Types of Hepatitis Explained: Hepatitis A, B, C, D and E — Causes, Spread and Prevention

Five viruses cause viral hepatitis: A, B, C, D and E. Hepatitis A and E spread through contaminated water and food and almost always clear on their own; B, C and D spread through blood and body fluids and can become lifelong, ending in cirrhosis or liver cancer. The exception is hepatitis E in pregnancy — up to 20–25% of women infected in the third trimester can die.
— Dr Chetan Kalal, DM Hepatology, Gleneagles Hospital Mumbai

A composite of a family I see every September. Two members of a Parel household turn yellow within a fortnight of each other after the rains. The first is a 9-year-old boy — fever for three days, then dark urine and a yellow tinge to his eyes. His test shows anti-HAV IgM, the marker of fresh hepatitis A. He is eating again in a week and back at school in three. The second is his 26-year-old aunt, seven months pregnant, living in the same flat and drinking the same water. Her jaundice does not settle. Within days she is drowsy, her clotting is deranged, and she is in our liver ICU with hepatitis E and acute liver failure.

Same monsoon, same tap, two different viruses, two very different outcomes. The letters matter. “Hepatitis” is not one disease but five viruses with different routes, time courses and endings, and most of the confusion I meet in clinic comes from treating them as interchangeable.

This guide is for the patient, parent or spouse who has just been told “it’s hepatitis” and wants to know which one, how it was caught, whether it will go away, and what the family should do. I have spent a decade in liver units where A and E fill the acute beds and B and C fill the cirrhosis and transplant lists; what follows is what I actually see, anchored to WHO and EASL guidance.

Hepatitis A, B, C, D and E at a glance

Split them in two. A and E enter through the mouth and leave on their own. B, C and D enter through blood and can stay for life. Everything else — who is at risk, which vaccine exists, whether treatment is needed — follows from that one division.

Hepatitis A and E: the monsoon viruses

These two travel together in India. Both are passed in the stool of an infected person and swallowed by the next — in sewage-contaminated water, in ice, in cut fruit and chaat handled with unwashed hands, in a shared flat where one child is already shedding virus. The surge begins once the rains flood drains into water lines, which is why the family above turned yellow in September rather than January.

Hepatitis A is overwhelmingly a childhood illness here; children often get a mild or silent infection and walk away immune for life. Adults who escaped it get a rougher ride — two to four weeks of fever, nausea, dark urine and jaundice — but, in the WHO’s words, almost everyone recovers fully. There is no chronic form. A “very small proportion” develop fulminant hepatitis, the liver shutting down.

Hepatitis E behaves the same way in most people, with a longer incubation (two to ten weeks), and then differs in two groups that matter enormously in this country. The first is pregnant women. In a prospective Delhi series of 220 pregnant women with jaundice from acute viral hepatitis, hepatitis E caused 60% of cases, and the women who had it were six times more likely to die than those with other hepatitis viruses, with more antepartum haemorrhage, stillbirth and preterm delivery. The WHO puts third-trimester mortality at up to 20–25%. No other common infection turns a healthy young woman into a liver-failure patient this fast.

The second group is anyone whose liver is already damaged. Hepatitis E landing on an unrecognised cirrhosis — alcohol, fatty liver, old hepatitis B — is a classic trigger for acute-on-chronic liver failure; in an AIIMS cohort of 368 ACLF patients it was the third commonest precipitant. Transplant recipients and others on immunosuppression are the only people in whom it becomes chronic, which is why EASL’s 2018 guideline asks for a blood PCR in them rather than antibodies alone.

Both viruses lead the causes of acute liver failure in India. The INASL consensus states plainly that viral hepatitis is the most frequent cause of ALF here, with anti-tuberculosis drugs second. In the AIIMS series of 1,462 ALF patients over thirty years, hepatitis E alone accounted for 28.7%; in the MAHAL trial I ran at ILBS on raised intracranial pressure in ALF, it was again the commonest cause, in a third of patients. The one consolation: hepatitis E–related ALF carries better survival than the other causes (55% without transplant in the AIIMS cohort, against 36% for hepatitis B), because the liver underneath is healthy and regenerates if we keep the patient alive long enough.

Hepatitis B, C and D: the blood-borne viruses

Here the danger is not speed but silence. A person can carry hepatitis B from birth, or hepatitis C from a transfusion twenty years ago, feel perfectly well, and present for the first time with ascites, a variceal bleed or a liver mass. The WHO’s 2024 report counted 254 million people living with hepatitis B and 50 million with hepatitis C, 1.3 million deaths a year from the two combined, and named India among the ten countries carrying nearly two-thirds of that burden. India’s own sentinel surveillance (2021) found 0.85% of people tested positive for hepatitis B and 0.29% for hepatitis C: roughly one in 118 and one in 345.

Hepatitis B

Spread through blood, semen and vaginal fluid — in India most often from an infected mother to her newborn, which is why so many adult carriers were infected before they could walk. Age at infection decides everything: about 95% of infected infants become chronic carriers, against fewer than 5% of adults. Chronic infection is controlled, usually long term, with daily antiviral tablets (tenofovir or entecavir) in those who meet treatment criteria; a true cure is uncommon. Not everyone needs treatment, but everyone needs follow-up, because the quiet phase can end. The vaccine is nearly 100% protective and India gives it at birth. For testing, treatment decisions and pregnancy in detail, read my post on hepatitis B versus hepatitis C.

Hepatitis C

Almost purely blood-borne: unsafe injections at small clinics, transfusions before blood screening, dialysis, shared needles, roadside tattoos. Around 70% of those infected stay infected. A positive anti-HCV antibody must be confirmed with HCV RNA, because a third of people clear the virus on their own and keep the antibody as a footprint. The important sentence: hepatitis C is curable. A short course of direct-acting antiviral tablets cures more than 95% of patients, India makes the generics, and the national programme supplies them free. There is no vaccine. My hepatitis C page covers genotypes and follow-up after cure.

Hepatitis D

The one most patients have never heard of, and the one I most want hepatitis B carriers to ask about. Hepatitis D is a defective virus that can only replicate inside a cell already infected with hepatitis B. Nearly 5% of people with chronic hepatitis B worldwide, about 12 million, carry it, and the WHO calls the combination the most severe form of chronic viral hepatitis, progressing to cirrhosis and liver cancer faster than hepatitis B alone. EASL’s 2023 guideline recommends testing every HBsAg-positive person for anti-HDV at least once. Treatment is difficult — pegylated interferon, and since 2023 bulevirtide in Europe — and strictly a specialist matter. Prevention is simple: the hepatitis B vaccine blocks hepatitis D as well.

How each type of hepatitis is tested

The first test in anyone with jaundice is a liver function panel, which says how inflamed the liver is, with a prothrombin time or INR, which says whether it is failing. Neither names the virus. For that the tests are specific, and knowing them stops a lot of needless panic over reports.

Hepatitis A — anti-HAV IgM. Positive means infection in the last few weeks; anti-HAV IgG only means past infection or vaccination.

Hepatitis B — HBsAg to screen; positive beyond six months means chronic. Then HBV DNA for activity, HBeAg, anti-HBc (ever exposed) and anti-HBs (immune, from vaccine or recovery). Anti-HBs positive with HBsAg negative is protected, not infected.

Hepatitis C — anti-HCV antibody to screen, HCV RNA to confirm. Antibody positive with RNA negative is a cleared infection and needs no treatment.

Hepatitis D — anti-HDV antibody in every HBsAg-positive person, then HDV RNA if positive.

Hepatitis E — anti-HEV IgM for recent infection; HEV RNA by PCR in transplant recipients and others on immunosuppression, where antibodies may never form.

Once the virus is named, a FibroScan or ultrasound tells us whether the chronic ones have already scarred the liver. Normal enzymes are not proof of a healthy liver.

Prevention and vaccines for each type

For A and E, prevention is water. Boiled or properly filtered drinking water, no ice of unknown origin, no roadside cut fruit or chaat during the rains, hands washed with soap before eating and after the toilet. When one family member has hepatitis A or E, separate utensils are unnecessary; clean hands are not.

A safe, effective injectable hepatitis A vaccine is available in India, though it is not part of the government’s routine childhood schedule. Ask your paediatrician or physician about it, particularly for children and for adults who grew up with piped water and may have escaped childhood infection.

For hepatitis E the ground shifted this year. The HEV 239 vaccine, licensed in China since 2011, was approved by the Drug Controller General of India and launched in January 2026 for adults aged 18 to 65. It is not yet in any international guideline — EASL’s 2018 recommendations predate it — and who should receive it is a conversation to have with a physician, not a decision to make from a blog. I expect women planning pregnancy and people with cirrhosis to be the groups where it earns its place.

For hepatitis B the vaccine is the single best investment in liver health India has made. Every newborn is due a dose within 24 hours of birth, then at 6, 10 and 14 weeks; babies of HBsAg-positive mothers also receive hepatitis B immunoglobulin, which is why the programme screens every pregnant woman. An unvaccinated adult can take the course at any age, and should — it protects for at least 20 years and probably for life, and against hepatitis D in the same stroke.

For hepatitis C there is no vaccine. Prevention is single-use needles, screened blood, licensed tattoo studios, and never sharing razors or syringes. Cure is the other half of prevention: a person who has been treated cannot pass it on.

When to see a hepatologist

Most hepatitis A and E in a healthy adult needs a physician, rest and patience, not a transplant unit. But some presentations should reach a liver specialist the same day, because the window in acute liver failure is measured in hours.

Go urgently if a jaundiced person becomes drowsy, confused or unusually irritable; if there is bleeding from the gums or nose, or vomiting of blood; if a pregnant woman develops jaundice at any stage; if jaundice appears in someone with known cirrhosis, fatty liver or heavy alcohol use; or if jaundice has not begun to fade after three to four weeks. In children, drowsiness and refusal to eat matter more than the depth of the yellow.

Go soon, not urgently, if any report — pre-employment, antenatal, blood donation, pre-operative — shows HBsAg or anti-HCV positive. Both are far easier to deal with while you feel well than at the point of ascites or bleeding, and both carry implications for your spouse and children that are best handled once, properly. Our liver clinic in Mumbai sees patients from across Maharashtra and abroad for exactly this.

References

1. World Health Organization. Hepatitis A fact sheet. 28 July 2026. who.int/news-room/fact-sheets/detail/hepatitis-a
2. World Health Organization. Hepatitis B fact sheet. 28 July 2026. who.int/news-room/fact-sheets/detail/hepatitis-b
3. World Health Organization. Hepatitis C fact sheet. 28 July 2026. who.int/news-room/fact-sheets/detail/hepatitis-c
4. World Health Organization. Hepatitis D fact sheet. 28 July 2026. who.int/news-room/fact-sheets/detail/hepatitis-d
5. World Health Organization. Hepatitis E fact sheet. 28 July 2026. who.int/news-room/fact-sheets/detail/hepatitis-e
6. World Health Organization. WHO sounds alarm on viral hepatitis infections claiming 3500 lives each day (Global Hepatitis Report 2024). 9 April 2024. who.int/news/item/09-04-2024
7. Press Information Bureau, Government of India. India’s fight to combat hepatitis (National Viral Hepatitis Control Programme backgrounder). 27 July 2026. static.pib.gov.in (PDF)
8. Patra S, Kumar A, Trivedi SS, Puri M, Sarin SK. Maternal and fetal outcomes in pregnant women with acute hepatitis E virus infection. Ann Intern Med. 2007;147(1):28–33. PMID 17606958. doi:10.7326/0003-4819-147-1-200707030-00005
9. Shalimar, Kedia S, Gunjan D, et al. Acute liver failure due to hepatitis E virus infection is associated with better survival than other etiologies in Indian patients. Dig Dis Sci. 2017;62(4):1058–1066. PMID 28130708. doi:10.1007/s10620-017-4461-x
10. Shalimar, Kedia S, Mahapatra SJ, et al. Severity and outcome of acute-on-chronic liver failure is dependent on the etiology of acute hepatic insults: analysis of 368 patients. J Clin Gastroenterol. 2017;51(8):734–741. PMID 28296656. doi:10.1097/MCG.0000000000000823
11. Anand AC, Nandi B, Acharya SK, et al. Indian National Association for the Study of the Liver consensus statement on acute liver failure (Part 1): epidemiology, pathogenesis, presentation and prognosis. J Clin Exp Hepatol. 2020;10(4):339–376. PMID 32655238. doi:10.1016/j.jceh.2020.04.012
12. Kalal CR, Maiwall R, Choudhary A, et al. Mannitol is comparable to hypertonic saline for raised intracranial pressure in acute liver failure (MAHAL Study): a randomized controlled trial. Dig Dis. 2021;40(5):607–615. PMID 34763338. doi:10.1159/000520229
13. European Association for the Study of the Liver. EASL Clinical Practice Guidelines on hepatitis E virus infection. J Hepatol. 2018;68(6):1256–1271. PMID 29609832. doi:10.1016/j.jhep.2018.03.005
14. European Association for the Study of the Liver. EASL Clinical Practice Guidelines on hepatitis delta virus. J Hepatol. 2023;79(2):433–460. PMID 37364791. doi:10.1016/j.jhep.2023.05.001
15. European Association for the Study of the Liver. EASL Clinical Practice Guidelines on the management of hepatitis B virus infection. J Hepatol. 2025;83(2):502–583. PMID 40348683. doi:10.1016/j.jhep.2025.03.018
16. European Association for the Study of the Liver. EASL recommendations on treatment of hepatitis C: final update of the series. J Hepatol. 2020;73(5):1170–1218. PMID 32956768. doi:10.1016/j.jhep.2020.08.018
17. Dr. Reddy’s Laboratories. Dr. Reddy’s launches Hevaxin, a novel recombinant hepatitis E vaccine in India (press release). 6 January 2026. drreddys.com (PDF)