TABLE 4—
Hepatitis Viruses: Discovery, Incubation Period, Transmission, Clinical Severity, and Chronicity
| Characteristic | HAV | HBV | HCV | HDV | HEV |
| Discovery68–96 | 1973: Virus visualized on immune electron microscopy; 1979: grown in mammalian cells; 1987: genome sequenced.68–71 | 1964: Identification of antigen in leukemia patients; 1967: identification of Australia antigen; 1979: genome sequenced.72–76 | 1974, 1975: Parenteral non-A non-B hepatitis identified; 1978: transmission to chimpanzees; 1989: virus cloned; 1989: antibody assay.77–86 | 1977: Detection of delta antigen; 1980: association of delta antigen with hepatitis B; 1980: transmission of delta antigen to chimpanzees; 1987: genome sequenced.87–92 | 1978: non-A, non-B hepatitis transmitted and identified during epidemic in Delhi; 1970: partial cloning; 1991: genome sequenced.93–96 |
| Incubation, d,97 range (mean) | 15–45 (30) | 30–180 (60-90)a | 15–160 (90) | 30–180 (60-90) | 14–60 (40) |
| Onset97 | Acute | Insidious or acute | Insidious | Insidious or acute | Acute |
| Clinical severity97 | Mild | Occasionally severe | Moderate | Occasionally severe | Mild |
| Fulminant,97 % | 0.1 | 0.1–1 | 0.1 | 5–20 | 1–2 (20% in pregnant women) |
| Progression to chronicity97 | None | 1%–10% (90% of neonates) | 75%–80% | Common (invariable in HDV superinfection) | None |
Note. HAV = hepatitis A virus; HBV = hepatitis B virus; HCV = hepatitis C virus; HDV = hepatitis D virus; HEV = hepatitis E virus.
In two thirds of hepatitis B patients, no identifiable percutaneous exposure is identified. Hepatitis B surface antigen (HbsAg) has been identified in almost every body fluid of infected persons, although saliva is less infectious than serum.