Hepatitis B and C Explained — How They Damage the Liver

Hepatitis B and hepatitis C together cause an estimated 1.3 million deaths a year, according to the World Health Organization (WHO), and most of those deaths are preventable. Hepatitis B has had a safe vaccine since the 1980s. Hepatitis C became curable with a short course of pills after 2013. Yet most people carrying either virus do not know it, because both can smolder in the liver for decades without a single symptom. This article explains what the two viruses are, how they get into liver cells, why the damage builds so slowly, and why one of them can now be cured while the other can only be held in check.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. Information here reflects current research, but every person's situation differs.

Five hepatitis viruses, five different families

"Hepatitis" simply means inflammation of the liver. Many things can cause it, including alcohol, certain drugs, and autoimmune disease, but five unrelated viruses are named hepatitis A through E because they all target liver cells. They share a letter scheme, not a family tree.

Virus	Genetic material	Main route of spread	Chronic infection?	Vaccine?
Hepatitis A (HAV)	RNA (picornavirus)	Contaminated food and water	No	Yes
Hepatitis B (HBV)	Partly double-stranded DNA (hepadnavirus)	Blood, semen, mother to child	Yes	Yes
Hepatitis C (HCV)	RNA (flavivirus family)	Blood	Yes, in most cases	No
Hepatitis D (HDV)	Circular RNA, needs HBV	Blood, alongside HBV	Yes	Indirectly, through the HBV vaccine
Hepatitis E (HEV)	RNA (hepevirus)	Contaminated food and water	Rarely	Yes, in some countries

WHO notes that hepatitis A and E are most common where clean water is scarce, are usually mild, and that safe, effective vaccines exist for both (WHO, hepatitis overview). The three bloodborne viruses, B, C, and D, are the ones that cause lifelong infection. B and C account for nearly all of the deaths, so they get the rest of this article.

Hepatitis C belongs to the same broad virus family as dengue and yellow fever, which gives it a cousinship that explains some of its RNA biology. For a general primer on how any virus enters a cell and copies itself, see how viruses work from infection to replication.

The scale of the problem in 2026

WHO's most recent fact sheets give the following figures for 2024. For hepatitis B, 240 million people were living with chronic infection and about 1.1 million died, mostly from cirrhosis (advanced scarring) and hepatocellular carcinoma (the most common form of primary liver cancer). For hepatitis C, about 47 million people had chronic infection and roughly 239,000 died (WHO hepatitis B fact sheet; WHO hepatitis C fact sheet).

Older sources quote different totals, because WHO revises its modeling between reports. Comparisons across WHO reports therefore need care, and the 2024 figures above should not be read as a sudden fall in disease.

Two numbers matter more than the totals. Only 27% of people with hepatitis B knew their status in 2024, and only about 4.3% of those with chronic hepatitis B were on treatment (WHO). The viruses are not defeating medicine. They are slipping past it because nobody is looking.

Hepatitis B: a DNA virus that works like a retrovirus

HBV is among the smallest enveloped viruses that infect animals, about 42 nanometers across. Its genome is a tiny loop of DNA a little over 3,000 nucleotides long, which is minuscule next to the 3.1 billion base pairs in a human cell. It is a DNA virus with an unusual habit: to make copies of itself it passes through an RNA stage and then reverse-transcribes that RNA back into DNA, the same trick HIV uses.

That detour is the whole story of why hepatitis B is so persistent. The best analogy is a print shop that keeps its master printing plate in a vault. The shop can be shut down for months, but as long as the plate survives, it can restart production at any time.

How HBV gets into a liver cell

The virus needs a doorway, and in 2012 a team led by Wenhui Li found it. Working with tree shrew liver cells, they showed that a bile-acid transporter called NTCP (sodium taurocholate cotransporting polypeptide) is a functional receptor for hepatitis B and for hepatitis D (Yan et al., eLife, 2012). NTCP normally pulls bile salts out of the blood into liver cells. HBV has learned to ride in on it.

That finding helps explain why HBV targets the liver almost exclusively: NTCP is concentrated on the surface of hepatocytes (liver cells). It also gave drug developers a concrete target, since a drug that blocks NTCP could in principle keep the virus out.

The vault: cccDNA

Once inside, the viral DNA travels to the cell nucleus. Cellular repair enzymes convert the incomplete viral genome into a closed, fully double-stranded loop called covalently closed circular DNA, or cccDNA. Inside the nucleus, cccDNA behaves much like a miniature chromosome, and the cell's own machinery reads it to produce viral RNAs.

Those RNAs then do two jobs. Some are translated into viral proteins, including the surface protein HBsAg that blood tests detect. One long RNA, the pregenomic RNA, is packaged into a new capsid and reverse-transcribed into DNA by the viral polymerase. Fresh particles are then wrapped in an envelope and released.

Current antiviral drugs act on the reverse-transcription step. They stop new virus particles from forming, so the amount of virus in the blood can fall below the level a test can detect. They do not touch the cccDNA already sitting in the nucleus. That is why stopping treatment often lets the virus rebound, and why the standard drugs are described as suppressive rather than curative.

HBV DNA can also splice itself into the host's chromosomes. Integrated fragments cannot make complete new virus, but they can keep producing HBsAg and may disturb the genes around them. Researchers think this is one reason hepatitis B can lead to liver cancer even in people whose livers have not yet become cirrhotic.

Age at infection decides whether HBV becomes chronic

Hepatitis B behaves differently depending on how old you are when you catch it. WHO reports that chronic infection develops in fewer than 5% of adults who are infected, but in about 95% of infections acquired in infancy or early childhood (WHO).

Age at infection	Chance of chronic infection	Why
Infancy or early childhood	About 95%	The immature immune system tolerates the virus rather than clearing it
Adulthood	Under 5%	A mature immune response usually clears the virus within six months

The explanation is immunological. A newborn's immune system is trained to avoid overreacting to the unfamiliar molecules it meets, including those carried by its mother. When HBV arrives during that window, the immune system tends to accept it as part of the landscape. That is why mother-to-child transmission is the most important route in regions where hepatitis B is common, and why the birth dose of vaccine matters so much.

Most infected adults feel nothing or have a mild flu-like illness. When acute symptoms do appear, the CDC lists dark urine, clay-colored stools, fatigue, fever, joint pain, nausea, abdominal pain, and jaundice (yellowing of the skin and eyes), typically beginning around 90 days after exposure (CDC, About hepatitis B).

The five phases of chronic hepatitis B

Chronic HBV is not a single steady state. The European Association for the Study of the Liver (EASL) 2017 guidelines describe five phases, defined by three measurements: whether the e antigen (HBeAg, a secreted viral protein) is present, how much HBV DNA is in the blood, and the level of the liver enzyme ALT, which leaks out of damaged liver cells (EASL 2017 guidelines).

Phase	Name	Typical pattern
I	HBeAg-positive chronic infection	High HBV DNA, normal ALT, little or no liver injury
II	HBeAg-positive chronic hepatitis	High HBV DNA, raised ALT, active inflammation, progressive scarring
III	HBeAg-negative chronic infection	Low viral load, normal ALT (formerly the "inactive carrier" state)
IV	HBeAg-negative chronic hepatitis	Detectable virus, raised ALT, ongoing liver injury
V	HBsAg-negative phase	Surface antigen gone, though low-level viral DNA may persist

The guidelines stress that people do not move through these phases in a fixed order, and some fall in a gray zone between them. Doctors therefore repeat tests over time before deciding whether to treat. As a general rule, EASL's criteria point toward treatment when viral DNA is above 2,000 IU/mL together with raised ALT or moderate liver injury on biopsy, and when a person with cirrhosis has detectable virus.

Reading a hepatitis B blood test

Hepatitis B diagnosis relies on a small set of antigen and antibody markers. Reading them together is like reading a three-gauge dashboard.

HBsAg	Total anti-HBc	Anti-HBs	Usual interpretation
Negative	Negative	Negative	Never infected, not vaccinated (susceptible)
Negative	Negative	Positive	Immune through vaccination
Negative	Positive	Positive	Immune after a resolved natural infection
Positive	Positive	Negative	Infected; further tests separate acute from chronic
Negative	Positive	Negative	Ambiguous; past infection, a false positive, or low-level infection

HBsAg is the virus's surface protein, so its presence means active infection. Anti-HBs is the protective antibody, the one a vaccine teaches the body to make. Anti-HBc is an antibody to the viral core, which appears only after real infection, never after vaccination. CDC defines chronic infection as being unable to clear the virus within six months (CDC), and it recommends that all adults be tested at least once in their lifetime, with more frequent testing for pregnant women in each pregnancy and others with ongoing exposure.

For background on how antibodies recognize their targets, see antibody structure and immune defense.

The hepatitis B vaccine

The first hepatitis B vaccines, introduced in the early 1980s, were made from the blood plasma of chronic carriers. They were effective, but the supply was limited and people understandably worried about their source. They were replaced by a recombinant vaccine, in which the gene for the surface protein is inserted into yeast cells that manufacture the protein in vats.

Because the vaccine contains only a harmless fragment of the virus, it cannot cause infection. WHO says protection lasts at least 20 years and probably for life, so boosters are generally not needed. The standard schedule is a birth dose within 24 hours of delivery followed by two or three further doses at least four weeks apart. CDC recommends vaccination for all infants, for children and adolescents younger than 19 who have not been vaccinated, for adults aged 19 to 59, and for older adults with risk factors.

What the Taiwan data show

Taiwan began a national newborn vaccination program in July 1984, which gave researchers an early look at what mass vaccination does. In a 1997 paper in the New England Journal of Medicine, Mei-Hwei Chang and colleagues analyzed registry data on liver cancer in children. Among children aged 6 to 14, the average annual incidence of hepatocellular carcinoma fell from 0.70 per 100,000 in 1981 to 1986, to 0.57 in 1986 to 1990, and to 0.36 in 1990 to 1994 (Chang et al., NEJM, 1997). Among children aged 6 to 9, the rate dropped from 0.52 per 100,000 in those born in 1974 to 1984 to 0.13 in those born in 1984 to 1986.

The study was observational, so it shows an association, not a controlled proof. But the size of the effect, and the fact that other childhood cancers did not change, is why the hepatitis B vaccine is widely described as one of the first vaccines to prevent a cancer. The more widely known human papillomavirus vaccine works on the same principle; see HPV explained. For the wider history of immunization, see how vaccines were invented and the polio vaccine story.

The mechanism behind vaccine protection is the same as for any other vaccine: the immune system builds memory cells that respond within hours of a real exposure. How vaccines train memory B cells walks through that process.

Treating hepatitis B: control without cure

WHO recommends two oral antivirals as the backbone of treatment for chronic hepatitis B: tenofovir and entecavir. Both are nucleos(t)ide analogues, molecules that resemble the building blocks of DNA closely enough that the viral polymerase picks them up and stalls. They are taken daily, often for years or for life, and they are very good at driving viral DNA in the blood to undetectable levels and slowing liver damage.

Pegylated interferon is the alternative. It is an injected protein that boosts the immune response, given for a fixed period, often 48 weeks, and helps a minority of patients clear the surface antigen. Side effects such as flu-like symptoms, fatigue, and mood changes make it a harder choice.

The gap between the tools and the need is large. In 2024 only about 10 million people, 4.3% of those with chronic infection, were on treatment. WHO's 2024 guidelines broaden eligibility, and the agency estimates that more than half of people with chronic infection will qualify for treatment depending on setting.

Why a true cure is hard and what a "functional cure" means

With today's drugs, patients who lose HBsAg and stay well off treatment are uncommon. Researchers therefore talk about a functional cure: undetectable HBV DNA and undetectable HBsAg for at least 24 weeks after all treatment stops. It is a lower bar than eliminating every viral genome, since cccDNA and integrated fragments may remain, but it describes a state in which the virus is silent and the patient no longer needs drugs.

In 2026 the first late-stage data for a drug aimed at that target appeared. Bepirovirsen, an antisense drug developed by Ionis and GSK that is designed to bind viral RNA, was tested in two phase 3 trials, B-Well 1 and B-Well 2, in adults who were already taking a nucleos(t)ide analogue and had HBsAg of 3,000 IU/mL or less. After six months of treatment, 19% of pooled bepirovirsen recipients (233 of 1,220) had a functional cure 24 weeks after stopping, compared with none of 614 on placebo. In people with HBsAg at or below 1,000 IU/mL at the start, the figure was 26% (HCPLive summary of the NEJM paper by Hou et al.).

Two cautions apply. Most participants did not reach functional cure, and the 26% figure comes from a subgroup defined by starting antigen level. Experts quoted in coverage of the trials also said the durability of the response needs longer follow-up. The US Food and Drug Administration (FDA) accepted the application for priority review with an action date of October 26, 2026, so a regulatory decision is imminent as this article is updated. Until a drug is approved and tracked in practice, hepatitis B remains a condition managed rather than cured.

Hepatitis D: the satellite that needs hepatitis B

Hepatitis D virus is a small, circular RNA virus that cannot assemble itself without the envelope proteins of HBV. WHO states that hepatitis D infection cannot occur in the absence of hepatitis B. About 5% of people with chronic hepatitis B, an estimated 12 million people, are also infected with HDV (WHO hepatitis D fact sheet).

Chronic hepatitis D is considered the most severe form of chronic viral hepatitis, progressing faster to liver failure and cancer. For years the only option was pegylated interferon, which helped only a minority of treated patients, with frequent relapse. The European Medicines Agency approved bulevirtide, a drug that blocks the NTCP doorway the virus uses, in 2023 for adults with compensated liver disease. The HBV vaccine also prevents HDV, because without HBV the satellite virus has nowhere to live.

Hepatitis C: the virus that can be cured

Hepatitis C virus carries a single strand of RNA inside an enveloped particle, and its genome is considerably longer than HBV's tiny loop. Seven major genotypes exist, each with several subtypes. Unlike HBV, it never writes itself into the cell's DNA and has no nuclear vault. Everything it does happens in the cytoplasm, the fluid outside the nucleus, and that single fact is why a cure is possible. If drugs can stop replication long enough for infected cells to turn over, there is no hidden template left to reignite the infection.

How HCV infects a liver cell

HCV enters hepatocytes by binding several surface proteins at once, including CD81, SR-BI, claudin-1, and occludin, and then being engulfed in a bubble of membrane. Once inside, the genome acts directly as messenger RNA. The cell's ribosomes read it and make one long protein, which viral and cellular enzymes cut into the structural and nonstructural proteins the virus needs.

Those pieces rebuild the cell's internal membranes into replication factories. New viral RNA is copied there, and new particles assemble near fat droplets, with the virus borrowing the cell's lipid-handling machinery to travel out as a particle coated in lipoproteins. This tight link with fat metabolism is one reason hepatitis C and fatty liver disease can interact.

The viral polymerase has no proofreading function, so copying errors are frequent. Within a single infected person the virus exists as a cloud of closely related variants. This is the main reason attempts at a vaccine have failed so far: the immune system and any vaccine-induced antibodies chase a moving target.

Discovery: the hunt for the missing virus

By the 1970s, researchers led by Harvey Alter at the US National Institutes of Health had shown that most hepatitis that followed blood transfusions was caused by neither hepatitis A nor B. For about a decade, this "non-A, non-B hepatitis" had no identified cause. In 1989, a team at the Chiron Corporation led by Michael Houghton reported the cloning of the virus, and a blood test followed.

The impact on transfusion safety was dramatic. The Lasker Foundation notes that screening methods built on the discovery lowered the risk of transfusion-linked hepatitis in the United States from 30% in 1970 to "virtually zero" in 2000 (Lasker Foundation). Charles Rice later helped build the lab system that let researchers study how the virus replicates, a system later used to develop treatment. Alter, Houghton, and Rice shared the 2020 Nobel Prize in Physiology or Medicine.

How often HCV turns chronic

WHO states that about 70% of people exposed to hepatitis C develop chronic infection (range 55% to 85%), while about 30% clear the virus within six months without treatment. Among those with chronic infection, 15% to 30% develop cirrhosis within 20 years (WHO hepatitis C fact sheet).

Acute infection often passes unnoticed. Fatigue and a vague malaise are common, and jaundice is uncommon, so a large share of people discover the infection only through a routine screening test or after liver damage has built up.

The direct-acting antiviral revolution

Before 2011, hepatitis C treatment meant 24 to 48 weeks of weekly interferon injections plus ribavirin, a drug taken by mouth. Cure rates were well below those of modern drugs, and the side effects included severe fatigue, anemia, and depression. Many people with advanced disease could not tolerate the regimen at all.

The turning point was a new class called direct-acting antivirals, or DAAs. Instead of stimulating the immune system, they hit the virus's own enzymes. Three targets matter:

• NS3/4A protease, the scissors that cut the long viral protein into usable pieces.
• NS5A, a protein that organizes replication and assembly.
• NS5B polymerase, the enzyme that copies viral RNA. Sofosbuvir, approved by the FDA in late 2013, is a nucleotide analogue that jams this enzyme.

Giving two or three DAAs together works like locking a door with several bolts at once. The virus would need simultaneous resistance mutations at each target, which is far rarer than a single mutation. The same logic transformed HIV treatment.

Regimen (brand)	Targets	Typical course
Sofosbuvir plus velpatasvir (Epclusa)	NS5B plus NS5A	12 weeks, effective across genotypes
Glecaprevir plus pibrentasvir (Mavyret)	NS3/4A plus NS5A	8 weeks for many people without cirrhosis

The CDC says that most treatments involve 8 to 12 weeks of oral medication, cure more than 95% of patients, and usually cause few side effects (CDC, About hepatitis C). WHO adds that in many low- and middle-income countries a curative course of sofosbuvir and daclatasvir costs less than US$50, and that treatment is usually 12 to 24 weeks depending on whether cirrhosis is present. Exact regimens and durations depend on genotype, prior treatment, and liver status, which is why doctors follow guidelines such as those from the American Association for the Study of Liver Diseases.

What "cured" means

Doctors measure cure as a sustained virologic response, or SVR: no detectable HCV RNA in the blood 12 weeks after treatment ends. After SVR, relapse is rare, and the infection is considered eliminated. It does not leave lasting protection. The CDC notes that people who have cleared the virus or been cured can be infected again, so someone with ongoing exposure, such as sharing injection equipment, remains at risk.

Cure also does not rewind all the damage. If a liver was already cirrhotic, the scarring may improve somewhat but often does not vanish, and the risk of liver cancer, though reduced, does not return to zero. People with cirrhosis therefore usually continue to be monitored after cure.

A safety note: hepatitis B reactivation

A subtle problem surfaced soon after DAAs reached the market. In 2016, the FDA required a boxed warning, its strongest label warning, after reports of hepatitis B reactivation, some of them serious, in patients treated with HCV DAAs. The likely reason is that HCV and HBV suppress one another inside the liver. When the dominant virus is removed, a quiet cccDNA reservoir can wake up. The practical consequence is that anyone starting DAAs is now screened for hepatitis B first.

How hepatitis B and C spread

Both viruses travel in blood and certain body fluids, and a microscopic amount can be enough. The routes differ in proportion.

Route	Hepatitis B	Hepatitis C
Mother to child at birth	Dominant route where HBV is common	Possible, less common
Sharing injection equipment	Yes	Main route in many high-income countries
Unsafe medical injections or unscreened blood	Yes	Yes
Sex	Yes, via semen	Less common
Casual contact (hugging, sharing food, kissing, coughing)	No	No

CDC states that HBV is not spread by kissing, sharing utensils, sneezing, coughing, hugging, breastfeeding, or food or water, and that there is no evidence HCV spreads through utensils, hugging, kissing, holding hands, coughing, or sneezing. In the US, CDC data show that 43% of acute hepatitis C cases with known risk information in 2023 were associated with injection drug use (CDC). WHO identifies unsafe health-care injections and unscreened transfusions as major routes in other settings.

Blood screening has largely closed the transfusion route in countries that test donations. The remaining burden comes from injection equipment, birth, and unsafe medical procedures.

Why liver damage builds so slowly

Neither virus kills liver cells very efficiently by itself. Most of the harm comes from the immune system doing its job too long. T cells recognize infected hepatocytes by the viral fragments displayed on their surfaces, and kill them. Meanwhile the liver, which has a remarkable ability to regrow, replaces them.

Picture a forest that burns lightly every year. Each fire is survivable, and the trees come back. After decades of fires, though, the soil changes, the character of the forest changes, and tough scar-like growth replaces what grew before. In the liver that growth is fibrous scar tissue, and the process runs like this:

1. Chronic inflammation kills infected cells, and regeneration replaces them.
2. Scar tissue (fibrosis) accumulates in the spaces between liver cells.
3. Fibrosis spreads until it distorts the liver's architecture. This is cirrhosis.
4. A cirrhotic liver cannot filter blood or make clotting factors and proteins well. Complications include fluid buildup, bleeding from swollen veins, and confusion from toxins that build up in the blood.
5. Repeated cycles of cell death and regrowth raise the risk of a cell acquiring a cancer-causing mutation.

For a deeper look at the organ itself, see how the liver works, and for what the cancer step involves, what causes cancer. The immune side of the story, how killer T cells identify infected cells, is covered in how the immune system fights viruses step by step.

Hepatitis B has one extra route to cancer. Because the viral DNA can integrate into liver cell chromosomes and the viral protein HBx can alter host gene regulation, HBV can drive liver cancer without prior cirrhosis. Hepatitis C cancers, by contrast, mostly arise in livers that are already cirrhotic, which is why people with cirrhosis from either virus are usually offered regular liver ultrasound surveillance.

How the two viruses compare

Feature	Hepatitis B	Hepatitis C
Genome	Partly double-stranded DNA, roughly 3,000 nucleotides	Single-stranded RNA, considerably longer
Persistent nuclear reservoir	Yes (cccDNA)	No
Vaccine	Yes, highly effective	None
Cure	Rare with current drugs; functional cure under study	More than 95% with DAAs
Chronic infection after exposure	Under 5% in adults, about 95% in infants	About 70% overall
People with chronic infection (WHO, 2024)	240 million	About 47 million
Deaths (WHO, 2024)	About 1.1 million	About 239,000
Treatment uptake (WHO, 2024)	About 10 million people, 4.3% of those with chronic infection	About 13 million had received DAAs by the end of 2024
Main route	Mother to child, blood, sex	Blood, especially injection equipment

Hepatitis B is more common and more deadly, but it can be prevented. Hepatitis C is rarer and cannot be prevented by vaccine, but it can be cured. The two diseases therefore call for different public health strategies: universal infant vaccination for one, and widespread testing plus cheap generic drugs for the other.

The diagnostic gap and the 2030 targets

The biggest obstacle is not scientific. WHO estimates that 27% of people with hepatitis B knew their status in 2024. For hepatitis C, about 68 million people were infected at some point between 2015 and 2024, and only 36% of them knew their diagnosis, about 24 million. By the end of 2024 around 13 million had received DAAs, and 11 million diagnosed people had not yet started treatment (WHO hepatitis C fact sheet).

In the United States, CDC estimates that about 640,000 adults live with chronic hepatitis B, and about half of people with hepatitis B do not know they are infected. For hepatitis C, an estimated 2.4 million to 4 million people were infected from 2017 to 2020. CDC recommends testing for all adults at least once, for all pregnant women (HCV in each pregnancy, HBV in each pregnancy), and for anyone recently exposed.

WHO's 2022 to 2030 strategy sets out ambitious goals, measured against 2015: a 90% reduction in new infections, to 520,000 per year, and a 65% reduction in deaths, to 450,000 per year (WHO, hepatitis topic page). For hepatitis B in children, the target is chronic infection prevalence of 0.1% in under-fives by 2030. WHO puts the 2024 figure at 0.6%, but the African region sits at 1.4%.

Each virus has a different path to the finish line. For hepatitis C, nothing scientific is missing: the pills exist, and costs have fallen to a point where a course can be bought for under US$50 in many countries. What is missing is testing and linkage to care. For hepatitis B, vaccination and early treatment can shrink new infections, but a true cure is the remaining scientific hurdle.

Common misunderstandings

"Hepatitis is spread by casual contact." Hepatitis A and E spread through contaminated food and water, but B and C do not spread through hugging, shared meals, or sneezing. The bloodborne viruses need blood or certain body fluids to reach the bloodstream.

"If I feel fine, I'm fine." Chronic infection with either virus often produces no symptoms for decades. Fatigue, jaundice, and swelling arrive late, when the liver is already damaged.

"Hepatitis C is incurable." That was true before 2013. It is no longer true. More than 95% of people who complete DAA therapy are cured.

"A cure means I can't catch it again." HCV cure does not confer immunity, and reinfection is possible.

"The hepatitis B vaccine is only for infants." CDC recommends it for adults aged 19 to 59 and for older adults at higher risk.

"All liver cancer comes from alcohol." Alcohol is a major cause, but chronic hepatitis B and C are leading causes worldwide, which is why vaccination and testing double as cancer prevention.

The takeaway

Hepatitis B and hepatitis C attack the same organ and spread through the same bodily fluids, but their biology sets them on opposite tracks. B hides a copy of its genome in the nucleus, which makes it controllable and preventable but hard to cure. C lives entirely in the cytoplasm, which makes a vaccine impossible so far, but lets three drugs working together erase it within weeks. What both share is time: they damage the liver slowly enough that a single blood test, taken years before symptoms, can change the outcome. The tools to prevent most hepatitis B deaths and cure nearly all hepatitis C already exist, and the open question is how quickly testing reaches the people who need it.

Frequently Asked Questions

Q: Should I get tested for hepatitis B and C? A: CDC recommends that all adults be tested for hepatitis B and for hepatitis C at least once in their lifetime, and that pregnant women be tested during each pregnancy. People with ongoing exposure may need more frequent testing. Because both infections are usually silent for decades, testing is the only reliable way to know.

Q: How is hepatitis B diagnosed? A: A blood panel measures HBsAg (a sign of current infection), anti-HBs (protective antibody, from vaccination or recovery), and total anti-HBc (a sign of past or current infection). In people with chronic infection, HBV DNA quantifies the viral load, and liver enzymes and imaging show whether the liver is being damaged.

Q: How is hepatitis C diagnosed? A: Screening starts with an HCV antibody test. If it is positive, an HCV RNA test shows whether the infection is still active, because some people clear the virus on their own but remain antibody-positive for life. Q: I was vaccinated against hepatitis B as a baby. Am I still protected? A: Probably yes. WHO says protection lasts at least 20 years and likely for life, and routine boosters are not generally recommended for people with healthy immune systems. If you are in a high-risk group, or work in health care, a doctor can check your antibody level.

Q: Can hepatitis C be cured permanently? A: In more than 95% of people, yes. A sustained virologic response, meaning no detectable virus 12 weeks after treatment ends, is considered a cure. A cured person can be reinfected through a new exposure, and anyone with cirrhosis still needs follow-up because the scarring and liver cancer risk may persist.

Q: Can hepatitis B be spread by kissing? A: CDC says hepatitis B is not spread through kissing or sharing utensils, although the virus can be found in saliva. The relevant routes are blood, semen, and birth.

Q: Why is there no hepatitis C vaccine? A: The virus mutates quickly, with a polymerase that makes frequent copying errors, so antibodies aimed at one variant often miss others. Candidate vaccines have so far not produced reliable protection in people. Because modern drugs cure most patients, the urgency for a vaccine has also been lower than it was for hepatitis B.

Q: What does cirrhosis mean for life expectancy? A: It depends heavily on the stage and the cause. Compensated cirrhosis, in which the liver still performs its main jobs, can remain stable for years, especially once the underlying virus is controlled. Decompensated cirrhosis, marked by fluid buildup, bleeding, or confusion, is far more serious and may call for a transplant evaluation. A hepatologist can give a person-specific outlook.

Sources

• WHO. Hepatitis B fact sheet; Hepatitis C fact sheet; Hepatitis D fact sheet; Hepatitis overview and 2030 targets.
• CDC. About hepatitis B; About hepatitis C.
• Yan H, et al. Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus. eLife, 2012. Link.
• Chang MH, et al. Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children. N Engl J Med, 1997;336:1855-1859. Record.
• European Association for the Study of the Liver. EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection. J Hepatol, 2017;67:370-398. Record.
• Hou JL, et al. Phase 3 results of bepirovirsen treatment for chronic hepatitis B virus infection. N Engl J Med, 2026. Summary.
• Lasker Foundation. 2020 Nobel Prize in Medicine.

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