HEPATITIS B VIRUS DNA, ULTRASENSITIVE, QUANTITATIVE, REAL-TIME PCR
- HEPATITIS B VIRUS DNA, ULTRASENSITIVE, QUANTITATIVE, REAL-TIME PCR
- Start Date
- Expiration Date
- HBV Viral Load
- CPT Codes
- Reference Test
- Transport Info
Centrifuge and immediately transfer serum to separate plastic tube
Separate specimens must be submitted when multiple tests are ordered
- Fasting Required?
- Patient Instructions
- Reference Range
Quantitative Real-Time Polymerase Chain Reaction (RT-PCR
This test is useful for monitoring the response to treatment in chronically infected HBV patients.
The laboratory diagnosis and monitoring of both acute and chronic infections due to hepatitis B virus (HBV) involves the use of several of the following tests: hepatitis B surface antigen (HBsAg), the e antigen (HBeAg), antibody to the core antigen (anti-HBc), antibody to the e antigen (anti-HBe), and antibody to the surface antigen (anti-HBs). Immunity conferred by the HBV vaccine can also be assessed by measuring levels of anti-HBs (although the CDC does not recommend post-vaccination testing). Groups of HBV tests are recommended for the following clinical situations: (1) suspected acute viral hepatitis, HBsAg, IgM anti-HBc; (2) chronic hepatitis, HBsAg, anti-HBc, and anti-HBs; and (3) monitoring chronic HBV infection, HBsAg, HBeAg, anti-HBs, anti-HBe, and quantitative or qualitative HBV DNA. The result pattern of these tests are particularly helpful in differentiating acute hepatitis, chronic hepatitis, and the chronic carrier state. The pattern of reactivity is reflective of the natural course of infection. HBsAg usually becomes detectable 2 weeks to 2 months before clinical symptoms, and as little as 2 weeks after infection. It is usually present for 2 to 3 months. Five to 10 percent of patients will have persistent HBsAg levels beyond 6 months (chronic carrier, chronic hepatitis). The EIA test will detect 100 pg/mL or more of HBsAg. All positive HBsAg are further tested using the HBsAg confirmation test. About 5% of positive HBsAg's are false positives and will not neutralize in the confirmatory assay. Anti-HBc IgM first becomes detectable at about the same time as clinical symptoms appear and serum transaminases rise. It will usually persist for several months and occasionally up to a year. Anti-HBc IgG appears soon after IgM and will persist for years, ultimately disappearing in some patients. IgM may be present in cases of chronic hepatitis. The appearance of anti-HBs usually follows the disappearance of HBsAg. It persists for years and is associated with relative or absolute immunity. In patients who have received the HBV vaccine, this antibody should be the only one to appear in responders. Response depends strongly on age, sex, obesity, and general health. About 95% of healthy, thin women in their 20's will develop antibodies after a three-dose course. Twenty-five to 50 percent of non-responders will ultimately seroconvert after a repeat course. Assessing responsiveness in vaccinees is only recommended in selected subgroups (e.g., those with high prevalence of infection or health care workers). Levels less than 10 IU/L are considered negative and non-protective. The HBeAg appears in close association with HBsAg, but normally does not persist as long. Its presence is generally associated with higher infectivity, but it is of limited usefulness diagnostically. The development of anti-HBe coincides with the disappearance of e antigen. This is usually after the appearance of anti-HBc and before that of anti-HBs. Anti-HBe often disappears, but its persistence has been associated with chronic hepatitis and the chronic carrier state. It does not confer protection. The typical case of acute HBV hepatitis will be characterized by the presence of HBsAg and anti-HBc IgM. The latter is particularly helpful in HBsAg-negative cases. It is not recommended to rely solely on surface antigen determinations for diagnosing acute infection. In the antigen-negative cases, the presence of IgM and total anti-HBc and the presence of HBV DNA, in the absence of anti-HBs, will help to confirm the acute case. In chronic hepatitis, HBsAg will be present together with anti-HBc, but without anti-HBs. HBeAg may or may not be present. The newest molecular test, "Hepatitis B Virus DNA, Ultra Sensitive Quantitative PCR," is useful for monitoring the response to treatment in chronically infected HBV patients. For example, decreases of nearly 100-fold were observed in patients receiving 100 mg/day of lamivudine for one year. Changes less than 5- fold are not medically significant (Lai CL). In a more recent Chinese study examining chronic hepatitis B patients, it was found that patients treated with lamivudine for three consecutive years exhibited enhanced seroconversion rates for antibody directed to HBeAg and 20% of treated patients did not have detectable HBV DNA (Nancy WY). Approximately 1% of blood donors will have a positive anti-HBc and negative HBsAg. These donors should be further evaluated by measuring anti-HBs. Most of these donors will have a negative anti-HBs (see Draelos, et al.). Vaccinating donors with this pattern of results showed that the anti-HBc was a cross-reacting antibody.