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Hepatitis C is now curable in 8–12 weeks. Hepatitis B can be suppressed for life, preventing cirrhosis and liver cancer. If you are HBsAg or HCV-positive, do not wait — treatment works best before fibrosis advances.
Hepatitis B is caused by a DNA virus (HBV). India is a high-prevalence country, with most infections acquired at birth (vertical transmission) or in early childhood. Chronic HBV carries a lifetime risk of cirrhosis (15–40%) and hepatocellular carcinoma (HCC, 2–5% per year in cirrhotic patients).
Not all HBsAg-positive people are the same. Your phase determines whether you need treatment now, soon, or monitoring only.
| Phase | HBeAg | HBV DNA | ALT | Liver Damage | Action |
|---|---|---|---|---|---|
| Immune Tolerant | + | Very high | Normal | Minimal | Monitor; treatment criteria evolving |
| Immune Active (HBeAg+) | + | High | Elevated | Active | Treat |
| Inactive Carrier | − | Low/undetectable | Normal | Minimal | Monitor 6-monthly |
| HBeAg-negative hepatitis | − | Moderate-high | Elevated | Active | Treat |
| Cirrhotic | ± | Any level | Variable | Advanced | Treat regardless of DNA level |
Hepatitis C (HCV) is an RNA virus transmitted through blood-to-blood contact. Unlike HBV, HCV has no vaccine — but unlike HBV, it can be cured. India's most common genotypes are Genotype 1, 3, and 4. Modern DAAs are pan-genotypic — they work against all genotypes without needing to know yours.
All HCV RNA-positive patients should be treated — regardless of fibrosis stage. There is no benefit to waiting.
| Regimen | Duration | Genotype | Note |
|---|---|---|---|
| Sofosbuvir + Velpatasvir (Epclusa) | 12 weeks | All genotypes | Pan-genotypic, preferred first-line |
| Glecaprevir + Pibrentasvir (Mavyret) | 8 weeks | All genotypes | Non-cirrhotic patients; 12 weeks with cirrhosis |
| Sofosbuvir + Daclatasvir | 12–24 weeks | 1, 2, 3, 4 | Widely affordable; effective in India context |
| Ledipasvir + Sofosbuvir | 12 weeks | Genotype 1, 4 | Genotype-specific; less commonly used now |
SVR12 rate with modern DAAs: >95% in non-cirrhotic; 90–95% in compensated cirrhosis.
Acute viral hepatitis from contaminated food and water. Self-limiting — resolves in 4–8 weeks with supportive care. Does not cause chronic infection. However, Hepatitis A superimposed on pre-existing liver disease (e.g., HBV cirrhosis) can cause acute-on-chronic liver failure requiring ICU care. Vaccine available and recommended for all children and at-risk adults.
Hepatitis D virus (HDV) can only infect patients who already have Hepatitis B — it requires HBV to replicate. Coinfection (HBV + HDV simultaneously) is usually self-limiting. Superinfection (HDV in a chronic HBV carrier) causes rapid cirrhosis progression. Bulevirtide is the first approved HDV treatment. Vaccination against HBV prevents HDV infection.
Acute infection from contaminated water, especially during monsoon flooding. Usually self-limiting in 4–6 weeks. However, in pregnant women (especially third trimester), HEV can cause fulminant hepatic failure with mortality up to 25%. Immunocompromised patients (post-transplant, HIV) can develop chronic HEV infection. No approved antiviral in India; supportive care, ribavirin in select cases.
Most patients have no symptoms for years. Screening catches disease at the treatable stage.
HBsAg, HBeAg, Anti-HBe, HBV DNA quantification (for HBV). Anti-HCV, HCV RNA, HCV genotype (for HCV). Plus LFTs, CBC, INR, albumin, and HBsAb status in contacts.
Fibroscan elastography (available at Dhaara Liver Clinic) gives fibrosis stage F0–F4 without biopsy. Liver biopsy when Fibroscan is inconclusive or when biopsy changes management. FIB-4 score as initial triage.
For HBV: treat if criteria met, otherwise monitor 6-monthly. For HCV: all RNA-positive patients should be treated — choose DAA regimen based on cirrhosis status, co-medications, and affordability.
HBV DNA at 3 months, 6 months, 12 months to confirm viral suppression. HCV RNA at week 4 and 12 weeks post-treatment (SVR12) to confirm cure. Resistance testing when breakthrough occurs.
6-monthly liver ultrasound + AFP for all cirrhotic patients; for HBV patients with high-risk features (age >40, family history, high DNA history); for HCV patients with F3–F4 fibrosis even after cure. Liver cancer caught at stage 1 is curable.
The 3-dose series (0, 1, 6 months) gives >95% protection. Check anti-HBs after vaccination — a level >10 IU/L confirms immunity.
There is currently no vaccine for HCV. Prevention depends on avoiding blood-to-blood exposure: ensure sterilised instruments at dental, surgical, and barber procedures; never share razors, blades, or nail equipment; use sterile needles.
Strongly recommended for all adults with pre-existing liver disease (HBV, HCV, MASLD, cirrhosis). HAV superinfection on chronic liver disease can be fatal. Two-dose vaccine series at 0 and 6–12 months.
Yes — Hepatitis C is now one of the most curable chronic viral infections in medicine. Modern Direct Acting Antiviral (DAA) tablets achieve cure rates above 95% in just 8–12 weeks. Cure means SVR12: undetectable HCV RNA in your blood 12 weeks after completing treatment. Once achieved, the virus is gone permanently. The liver gradually recovers, cirrhosis risk drops by 90%, and liver cancer risk by 75%. All HCV RNA-positive patients should be treated without delay — there is no good reason to wait.
Complete cure — defined as loss of HBsAg from the blood — occurs in fewer than 5% of treated patients. However, antiviral therapy (Tenofovir or Entecavir) suppresses HBV DNA to undetectable levels, which effectively halts the disease. With HBV DNA suppressed: cirrhosis stops progressing, liver cancer risk drops by 70–80%, liver function improves, and life expectancy approaches normal. Treatment is typically lifelong but involves a single daily tablet with minimal side effects. Think of it as managing HBV the way we manage blood pressure — not a cure, but complete control.
Not necessarily right now, but you do need a proper specialist assessment. Normal ALT does not mean safe — many people in the "immune tolerant" or "inactive carrier" phase have normal enzymes but active viral replication and ongoing liver injury. You need HBV DNA quantification, HBeAg/Anti-HBe testing, and Fibroscan to determine your exact phase. Treatment is indicated if DNA is high and fibrosis exists, even with normal ALT. Inactive carriers need 6-monthly monitoring. Never assume you are "safe" based only on normal LFTs.
Yes — this is urgent and important. HBV spreads through blood, sexual contact, and from mother to child during birth. All household contacts (spouse, children, parents, siblings sharing the same home) and sexual partners should be tested for HBsAg and anti-HBs immediately. Anyone who tests negative and has no anti-HBs (no immunity) should receive the 3-dose Hepatitis B vaccine series (0, 1, 6 months). This single action prevents transmission and potentially saves your family members from developing chronic hepatitis, cirrhosis, and liver cancer.
HCC (hepatocellular carcinoma) surveillance means 6-monthly liver ultrasound plus AFP blood test to detect liver cancer at an early, curative stage. It is essential for: all HBV or HCV patients with cirrhosis; HBV-infected men over 40 years with high viral load; HBV patients with a family history of HCC; HCV patients who had fibrosis stage F3–F4 at treatment, even after cure. Liver cancer found at 1–2 cm can be cured with ablation or resection. Found at stage 3–4 (which typically causes symptoms), treatment options are very limited. Surveillance literally saves lives — never skip it.
No. Hepatitis C requires blood-to-blood contact to transmit. It cannot spread through: toilet seats, hugging, kissing, sneezing, coughing, sharing plates or glasses, food or water. Common transmission routes in India: unsterilised medical, dental, or barber instruments; shared razors at home; blood transfusions before 1992; tattooing with unclean needles; needlestick injuries. HCV is very rarely transmitted sexually (in heterosexual couples without other risk factors). If you have been diagnosed, your household members do not need to be isolated — but do not share razors or nail cutters.
Yes — there is no lasting immune protection after HCV infection or cure. You can be reinfected if re-exposed. However, your cure is real — the virus from your original infection is permanently gone, and your liver damage risk from that infection has stopped. Post-cure, you should continue HCC surveillance if you had significant fibrosis. Avoid re-exposure by ensuring sterilised instruments at all medical and dental procedures and not sharing sharp personal items. Reinfection is rare if you follow standard precautions.
Yes — HBV/HCV coinfection occurs, most often in people with a history of blood transfusions, injection drug use, or high-risk procedures. Coinfection accelerates liver damage more than either infection alone. Importantly, starting HCV DAA treatment in a coinfected patient can cause HBV reactivation — a potentially serious event. HBV DNA must be monitored throughout HCV treatment, and HBV antiviral therapy may need to run concurrently. This requires specialist hepatology management, not self-treatment.