General Virology & Hepatitis Viruses: Structure to Disease

Viruses are obligate intracellular parasites: a packet of nucleic acid wrapped in a protein capsid, sometimes with a lipid envelope, that can only replicate inside a living cell. The hepatitis viruses A through E all inflame the liver, yet they could hardly be more different: A and E spread through contaminated food and water and never become chronic, while B, C and D spread through blood and sex and can smoulder for decades into cirrhosis and liver cancer.

This matters because viral hepatitis kills over a million people a year worldwide, mostly through chronic hepatitis B and C, while hepatitis B vaccine and hepatitis C cure are among medicine's greatest victories.

Key Concepts

• Virion structure: nucleic acid (DNA or RNA, single or double stranded) plus capsid, with or without an envelope stolen from the host cell; envelopes make viruses vulnerable to soap and disinfectants.
• Replication cycle: attachment, penetration, uncoating, genome replication, assembly and release; antivirals block specific steps.
• Hepatitis A: picornavirus, faeco-oral spread, acute self-limiting illness, never chronic; vaccine available.
• Hepatitis B: hepadnavirus with partially double-stranded DNA; spreads by blood, sex and birth; can become chronic; markers are HBsAg (infection), anti-HBs (immunity, protective at 10 mIU per mL or more), anti-HBc (past or current infection) and HBeAg (high infectivity).
• Hepatitis C: flavivirus with single-stranded RNA; blood-borne; most infections become chronic but direct-acting antivirals cure over 95 percent in 8 to 12 weeks; no vaccine.
• Hepatitis D: defective virus that can only replicate inside someone already infected with hepatitis B.
• Hepatitis E: faeco-oral like A, but can cause fulminant liver failure in pregnant women.

How It Works

1. A blood sample is tested for HBsAg; positive means current hepatitis B infection.
2. Anti-HBs is checked; positive without HBsAg means immunity from vaccine or past recovery.
3. Anti-HBc IgM positive indicates acute infection, while IgG alone indicates past infection.
4. HBeAg positive signals high viral replication and high infectivity; anti-HBe suggests lower replication.
5. High HBV DNA with liver inflammation means starting antivirals such as tenofovir.

Worked Example

A woman with chronic hepatitis C has a viral load of 2,000,000 IU per mL and starts a 12-week course of sofosbuvir plus velpatasvir. Step 1: baseline log load = log10 of 2,000,000, which is about 6.3. Step 2: at 12 weeks after finishing treatment, her viral load is below 15 IU per mL (undetectable); log10 of 15 is about 1.2. Step 3: the drop is 6.3 minus 1.2 = 5.1 logs, and an undetectable load 12 weeks post-treatment (SVR12) defines cure.

Common Misconceptions

• "All hepatitis spreads by touch or sharing food." Only A and E are faeco-oral; B, C and D need blood, sexual or birth exposure, and casual contact is safe.
• "The hepatitis B vaccine can give you hepatitis." The vaccine contains only recombinant surface protein.
• "Hepatitis C has a vaccine like hepatitis B." It does not, because the virus mutates too fast; prevention relies on safe blood, safe injections and screening, while cure relies on direct-acting antivirals.

Real-World Applications

• Blood safety: every donated unit is screened for HBsAg, anti-HCV and HIV.
• Birth-dose vaccination: hepatitis B vaccine within 24 hours of birth, plus immunoglobulin for babies of infected mothers.
• National viral hepatitis programmes: free testing and direct-acting antivirals for hepatitis C.
• Liver cancer prevention: treating chronic hepatitis B and curing hepatitis C sharply cut hepatocellular carcinoma risk.

Viruses replicate only inside cells through a fixed cycle that antivirals interrupt, and the five hepatitis viruses split into faeco-oral acute types and blood-borne chronic types. Serology decodes hepatitis B status step by step, vaccine prevents it, and direct-acting antivirals cure hepatitis C.