Laboratory diagnosis (Fig. 1) and monitoring of acute and chronic HBV infections involve the use of several of the following tests (Tables 1 and 2):

1. Hepatitis B surface antigen (HBsAg)

2. Hepatitis B e antigen (HBeAg)

 3. Hepatitis B core antibody, total or IgM (anti-HBc)

4. Hepatitis B e antibody (anti-HBe)

 5. Hepatitis B surface antibody (anti-HBs)

6. Hepatitis B viral DNA by polymerase chain reaction (PCR, qualitative and quantitative)

Fig1. Hepatitis B virus testing algorithm. (From ARUP Laboratories: Hepatitis B virus testing algorithm, 2012 [http://www.arupconsult.com/ Algorithms/HBV.pdf].)

Table1. Serologic Markers for Hepatitis B Virus (HBV) Infection

Table2. Interpretation of Hepatitis B Panel

Serum testing procedures may be performed by qualitative chemiluminescent immunoassay, qualitative EIA, quantitative real-time PCR, quantitative real-time PCR–nucleic acid sequencing, or real-time PCR with reflex to genotype. Immunohistochemistry may be used to detect HBsAg in liver tissue samples.

Hepatitis B Surface Antigen

 Serum HBsAg is a marker of HBV infection. Antibodies against HBsAg signify recovery. The initial detectable marker found in serum during the incubation period of HBV infection is HBsAg. HBsAg usually becomes detectable 2 weeks to 2 months before clinical symptoms and as soon as 2 weeks after infection. This marker is usually present for 2 to 3 months. This procedure screens for the presence of the major coat-protein of the virus (HBsAg) in serum and is considered to be the most reliable method of choice for preventing the transmission of HBV via blood. The presence of HBsAg indicates active HBV infection, acute or chronic.

The titer of HBsAg rises and generally peaks at or shortly after the onset of elevated liver serum enzyme levels (e.g., ALT, SGPT). Clinical improvement of the patient’s condition and a decrease in serum enzyme concentrations are paralleled by a fall in the titer of HBsAg, which subsequently disappears. There is variability in the duration of HBsAg positivity and in the relationship between clinical recovery and the disappearance of HBsAg (Fig. 23-6). About 5% of positive HBsAg values are false-positive results.

Serologic and clinical patterns observed during acute hepatitis B viral infection. (Adapted from Hollinger FB, Dreesman GR Rose RN, Friedman H, editors: Manual of clinical immunology, ed 2, Washington, DC, 1980, American Society for Microbiology.)

Among persons infected with HBV with detectable HBsAg in their serum, not all the HBsAg represents complete Dane particles. HBsAg-positive serum also contains two other virus-like structures, which are incomplete spherical and tubular forms consisting entirely of HBsAg and devoid of HBcAg, DNA, or DNA polymerase. The incomplete HBsAg particles can be present in serum in extremely high concentrations and form the bulk of the circulating HBsAg.

Hepatitis B–Related Antigen

 A hepatitis B–related antigen, HBeAg, is found in the serum of some HBsAg-positive patients. HBV DNA and DNA polymerase will appear along with HBeAg. These are all indicative of active viral replication. HBeAg is rarely found in the absence of HBsAg. HBeAg appears to be associated with the HBV core; however, the relationship between HBeAg and the structure of HBV is unclear. HBeAg appears to be a reliable marker for the presence of high levels of virus and a high degree of infectivity.

Hepatitis B Core Antibody

 During the course of most HBV infections, HBsAg forms immune complexes with the antibodies produced as part of the recovery process. Because the HBsAg contained in these complexes is usually undetectable, HBsAg disappears from the serum of up to 50% of symptomatic patients. During this phase, an indicator of a recent hepatitis B infection is anti HBc, the antibody to the core antigen. The time between the disappearance of detectable HBsAg and the appearance of detectable antibody to HBsAg (anti-HBs) is called the anti-core window or hidden antigen phase of HBV infection. This window phase may last for a few weeks, several months, or 1 year, during which anti-HBc may be the only serologic marker. Anti-HBc is found in 3% to 5% of individuals. Of 100 anti-HBc–positive persons, 97 will have anti-HBs, 2 will have HBsAg, and 1 may have only anti-HBc.

Testing for antibody to the core of the virus (anti-HBc) may provide an additional advantage and lead to the identification of a person recently recovered from an HBV infection who may still be infectious. EIA or microparticle EIA is the method of choice.

An anti-HBc test is the Corzyme test (Abbott Laboratories, Abbott Park, Ill) EIA. The most recent assay to be developed is the test for anti-HBc IgM. This is considered a reliable marker during the window period, diagnostic of acute infection, when most other markers may be absent. The IgM anti HBc titer rises rapidly in the acute phase and becomes negative in most patients in 3 to 9 months, although it may persist for many years.

Antibodies to HBeAg and HBsAg

HBeAg is a serum marker of active viral replication. Antibodies to HBeAg (anti-HBe) and HBsAg (anti-HBs) develop during convalescence and recovery from HBV infection. The development of anti-HBe in a case of acute hepatitis is the first serologic evidence of the convalescent phase. Antibody to HBsAg (anti-HBs), unlike anti-HBc and anti-HBe, does not arise during the acute disease; it is manifested during convalescence. Anti-HBs is a serologic marker of recovery and immunity. Anti-HBs is probably the major protective antibody in this disease. Thus, hepatitis B immune globulin is so named because it contains high levels of anti-HBs.

Hepatitis B Viral DNA

 Current tests the assessment of HBV infections are the qualitative and quantitative measures of HBV DNA by molecular methods (e.g., PCR). In the qualitative assay, a highly con served region of the surface gene of HBV is detected at a level as low as 1.5 × 10⁴ copies of the viral genome/mL. This assay may be of value in confirming HBV infection in patients with questionable results. A less sensitive quantitative assay that uses an RNA probe is available for monitoring therapeutic responsiveness in chronically infected patients.

اخر الاخبار

اخبار العتبة العباسية المقدسة

قسم شؤون المعارف ينظم دورة متقدمة في تحقيق المخطوطات لملاكاته

قسم الشؤون الفكرية يصدر العدد العشرين من مجلة دراسات إفريقية

المجمَع العلمي يكرم الأساتذة المشاركين في مشروع الدورات القرآنية الصيفية في كربلاء

العتبة العباسية المقدسة تختتم فعاليات البرنامج المركزي الأسبوعي لمنتسبيها

المزيد

الآخبار الصحية

تحذير من "عدوى بكتيرية" تسبب نوبات قلبية

ماذا يحصل لجسمك عند التوقف عن استخدام الزيت في الطهي؟

الأمل في كبسولة.. "فيتامين شهير" يبطئ التقدم في العمر

اشتهاء أطعمة بشكل مفاجئ.. ناقوس خطر للسرطان ؟!

المزيد

الآخبار التكنلوجية

زلزال أفغانستان يحصد أكثر من ألف قتيل.. ويدمر آلاف المنازل !

ناجٍٍ وحيد من انزلاق أرضي.. دمّر قرية سودانية بأكملها !

نهر الفرات.. مورد مائي بين الندرة والتقاسم

ما السر وراء مشية إيلون ماسك الغريبة والسريعة ؟

المزيد

مواضيع ذات صلة

Pathogenesis and clinical significance of HIV

Transmission of HIV

HIV replication

Hepatitis D

Prevention and Treatment of hepatitis B

Differentiating Acute and Chronic Hepatitis and the Chronic Carrier State

Flaviviridae

Togaviridae

Caliciviridae

Picornaviridae

Epidemiology of Hepatitis B

Hepatitis A