A vaccine — post-exposure prophylaxis of susceptible contacts works: in a cohort of 3,550 outbreak exposures, effectiveness was 97.6 percent for one dose of vaccine versus 98.3 percent for immunoglobulin (difference not significant), which supports the preferential use of vaccination over immunoglobulin to prevent secondary cases.^[17]

Hepatitis B vaccine — Engerix-B 20 microgram intramuscularly (adults and children over 10) at 0, 1, and 6 months; paediatric dose 10 microgram for under 10. The universal birth dose within 24 hours of birth is the WHO and AASLD cornerstone of vertical-transmission prevention. Anti-HBs over 10 mIU/mL means a responder; 5 to 10 percent of immunocompetent adults are non-responders (age over 40, obesity, smoking, immunosuppression, renal failure) and need a repeat series. No HCV or HEV vaccine is universally available (an HEV vaccine is licensed in China only).^[1][4]

The vertical-transmission package — the trial evidence behind the bundle:^[11][15]

• Maternal tenofovir disoproxil fumarate 300 mg orally once daily from 30 to 32 weeks of gestation (continued until postpartum week 4) for HBeAg-positive mothers with HBV DNA over 200,000 IU/mL — mother-to-child transmission at postpartum week 28 fell from 18 percent to 5 percent.
• All infants received immunoprophylaxis alongside the maternal tenofovir in the trial.
• EASL lists prevention of mother-to-child transmission in pregnant women with high viremia as a treatment indication in its own right.^[11][15]

HEV in pregnancy — the special catastrophe

HEV in pregnancy (second and third trimester) carries a uniquely high risk of acute liver failure, with maternal mortality of 20 to 25 percent. The mechanisms are immune modulation by pregnancy hormones, suppression of T-helper-1 responses, high viral replication, and increased hepatocyte susceptibility. The fetus suffers high rates of prematurity, stillbirth, and vertical transmission. Test HEV urgently in any pregnant woman with acute hepatitis — and remember ribavirin is contraindicated in pregnancy (teratogenic). Management is supportive, with urgent delivery if fulminant.^[8]

How viral hepatitis patients come to harm — the preventable list

• Missing HBV reactivation on rituximab, chemotherapy, or high-dose steroids — fatal and entirely preventable with prophylaxis.^[1]
• Overlooking HEV in a pregnant woman with acute hepatitis — high fulminant rate.^[8]
• Assuming a positive anti-HCV antibody means active infection — confirm with HCV RNA; a positive antibody with negative RNA is resolved.^[2]
• Not checking HBV status before DAAs for HCV — reactivation is a boxed warning.^[2][3]
• Confusing IgM anti-HBc with HBsAg in the window period — IgM anti-HBc is the most sensitive marker of acute HBV.^[1]
• Stopping nucleos(t)ide therapy in HBV cirrhosis — fatal flare and decompensation; therapy is indefinite.^[1]
• Forgetting that HBV causes HCC without cirrhosis — surveillance applies to high-risk chronic HBV even without cirrhosis.^[1]
• Prophylactically correcting the INR with fresh frozen plasma in acute liver failure — it erases the prognostic and transplant marker.^[8][9]

The trials and guidelines that set the standard

^{[5] [6]}

The guideline framework: the AASLD 2018 HBV guidance (Terrault) set the treatment indications and first-line agents; the AASLD-IDSA HCV Guidance 2018 and 2023 update introduced universal one-time adult and pregnancy screening and the pan-genotypic regimens; Lok and McMahon 2007 codified the four immunological phases of chronic HBV; the Polaris Observatory 2017 mapped the global HCV prevalence (about 1 percent, 71 million) and genotype distribution; Baveno VII 2022 set the cirrhosis and portal-hypertension thresholds that govern HCC and variceal surveillance.^{[1][2][4][7][10]}

Special populations — what changes

Pregnancy. HBV: EASL makes prevention of mother-to-child transmission in pregnant women with high viremia a treatment indication — in the NEJM trial, maternal TDF 300 mg daily from 30 to 32 weeks (HBeAg-positive, HBV DNA over 200,000 IU/mL) with infant immunoprophylaxis cut transmission from 18 percent to 5 percent at postpartum week 28. HCV: the AASLD-IDSA guidance keeps its emphasis on universal screening, and cure comes from 8 to 12 weeks of pan-genotypic DAAs — SVR12 99 percent with 12 weeks of sofosbuvir-velpatasvir (ASTRAL-1) and 99.7 percent with 8 weeks of glecaprevir-pibrentasvir (EXPEDITION-8).^{[11][15][3][12][13]}

Neonates and children. Perinatal HBV transmission is the commonest global route; 90 percent become chronic without immunoprophylaxis — prevented by the universal birth-dose vaccine plus HBIG. The paediatric HBV vaccine dose is half the adult. HCV vertical transmission is 5 percent with no prophylaxis; treat later, DAAs approved from age 3.^[1]

The immunosuppressed (HIV, transplant, chemotherapy). High risk of HBV reactivation: screen all and give prophylactic tenofovir or entecavir for high-risk regimens. HCV-HIV co-infection accelerates fibrosis — treat both, with careful DAA-antiretroviral interaction checks.^[1]

End-stage renal disease or dialysis. Prefer entecavir (dose-adjusted to eGFR) or TAF over TDF (nephrotoxicity); double the HBV vaccine dose and schedule extra doses; screen regularly for HBV and HCV (outbreak risk in dialysis units).^[1]

Decompensated cirrhosis. Refer for transplant evaluation; HBV — continue tenofovir or entecavir (avoid Peg-IFN, contraindicated); HCV — sofosbuvir-based regimens with ribavirin, cautious and specialist-led; HCC surveillance mandatory.^[8][10]

The mantra, and the mnemonics

The mantra: vowels enteric, consonants blood-borne; ninety percent of neonates; suppress HBV for life, cure HCV in weeks — and never give chemotherapy without screening for HBV.^[1][2]

^{[1] [11] [1]}

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)ShowHide

The 28-year-old with anorexia, dark urine, jaundice, tender hepatomegaly, an ALT over 1000, and a lost taste for cigarettes. What is the first investigation, and what marker proves acute HBV in the window period? Model: This is acute viral hepatitis — the lost taste for cigarettes is the classic pearl. The first investigation is serology to name the virus: IgM anti-HAV, HBsAg and IgM anti-HBc, anti-HCV and HCV RNA, and IgM anti-HEV (especially if pregnant or in an endemic region). The marker that proves acute HBV in the window period — when HBsAg has waned and anti-HBs has not yet appeared — is IgM anti-HBc, the most sensitive marker of acute HBV and the single most-tested serological fact. INR is normal here, so this is not acute liver failure — manage supportively and monitor the INR and encephalopathy.^[1]

Stem 2 — the HBsAg-positive patient starting rituximab (answer)ShowHide

A 62-year-old with known HBsAg-positive chronic HBV is about to start rituximab for lymphoma. What must you do, and what is the dose? Model: Start prophylactic tenofovir 300 mg orally once daily (or entecavir 0.5 mg daily). EASL is explicit that prevention of HBV reactivation in patients requiring immunosuppression or chemotherapy is a treatment indication, and the treatment of choice is the long-term potent nucleos(t)ide analogue with a high barrier to resistance — entecavir, tenofovir disoproxil, or tenofovir alafenamide. Do not wait for reactivation — HBV reactivation on rituximab can be fulminant and fatal, and this is the single most preventable death in viral hepatitis.^[11][15][16]

Stem 3 — the pregnant woman with acute hepatitis and a high ALT (answer)ShowHide

A 26-year-old in her third trimester presents with acute hepatitis and an ALT of 1200. What virus must you test for urgently, and why does it matter? Model: Test HEV urgently — IgM anti-HEV. HEV in pregnancy carries a uniquely high risk of acute liver failure, with maternal mortality of 20 to 25 percent, driven by immune modulation, high viral replication, and increased hepatocyte susceptibility. The fetus is at risk of prematurity, stillbirth, and vertical transmission. Management is supportive, with urgent delivery if fulminant — and ribavirin is contraindicated in pregnancy because it is teratogenic. Check the INR and encephalopathy to grade severity; an INR over 1.5 with encephalopathy means acute liver failure and a transplant-centre referral.^[8]

References18ShowHide

1. [1]Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance Hepatology, 2018.PMID 29405329
2. [2]AASLD-IDSA HCV Guidance Panel. Hepatitis C Guidance 2018 Update: AASLD-IDSA Recommendations for Testing, Managing, and Treating Hepatitis C Virus Infection Clin Infect Dis, 2018.PMID 30215672
3. [3]Bhattacharya D, Aronsohn A, Price J, et al. Hepatitis C Guidance 2023 Update: AASLD-IDSA Recommendations for Testing, Managing, and Treating Hepatitis C Virus Infection Clin Infect Dis, 2023.PMID 37229695
4. [4]Lok ASF, McMahon BJ. Chronic hepatitis B Hepatology, 2007.PMID 17256718
5. [5]Marcellin P, Heathcote EJ, Buti M, et al. Tenofovir disoproxil fumarate versus adefovir dipivoxil for chronic hepatitis B N Engl J Med, 2008.PMID 19052126
6. [6]Afdhal N, Zeuzem S, Kwo P, et al. Ledipasvir and sofosbuvir for untreated HCV genotype 1 infection N Engl J Med, 2014.PMID 24725239
7. [7]Polaris Observatory HCV Collaborators. Global prevalence and genotype distribution of hepatitis C virus infection in 2015: a modelling study Lancet Gastroenterol Hepatol, 2017.PMID 28404132
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9. [9]Bernal W, Wendon J. Acute liver failure N Engl J Med, 2013.PMID 24369077
10. [10]de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VII - Renewing consensus in portal hypertension J Hepatol, 2022.PMID 35120736
11. [11]European Association for the Study of the Liver. EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection J Hepatol, 2017.PMID 28427875
12. [12]Feld JJ, Jacobson IM, Hézode C, et al. Sofosbuvir and Velpatasvir for HCV Genotype 1, 2, 4, 5, and 6 Infection N Engl J Med, 2015.PMID 26571066
13. [13]Brown RS Jr, Buti M, Rodrigues L, et al. Glecaprevir/pibrentasvir for 8 weeks in treatment-naïve patients with chronic HCV genotypes 1-6 and compensated cirrhosis: The EXPEDITION-8 trial J Hepatol, 2020.PMID 31682879
14. [14]Chahine EB, Kelley D, Childs-Kean LM. Sofosbuvir/Velpatasvir/Voxilaprevir: A Pan-Genotypic Direct-Acting Antiviral Combination for Hepatitis C Ann Pharmacother, 2018.PMID 29115151
15. [15]Pan CQ, Duan Z, Dai E, et al. Tenofovir to Prevent Hepatitis B Transmission in Mothers with High Viral Load N Engl J Med, 2016.PMID 27305192
16. [16]Chang TT, Gish RG, de Man R, et al. A comparison of entecavir and lamivudine for HBeAg-positive chronic hepatitis B N Engl J Med, 2006.PMID 16525137
17. [17]Parrón I, Planas C, Godoy P, et al. Effectiveness of hepatitis A vaccination as post-exposure prophylaxis Hum Vaccin Immunother, 2017.PMID 27925847
18. [18]Younossi ZM, Stepanova M, Feld J, et al. Sofosbuvir/velpatasvir improves patient-reported outcomes in HCV patients: Results from ASTRAL-1 placebo-controlled trial J Hepatol, 2016.PMID 26956698