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Chapter 106 : Hepatitis B and D Viruses

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Abstract:

Hepatitis B virus (HBV) was identified and characterized after the discovery of the Australia antigen by Blumberg and colleagues in 1965. The Australia antigen, now designated hepatitis B surface antigen (HBsAg), is detected in the sera of patients with both acute and chronic HBV. HBV infects hepatocytes, leading to an acute infection that resolves or a chronic infection lasting years. Safe and effective vaccines against HBV have been available since 1982. HBV infection is diagnosed by serological and molecular markers using serum or plasma. The laboratory diagnosis of HBV uses a combination of tests that detect virus-specific protein and nucleic acid as well as the host immune response to infection. The methods for identification of HBV infection use a combination of molecular, antigenic, and serological methods. Serologic tests for HBV-specific antibodies are used to determine the stage of disease and to establish immunity due to vaccination. Patients with chronic hepatitis that are hepatitis B e antigen (HBeAg) negative are more likely to have more advanced liver disease in spite of lower serum HBV DNA levels. The majority of individuals vaccinated for HBV have detectable levels of anti-HBs, but some test negative due to waning levels of anti-HBs. Hepatitis D virus (HDV) is a defective RNA virus that requires the presence of HBV for its replication. The laboratory diagnosis of HDV depends on the detection of specific antibodies, HDAg, and HDV RNA.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106

Key Concept Ranking

Infection and Immunity
0.604018
RNA Polymerase II
0.5140845
Hepatitis C virus
0.47730443
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Figures

Image of FIGURE 1
FIGURE 1

(A) The intact infectious HBV virion and the empty particles are shown. The two HBV particles (right) comprised of HBsAg are shown as elongated or tubular and as spherical particles. These particles vastly outnumber the virions. (Designed by University of Kansas Graphic Design Department.) (B) Electron micrograph of serum showing the presence of three distinct morphologic entities: 17- to 25-nm-diameter, pleomorphic, spherical particles (a); tubular or filamentous forms with diameters similar to those of the small particles (b); and 42- to 47-nm-diameter, double-shelled, spherical particles representing the hepatitis B virion (Dane particle) (c). Magnification, ×10. (C) Diagrammatic representation of HBV coding regions. The functioning genome is a double-stranded circular DNA molecule shown in the middle. RNA transcripts (arrows) are generated using both the plus-strand [(+)Strand] and minus-strand [(−)Strand] DNA templates. The largest transcript codes for the viral polymerase shown around the genome as the P transcript. The transcript for surface antigen (S) is produced as three separate transcripts, pre-S1, pre-S2, and S. The core protein is translated from the C transcript. HBeAg is coded within the HBc gene. The transactivating protein is encoded by the X transcript. (Designed by University of Kansas Graphic Design Department.)

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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Image of FIGURE 2
FIGURE 2

Worldwide distribution of chronic hepatitis B in 2006. Dark shading, ≥8% of the population (high HBsAg prevalence); medium shading, 2 to 7% of the population (intermediate HBsAg prevalence); light shading, <2% of the population (low HBsAg prevalence). For multiple countries, estimates of prevalence of HBsAg, a marker of chronic HBV infection, are based on limited data, and they might not reflect the current prevalence in countries that have implemented childhood hepatitis B vaccination. In addition, the prevalence of HBsAg might vary within countries by subpopulation and locality. The source for this figure is reference .

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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Image of FIGURE 3
FIGURE 3

Typical sequence of serologic markers in patients with acute HBV infection and with resolution of symptoms.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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Image of FIGURE 4
FIGURE 4

Typical sequence of serologic markers in patients with HBV infection that progresses to chronicity. In patients with chronic HBV infection, both HBsAg and IgG anti-HBc remain persistently detectable, generally for life. HBeAg is variably present in these patients.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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Image of FIGURE 5
FIGURE 5

Serologic course of HDV infection, with resolution when the virus is acquired as a coinfection with HBV.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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Image of FIGURE 6
FIGURE 6

Serologic course of HDV infection when the virus is acquired as a superinfection with HBV. Symptoms and ALT levels are shown to indicate the intermittent nature of symptoms and liver involvement.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
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References

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Tables

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TABLE 1

HBV markers in different stages of infection and convalescence

This description can be applied to early convalescence and to individuals who remain HBV DNA positive for prolonged periods in the absence of HBsAg.

Remote infection can be applied to individuals with anti-HBc in the absence of other serological markers, including DNA. These patients may or may not have anti-HBs. There is evidence that these patients may reactivate HBV during immunosuppression. HBsAg, complex antigen found on the surface of HBV and on 20- nm-diameter particles and tubular forms; HBcAg, antigen associated with the 27-nm-diameter core of HBV; HBeAg, protein that results from the proteolytic cleavage of the precore/core protein by cellular proteases and that is secreted as soluble protein in serum.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
Generic image for table
TABLE 2

Commercial systems for serological testing of HBV antigens and antibodies

CMIA, chemiluminescent microparticle immunoassay; CIA, chemiluminescent immunoassay; CEIA, chemiluminescent enzyme immunoassay; EIA, enzyme immunoassay (usually plate or well based); ELFA, enzyme-linked fluorescent assay; ECL-EIA, electrochemiluminescence enzyme immunoassay, MEIA, microparticle enzyme immunoassay.

All information on methods are derived from FDA submissions and manufacturers' information, when available. LOD, limit of detection; OD, optical density.

A, diagnostic use only; not for use in the evaluation of blood, blood products, or tissue/blood donors; B, diagnostic use and screening of blood, blood products, and/or tissue/blood donors; C, screening of blood, blood products, and/or tissue/blood donors only; D, evaluate postvaccination response.

All assays require positive results to be repeated and confirmed with a separate confirmation assay specific for each kit.

Serum includes specimens collected in serum separator tubes; plamsa includes collections in potassium EDTA, sodium citrate, sodium heparin, lithium heparin, and/or plasma separator tubes unless otherwise stated for a specific test.

Some reactive and/or gray zone/indeterminate results are repeated in duplicate or with a new specimen before results are reported. See package insert for specific instructions.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
Generic image for table
TABLE 3

Molecular assays used to detect HBV nucleic acid

Data from manufacturers' literature and websites.

CE-IVD, European Conformity In Vitro Diagnostic Medical Devices.

FDA-IVD, Food and Drug Administration In Vitro Diagnostic Product.

Verify instrumentation use with manufacturer's kit. Evaluated on the Roto-Gene instrument.

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
Generic image for table
TABLE 4

HBV genotypes and geographic circulation

Information derived from references , and .

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106
Generic image for table
TABLE 5

Antiviral agents and HBV mutations associated with resistance

Resistance is defined as virologic breakthrough confirmed by an increase on two consecutive occasions of HBV DNA levels by >1 log copies/ml during therapy. Data are derived from references , and .

Citation: Horvat R, Tegtmeier G. 2011. Hepatitis B and D Viruses, p 1659-1676. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch106

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