Enumerate, uh, the viruses, virus causing hepatitis. Name the markers of hepatitis B vi- virus infection. And their interpretation. How is he- hepatitis B virus infection prevented?
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Viruses Causing Hepatitis
At least six viruses are specifically designated as hepatitis viruses. Other viruses (EBV, CMV, yellow fever) can cause incidental liver inflammation, but the primary hepatitis viruses are:
| Virus | Family | Genome | Transmission | Chronicity |
|---|---|---|---|---|
| HAV (Hepatitis A) | Picornaviridae (Hepatovirus) | ssRNA (+) | Fecal-oral | None |
| HBV (Hepatitis B) | Hepadnaviridae | dsDNA (encodes reverse transcriptase) | Parenteral, sexual, perinatal | ~10% adults; ~90% neonates |
| HCV (Hepatitis C) | Flaviviridae | ssRNA (+) | Parenteral, sexual | ~85% |
| HDV (Hepatitis D / Delta) | Deltaviridae | ssRNA (-), circular | Parenteral, sexual (requires HBV) | 50-80% |
| HEV (Hepatitis E) | Hepeviridae (calici-like) | ssRNA (+) | Fecal-oral | Rare (severe in pregnancy) |
| HGV (Hepatitis G / GBV-C) | Flaviviridae | ssRNA | Parenteral | Not associated with clinical disease |
Key distinguishing features:
- HAV and HEV: fecal-oral, acute only, no carrier state
- HBV, HCV, HDV: spread via blood, body fluids, and sexual contact; all can become chronic
- HDV is a defective virus requiring HBsAg from HBV to form its envelope; HBV vaccination prevents HDV
- HCV causes chronicity in ~85% of patients, highest risk for cirrhosis and hepatocellular carcinoma (HCC) after long-term infection
(Sherris & Ryan's Medical Microbiology 8e, p. 479; Medical Microbiology 9e, Ch. 55)
Markers of Hepatitis B Virus Infection and Their Interpretation
The Markers
| Abbreviation | What it is |
|---|---|
| HBsAg | Hepatitis B surface antigen - envelope protein; forms 22 nm spherical and tubular particles in serum in excess; four subdeterminants (adw, ayw, adr, ayr) |
| HBcAg | Core antigen (nucleocapsid); found in nucleus of infected hepatocytes only - NOT detectable in serum directly |
| HBeAg | Glycoprotein associated with the core; best correlate of active viral replication and high infectivity; present only when HBsAg is also present |
| Anti-HBs | Antibody to HBsAg; protective; marker of resolved infection or successful vaccination |
| Anti-HBc (IgM) | Early antibody to core antigen; marker of ACUTE infection; present during the "window period" when HBsAg has cleared but anti-HBs not yet appeared |
| Anti-HBc (IgG) | Persists for life; marker of past or chronic infection; does NOT develop in response to vaccine |
| Anti-HBe | Antibody to HBeAg; appears as HBeAg clears; suggests reduced viral replication and lower infectivity |
(Sherris & Ryan's Medical Microbiology 8e, Table 13-2; Medical Microbiology 9e)
Serology Interpretation by Clinical State
The sequence of marker appearance in acute self-limiting HBV infection:
| Clinical State | HBsAg | HBeAg | Anti-HBc | Anti-HBe | Anti-HBs | Interpretation |
|---|---|---|---|---|---|---|
| Early (presymptomatic) | + | - | - | - | - | Earliest detectable marker; active infection |
| Early acute | + | + | - | - | - | Active replication; highly infectious |
| Acute (symptomatic) | + | + | + (IgM) | - | - | Classic acute hepatitis B |
| Window period | - | - | + (IgM) | +/- | - | HBsAg cleared, anti-HBs not yet appeared; only anti-HBc detectable |
| Late acute / Convalescence | + | - | + | +/- | - | HBeAg cleared; resolving |
| Resolved | - | - | + (IgG) | +/- | + | Immunity; past infection |
| Chronic (>6 months HBsAg+) | + | + | + (IgG) | - | - | No anti-HBs; persistent viral replication |
| Vaccinated | - | - | - | - | + | Anti-HBs only (no anti-HBc - key distinction from resolved natural infection) |
(Medical Microbiology 9e, Table 55.2)
Key interpretive rules:
- HBsAg present >6 months + IgG anti-HBc = chronic HBV infection
- IgM anti-HBc = acute infection (also present during window period)
- Anti-HBs alone (no anti-HBc) = vaccination only
- Anti-HBs + IgG anti-HBc = resolved natural infection
- HBeAg = best single marker of infectivity and active replication; its persistence in chronic disease signals ongoing high infectivity
- HBsAg and anti-HBs can never be detected simultaneously (antigen-antibody complexes block detection)
- HBV DNA by PCR is used to quantify viral load, monitor antiviral therapy, and detect occult infection
Prevention of Hepatitis B Virus Infection
Prevention operates at three levels: pre-exposure active immunization, post-exposure prophylaxis, and general infection-control measures.
1. Active Immunization (Vaccine)
- The HBsAg subunit vaccine is the cornerstone of prevention
- Original vaccine: derived from 22-nm HBsAg particles purified from plasma of chronically infected people
- Current recombinant vaccine: the S gene for HBsAg is inserted into yeast (Saccharomyces cerevisiae); the protein self-assembles into virus-like particles (VLPs) with alum adjuvant
- Schedule: three doses at 0, 1, and 6 months - produces protective anti-HBs (IgG)
- Heplisav-B: a newer adult vaccine (age ≥18) combining yeast-derived HBsAg with a CpG-ODN (TLR-9 stimulating) adjuvant - only two doses 1 month apart required, with improved immunogenicity
- Who should be vaccinated: all infants (universal), children, adolescents, and high-risk adults (healthcare workers, IV drug users, people with multiple sexual partners, household contacts of HBsAg carriers, hemodialysis patients, travellers to endemic areas)
- HBV vaccination also prevents HDV (since HDV requires HBsAg to replicate)
2. Post-Exposure Prophylaxis (PEP)
- Hepatitis B Immune Globulin (HBIG): provides passive short-term protection (3-6 months); given within 1 week of exposure
- HBIG + HBV vaccine combination is used for:
- Newborns of HBsAg-positive mothers (given at birth; prevents ~90% of perinatal transmission)
- Healthcare workers after needle-stick exposure to HBsAg-positive blood
- Sexual partners of newly diagnosed HBV cases
- Without intervention, >90% of perinatally infected infants develop chronic infection
3. General Prevention and Infection Control
- Blood supply screening: donated blood is routinely screened for HBsAg and anti-HBc, greatly reducing transfusion-transmitted HBV
- Safe sex practices: condom use reduces sexual transmission
- Harm reduction: avoiding needle sharing among IV drug users
- Universal precautions: gloves, protective clothing, and eye protection when handling blood or body fluids; special care with needles and sharps
- Disinfection: HBV-contaminated materials can be disinfected with 10% bleach; note that unlike most enveloped viruses, HBV is NOT readily inactivated by simple detergents
(Medical Microbiology 9e, Ch. 55; Sherris & Ryan's Medical Microbiology 8e, p. 502)
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