Interpretive Handbook

Hepatitis A

Hepatitis A virus (HAV) is endemic throughout the world, occurring most commonly, however, in areas of poor hygiene and low socioeconomic conditions. The virus, which is transmitted primarily by the fecal-oral route, is spread by close person-to-person contact and by food- and water-borne epidemics. Outbreaks frequently occur in overcrowded situations and in high-density institutions and centers, such as prisons and health-care or day-care centers. Viral spread by parenteral contact (with blood or oropharyngeal secretions) is possible but rare, because infected individuals are viremic for a short period of time (usually <3 weeks). There is little or no evidence of transplacental transmission from mother to fetus or of newborns contracting HAV infection during delivery.

Hepatitis B

Hepatitis B virus (HBV) is a DNA virus that is endemic throughout the world. The infection is spread primarily through percutaneous contact with infected blood products, eg, blood transfusion, sharing of needles by drug addicts. The virus is also found in virtually every type of human body fluid and is known to be spread through oral and genital contact. HBV can be transmitted from mother to child during delivery through contact with blood and vaginal secretions; it is not commonly transmitted transplacentally. After a course of acute illness, HBV persists in approximately 10% of patients; some of these chronic carriers are asymptomatic.

Hepatitis C

Hepatitis C virus (HCV) is an RNA virus that is a significant cause of morbidity and mortality worldwide. HCV is transmitted through contaminated blood or blood products, or through other close, personal contacts. It is recognized as the cause of most cases of posttransfusion hepatitis. HCV shows a high rate of progression (>50%) to chronic disease. In the United States, HCV infection is quite common, with an estimated 3.5 to 4 million chronic HCV carriers. Cirrhosis and hepatocellular carcinoma are sequelae of chronic HCV.

Screening to determine a patient's previous exposure to hepatitis

Determining immunity to hepatitis A and B

Determining if a patient has been infected following exposure to an unknown type of hepatitis

Hepatitis A virus (HAV) infection

Anti-HAV is usually detectable by the onset of symptoms (15-45 days after exposure). Serological diagnosis of acute HAV infection depends on the detection of IgM antibody and its presence indicates recent exposure and potential infectivity.

Hepatitis B virus (HBV) infection

Hepatitis B surface antigen (HBsAg) is the first serological marker present following HBV infection. A positive result is diagnostic of acute or chronic HBV infection and is associated with infectivity. In acute cases, HBsAg usually disappears 1 to 2 months following the onset of symptoms. Persistence of HBsAg for more than 6 months indicates development of either a chronic carrier state or chronic liver disease.

Hepatitis B core antibody (anti-HBc) IgM can be detected in serum shortly after the onset of symptoms and is usually present up to 6 months. Anti-HBc IgM may be the only serologic marker of a recent HBV infection and is detectable following the disappearance of HBsAg and prior to the appearance of hepatitis Bs antibody (anti-HBs) (ie, core window period).

Hepatitis C virus (HCV) infection

Anti-HCV is usually not detectable during the early months of infection with HCV. A negative chemiluminescence immunoassay (CIA) antibody test result does not exclude the possibility of exposure to or infection with HCV. Negative results in individuals with prior exposure to HVC may be due to antibody levels below the limit of detection of this assay or lack of reactivity to the HCV antigens used in this assay. Patients with recent infections with HCV may have false-negative results due to the time required for seroconversion (an average of 8 to 9 weeks). If HCV infection is suspected, qualitative HCV RNA testing is recommended.

See Advances in the Laboratory Diagnosis of Hepatitis C (2002) in Publications. Also see HBV Infection-Diagnostic Approach and Management Algorithm, Testing Algorithm for the Diagnosis of Hepatitis C, and Viral Hepatitis Serologic Profile in Special Instructions.

A positive CIA screen result suggests the presence of anti-HCV as a result of past or present HCV infection.

Positive hepatitis B surface antigen (HBsAg) test result should be reported by the attending physician to the State Department of Health as required by law in some states.

A weakly positive anti-hepatitis B core (HBc) test result unaccompanied by other hepatitis B serologic markers, elevated liver enzymes, or a history of risk factors may be a false-positive result.

Passively acquired anti-hepatitis B surface (HBs) (eg, transfusion, recent immune globulin treatment) does not signify immunity.

Anti-HBs may fall below detectable levels with time.

Infants born to hepatitis C infected mothers may have delayed seroconversion to anti-hepatitis C virus (HCV) antibody.

Not useful for detection of early acute hepatitis C infection.

Not useful for differentiation between resolved and chronic hepatitis C infections.

Performance characteristics have not been established for the following specimen characteristics:

1. Containing particulate matter

2. Heat inactivated specimens

HEPATITIS A ANTIBODY, IgG & IgM

Negative

HEPATITIS B SURFACE ANTIGEN

Negative

HEPATITIS B SURFACE ANTIBODY

Unvaccinated: negative

Vaccinated: positive

HEPATITIS B SURFACE ANTIBODY, QUANTITATIVE

Unvaccinated: <5.0

Vaccinated: > or =12.0

HEPATITIS B CORE TOTAL

Negative

HEPATITIS C VIRUS ANTIBODY SCREEN

Negative

1. Ergun GA, Miskovitz PF: Viral hepatitis: the new ABC's. Postgrad Med 1990 October;88(5):69-76

2. Sherlock S: Hepatitis B: the disease. Vaccine 1990;8 Suppl:S6-S9

3. Lemon SM: Type A viral hepatitis: epidemiology, diagnosis, and prevention. Clin Chem 1997 August;43:(8 pt 2)1494-1499

4. Ciocca M: Clinical course and consequences of hepatitis A infection. Vaccine 2000;18 Suppl 1: S71-74

5. Choo QL, Weiner AJ, Overby LR, et al: Hepatitis C virus: the major causative agent of viral non-A, non-B hepatitis. Brit Med Bull 1990 April;46(2):423-441