INTRODUCTION — Hepatitis B virus (HBV) infection remains a global public health problem despite the availability of an effective vaccine. A substantial number of children are infected, even in countries where infants are routinely immunized against HBV. Infected children in these countries usually are adoptees or children of immigrants or become infected in childhood. The epidemiology, clinical manifestations, screening, and diagnosis of HBV infection in children and adolescents are discussed below. The management of HBV infection in this age group is discussed separately. (See "Management of hepatitis B virus infection in children and adolescents".)
Other topic reviews with related material include:
EPIDEMIOLOGY — In the United States, the incidence of acute HBV in children <15 years was less than 0.02 cases per 100,000 population in 2015  and has fallen further to 0.0 per 100,000 population aged <19 years in 2019 . This represents an almost 90 percent decrease since 1991, when recommendations for universal HBV vaccination of infants were implemented. (See "Hepatitis B virus immunization in adults".)
In the United States and in several other non-endemic countries, most cases of acute HBV infection develop in patients with risk factors such as intravenous drug use or sexual contact with an infected individual, in those living in communities with a large proportion of immigrants from regions where HBV is endemic, and in certain groups where HBV is endemic (such as Native Americans, including Alaska Natives) . The majority of children with chronic HBV infections are immigrants from high-endemicity areas, have parents who were immigrants, or became exposed through other household contacts [4,5].
Worldwide, the population prevalence of HBV infection is highest in the Western Pacific region (primarily in China, Mongolia, Vietnam, Philippines, and Papua New Guinea) and African regions, as shown in this list and in this HBV prevalence map . Even within high-endemicity regions, there can be substantial variation in HBV prevalence between countries and subpopulations. As an example, in a comprehensive report on HBV in Asian and Pacific countries, HBV seroprevalence within Singapore varied in the three main ethnic groups, from 4.2 percent (3.4 to 5.0) in Chinese people, to 2.2 percent (0.7 to 3.6) in Malay people, and 0.6 percent (0.0 to 1.4) in Indian people . These findings demonstrate the limitations of the broad classification systems often used to report HBV endemicity and risk. (See "Epidemiology, transmission, and prevention of hepatitis B virus infection" and "Epidemiology, transmission, and prevention of hepatitis B virus infection", section on 'Epidemiology of chronic HBV'.)
In countries where HBV is endemic, perinatal transmission remains the most important cause of chronic infection because of high rates of disease in pregnant women. Perinatal transmission also occurs in non-endemic countries, including the United States, mostly in children of HBV-infected mothers who do not receive appropriate HBV immunoprophylaxis at birth [8,9]. (See "Epidemiology, transmission, and prevention of hepatitis B virus infection", section on 'Transmission of HBV'.)
CLINICAL MANIFESTATIONS — Infection with HBV is associated with characteristic changes in the serum levels of HBV antigens and antibodies (figure 1 and table 1). These markers are used to define different clinical phases of HBV infection.
Acute hepatitis B virus infection — Acute HBV infection in children has a variable course ranging from asymptomatic infection to fulminant hepatitis. Universal HBV vaccination has substantially reduced the frequency of fulminant hepatitis. As an example, mortality in Taiwan decreased from 5.36 to 1.71 per 100,000 during the last two decades of the 20th century .
Clinical manifestations of acute HBV infection in children who develop symptoms are similar to those in adults. The incubation period lasts one to four months. A serum sickness-like syndrome may develop during the prodromal period, followed by constitutional symptoms, anorexia, nausea, jaundice, and right upper quadrant discomfort. The symptoms and jaundice generally disappear after one to three months, but some patients have prolonged fatigue even after normalization of serum aminotransferase concentrations. On serologic testing, acute HBV infection is characterized by hepatitis B surface antigen (HBsAg) and immunoglobulin M antibody to hepatitis B core antigen (IgM anti-HBc) (figure 1). (See 'Interpretation' below and "Hepatitis B virus: Clinical manifestations and natural history".)
However, some features are seen more commonly in certain age groups:
●The proportion of patients progressing to chronic infection is much higher in neonates (up to 90 percent) compared with 1 to 5 percent in adults and intermediate values in young children.
●Most older children and adolescents have mild constitutional symptoms during acute HBV infection. Fulminant hepatitis is rare but can also be seen, particularly in infants born to mothers with hepatitis B e-antigen (HBeAg)-negative chronic HBV (ie, HBsAg-positive and HBeAg-negative) . HBV vaccination does not consistently protect against the development of fulminant hepatitis B in neonates or in immunocompromised individuals.
●Gianotti-Crosti syndrome (characterized by papular acrodermatitis of the face, extremities, and trunk, accompanied by lymphadenopathy) is seen in infants and young children with acute HBV infection, in whom it may be the only clinical manifestation. The syndrome is not specific to HBV infection, since it can be seen with other forms of viral infection as well. (See "Gianotti-Crosti syndrome (papular acrodermatitis)".)
Management of acute HBV infection is discussed separately. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Management of acute hepatitis B virus'.)
Chronic hepatitis B virus infection — Most children with chronic HBV infection are asymptomatic and grow and develop normally. Some children note vague right upper quadrant discomfort and fatigue.
Chronic HBV infection is occasionally associated with extrahepatic manifestations including polyarteritis nodosa and glomerulonephropathy; the latter is observed principally in children. HBV infection can induce both membranous nephropathy and, less often, membranoproliferative glomerulonephritis. The typical presentation is with nephrotic range proteinuria. Approximately 30 to 60 percent of children with HBV-related membranous nephropathy undergo spontaneous remission, usually in association with HBeAg to antibody to HBeAg (anti-HBe) seroconversion (ie, conversion from HBeAg-positive to -negative and from anti-HBe-negative to -positive [ie, appearance of HBeAb]). The incidence of HBV-associated membranous nephropathy is falling as rates of HBV vaccination increase . (See "Kidney disease associated with hepatitis B virus infection".)
On serologic testing, chronic HBV infection is characterized by persistently positive HBsAg. In contrast with acute HBV, total anti-HBc is usually positive (because of the immunoglobulin G [IgG] component), while IgM anti-HBc is negative (unless during a flare of chronic HBV) (figure 1 and table 2). (See 'Interpretation' below.)
Natural history — The natural history of chronic HBV infection in children is variable, depending upon age, mode of acquisition, and ethnicity. These differences are likely due to immune tolerance that develops when infection occurs at an early age. The exact mechanisms through which immune tolerance develops are unknown.
●Children with perinatally acquired HBV usually remain HBeAg-positive and have high levels of viral replication that may persist for years or even decades, although histologic injury is typically mild [13,14]. In an illustrative report from Taiwan that followed a cohort of children with HBV infection born before the implementation of universal HBV immunization, approximately 66 percent of children remained HBeAg-positive at 10 years of age . Rates of spontaneous seroconversion (loss of HBeAg) are less than 2 percent per year in children younger than three years of age and increase to approximately 8 percent per year during puberty and young adulthood [16,17]. In boys, the rate of seroconversion increases with testosterone levels and earlier onset of puberty . Similarly, in girls, earlier age of menarche (before 11.5 years of age) is associated with earlier spontaneous HBeAg seroconversion and a greater rate of HBV clearance . Children who seroconvert spontaneously tend to have higher alanine aminotransferase (ALT) levels early in life compared with those who do not seroconvert spontaneously. Annual rates of HBeAg seroconversion appear to be lower in Asian populations, but the cumulative rate of HBeAb seroconversion still reaches 50 percent by 25 years of age [20,21]. This may be because rates of HBeAg seroconversion are lower in populations with perinatal HBV transmission and in those with HBV genotype C compared with genotype B .
●By contrast, children with HBV infection that was not perinatally acquired (eg, those born in non-endemic countries and who acquired the infection through parenteral transmission) are very likely to clear HBeAg and HBV DNA from serum during the first two decades of life . In a 29-year longitudinal study of Italian children with chronic HBV who underwent HBeAg seroconversion, 95 percent (81/85) of those without cirrhosis had inactive HBV infection at most recent follow-up and 15 percent (13/89) cleared HBsAg . Despite the high rate of seroconversion, hepatocellular carcinoma (HCC) developed in 2 percent of the cohort over 20 years, underscoring the serious nature of chronic HBV infection.
Phases of chronic hepatitis B virus infection — Individuals with perinatally acquired chronic HBV infection typically enter an immune-tolerant phase, from which they eventually move on to an immune-active phase and thence to an inactive chronic HBV state or, occasionally, to spontaneous clearance of the infection. The timing of this progression varies between individuals, and the severity of liver injury may depend on the length of the immune-active phase. Although the phases are defined by laboratory findings (figure 2A-B), the combination of findings for some patients may not fall into a single category. Therefore, longitudinal assessment is often needed to clarify the phase of infection. Moreover, some patients may progress rapidly through one or more of these phases, so each step may not be clinically apparent. (See "Hepatitis B virus: Clinical manifestations and natural history".)
Immune-tolerant — This phase is characterized by normal or mildly elevated serum aminotransferase activity (eg, ALT <1.5 times the upper limit of normal) and evidence of active HBV replication (HBV DNA >20,000 international units/mL or 105 copies/mL) (figure 2A). HBsAg and HBeAg are positive. Young children with vertically transmitted disease typically enter this phase, which continues for months, years, or even decades, before entering the immune-active phase. In some literature, this phase is known as phase 1 (but note that the phases do not necessarily occur in numerical order in clinical situations) . Treatment of patients in this phase is not recommended, because patients are unlikely to respond and treatment with nucleoside or nucleotide analogs may induce drug resistance and even cross-resistance to newer medications. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Selection of patients for antiviral treatment'.)
The normal range of ALT levels varies with sex in children and by reporting laboratory. For the purposes of making treatment decisions about chronic hepatitis B, a consensus guidance suggests using an ALT threshold of <25 U/L for girls and <35 U/L for boys for consistency with recommendations in adults , although the true normal range for ALT may be somewhat lower . ALT values should also be interpreted in the context of the patient's prior ALT results.
Immune-active, HBeAg-positive (clearance) — This phase, sometimes known as phase 2, is characterized by elevated serum aminotransferase activity (eg, ALT >1.5 times the upper limit of normal) and active HBV replication (HBV DNA is typically >20,000 international units/mL or 105 copies/mL) (figure 2A). HBsAg and HBeAg are positive. The ALT threshold used to define this phase (and therefore as a criterion for treatment) has not been established. We advocate using a threshold of ALT >45 international units/L (which is 1.5 times the upper limit of normal in most laboratories). Lower ALT thresholds have been proposed , but this approach is more likely to lead to treatment of children in the immune-tolerant phase, when treatment is much less likely to be effective.
Patients in this phase often clear HBeAg and move into the inactive chronic HBV phase; this can occur spontaneously or in response to treatment. Children in this stage of HBV infection who do not spontaneously clear HBeAg within several months are at risk for progressive liver disease and are likely to benefit from treatment . Spontaneous clearance of HBeAg early in life is less likely for patients with genotype C as compared with other genotypes , although genotyping is not part of routine clinical care. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Selection of patients for antiviral treatment' and "Clinical significance of hepatitis B virus genotypes".)
Inactive chronic hepatitis B virus — This phase (sometimes referred to as the latent, nonreplicative or carrier phase or phase 3) is characterized by normal levels of serum aminotransferase activity and low or undetectable levels of HBV. HBsAg is positive and HBeAg is negative. Up to 20 percent of patients have one or more reversions to the HBeAg-positive immune-active phase, and 20 to 30 percent reactivate into HBeAg-negative HBV, which is described below . These reactivations may occur at any time, so regular monitoring is necessary. Patients with either inactive chronic HBV or reactivated chronic HBV remain at risk for complications of HBV such as HCC. (See 'Hepatocellular carcinoma' below and "Management of hepatitis B virus infection in children and adolescents", section on 'Monitoring'.)
Immune-active, HBeAg-negative (reactivation) — Among patients with inactive chronic HBV, 20 to 30 percent experience HBeAg-negative immune reactivation, also known as HBeAg-negative chronic HBV or HBeAg-negative replicative phase, or phase 4 . This phase is characterized by a sharp increase in viral DNA levels increase (typically >2000 international units/mL), and ALT is normal or elevated, but HBeAg remains undetectable. Most of these patients have HBV variants with precore or core promoter mutations. Patients in this phase tend to have more virulent liver disease; they should be monitored for complications, and antiviral therapy may be indicated. (See "Hepatitis B virus: Overview of management", section on 'HBeAg-negative chronic hepatitis'.)
Resolved hepatitis B virus (loss of HBsAg) — A small minority of patients who clear HBeAg also go on to clear the HBV infection, heralded by clearance of HBsAg and appearance of antibody to hepatitis Bs (anti-HBs; also written HBsAb), sometimes known as phase 5. The annual rate of this transition is probably around 1 percent in populations in which HBV is acquired perinatally [32-34]. Although HBV is still present in hepatocytes, these individuals rarely revert to active HBV infection. The risk of progressive liver disease is low, but they remain at risk for HCC, and surveillance is warranted. (See 'Hepatocellular carcinoma' below and "Hepatitis B virus: Clinical manifestations and natural history", section on 'Resolution of chronic HBV infection'.)
Progression to cirrhosis — Cirrhosis occasionally develops during childhood in individuals with chronic HBV infection. One of the largest studies included 292 consecutive children who were HBsAg-positive and had elevated serum ALT levels . Cirrhosis was found in 10 patients (3 percent) at a mean age 4.0±3.3 years. However, children with cirrhosis had a higher prevalence of hepatitis D virus (HDV) infection and were more likely to have had blood transfusions, suggesting that coinfection with HDV or hepatitis C virus (HCV) may have contributed to disease progression in some children.
Although frank cirrhosis is unusual during childhood, development of moderate or severe fibrosis is relatively common. In a series of 134 children with chronic HBV (mean age nine years), 60 percent had portal expansion without bridging fibrosis, 20 percent had bridging fibrosis, and 4 percent had cirrhosis . These findings suggest that many individuals with perinatally acquired chronic HBV are at risk for developing cirrhosis in the long term. (See "Hepatitis B virus: Clinical manifestations and natural history", section on 'Sequelae and prognosis of chronic HBV infection'.)
The risk of progression to cirrhosis among adults diagnosed with chronic HBV infection is discussed separately. The risk is higher among individuals from areas endemic for HBV infection, most of whom acquire the disease perinatally; for those with coinfections with HCV, HDV, or HIV; and for those with HBV genotype C. Individuals who abuse alcohol probably have accelerated disease progression. Men also have higher risk for exacerbations of HBV, cirrhosis, and HCC compared with women. In transgenic mice, HBV acts as a sex hormone-responsive virus, which may explain the lower rates of HCC and HBV viral load seen in women compared with men; human correlation is awaited [37,38]. (See "Hepatitis B virus: Clinical manifestations and natural history", section on 'Sequelae and prognosis of chronic HBV infection' and "Clinical significance of hepatitis B virus genotypes", section on 'Genotypes/serotypes-disease progression and HBeAg seroconversion'.)
Hepatocellular carcinoma — HCC in children and adults with HBV infection has been described in both Asian and Western populations [39-43]. Adults with perinatally acquired HBV develop HCC at a rate of approximately 5 percent per decade . The risk is related to the duration of disease, degree of histologic injury, and replicative state of the virus (HBV DNA levels). The risk is higher in patients who are HBeAg-positive for extended periods of time and for those with precore mutants. The risk is increased further in the presence of cirrhosis or concomitant infection with HCV or HIV. However, HCC has been described in children who had undergone early HBeAg seroconversion, indicating that there is still a risk for HCC even after viral replication ceases . (See "Epidemiology and risk factors for hepatocellular carcinoma", section on 'Hepatitis B virus'.)
Because of these risks, we suggest surveillance for HCC in individuals in all phases of HBV infection, including those who have undergone seroconversion (converted to HBeAg-negative), either spontaneously or after successful treatment. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Monitoring'.)
HBV genotype may influence HCC development in children differently than in young adults. In Taiwan, the majority of children with HCC and chronic HBV infection have HBV genotype B . In contrast, most studies in young adults report an association between HBV genotype C and HCC. (See "Clinical significance of hepatitis B virus genotypes", section on 'Hepatocellular carcinoma'.)
Universal childhood vaccination has led to a major decline in the incidence of HCC in endemic countries. In Taiwan, for example, the average annual incidence in children six to nine years of age has decreased from 0.7 to 0.57 to 0.36 per 100,000 between the years 1981 to 1986, 1986 to 1990, and 1990 to 1994, respectively . Long-term studies have substantiated this finding .
Who should be screened — The following groups should be screened for HBV infection [26,31,49]:
●Screen regardless of vaccination history:
•Individuals born in areas with high or intermediate prevalence of HBV (regions in which the prevalence of HBV disease is more than 2 percent), which includes many immigrants and internationally adopted children. These regions include all of Africa and Asia, Cape Verde islands, most of Eastern and Mediterranean Europe, the Caribbean, and parts of South America, as shown in this list and this HBV prevalence map. (See "Epidemiology, transmission, and prevention of hepatitis B virus infection", section on 'Epidemiology of chronic HBV'.)
•Infants born to mothers with chronic HBV infection (hepatitis B e-antigen [HBeAg]-positive or -negative).
Postvaccination testing of infants who received appropriate immunoprophylaxis at birth is discussed separately. (See "Hepatitis B virus immunization in infants, children, and adolescents", section on 'HBsAg-positive mother or mother with other evidence of HBV infection'.)
•Pregnant individuals. (See "Prenatal care: Initial assessment", section on 'Hepatitis B'.)
●Screen those who are not fully vaccinated (or who did not have HBV testing prior to vaccination) if they have risk factors for horizontal transmission (table 3) including:
•Children not vaccinated as infants who are living in communities where HBV is endemic, including children born to immigrant parents from endemic areas.
•Household and sexual contacts of individuals with HBV infection.
•People who engage in high-risk behaviors. This includes those who use intravenous or intranasal drugs, have unprotected sex with an infected partner or more than one partner, people who engage in unprotected anal intercourse, and those with a history of sexually transmitted disease.
•Any patient with hepatitis C virus (HCV) or HIV infection, due to common modes of transmission. Coinfection with HCV and HBV increases the risk for progressive liver disease, for hepatocellular carcinoma (HCC), and for HBV reactivation during treatment for HCV. (See "Hepatitis C virus infection in children".)
Screening is also warranted for any individual who requests screening, regardless of vaccination history or risk factors (because they may be reluctant to disclose or unaware of risk factors). In addition, testing for HBV infection is warranted for any individual with unexplained alanine aminotransferase (ALT) elevations (eg, >2 times the upper limit of normal), as part of a diagnostic evaluation.
For adults, a less selective approach is used for HBV screening because the older population has higher rates of HBV infection and lower vaccination rates compared with children. (See "Hepatitis B virus: Screening and diagnosis in adults".)
Screening tests — Screening for HBV infection should be performed by testing for hepatitis B surface antigen (HBsAg) and antibody to hepatitis Bs (anti-HBs). Simultaneous testing for anti-HBc is essential for patients who are undergoing HBV screening prior to commencing immunosuppressive therapy including biologic agents because this test will identify the rare patient with resolved infection who is anti-HBs negative (see "Hepatitis B virus reactivation associated with immunosuppressive therapy"). The Centers for Disease Control and Prevention suggests including anti-HBc as part of routine screening ("triple panel" screening, ie, anti HBs, HBsAg, and anti-HBc). This triple panel test can help identify persons who have an acute HBV infection (anti-HBc IgM positive), or help distinguish between patients who are immune due to prior infection (total anti-HBc positive) or immune due to vaccination (anti-HBc negative) .
Results are interpreted as follows (table 2):
●Positive HBsAg – Diagnostic of HBV infection. Anti-HBs will almost always be negative (except during a brief window period as an infection resolves).
●Negative HBsAg, negative anti-HBs – Excludes HBV infection. These patients are not immune and should be vaccinated (see "Hepatitis B virus immunization in infants, children, and adolescents"). The possibility of acute HBV infection should be considered in those with suggestive signs or symptoms; this diagnosis could be confirmed by measuring IgM antibody to hepatitis B core antigen (IgM anti-HBc). (See 'Acute hepatitis B virus infection' above.)
●Negative HBsAg, positive anti-HBs – Excludes HBV infection and confirms that the patient is immune.
●Positive anti-HBc – Implies past or current HBV infection. Very rarely, this may be a false positive, so the HBsAg and anti-HBs tests should be repeated if the result is unexpected. If total anti-HBc is positive and anti-HBs is negative, further testing for IgM anti-HBc is indicated to distinguish between acute and chronic HBV infection.
Diagnostic testing — If HBV infection is diagnosed by the screening tests above, the patient should be further evaluated with the following tests:
●Hepatitis B e-antigen (HBeAg)
●Antibody to HBeAg (anti-HBe)
●IgG and IgM antibodies to hepatitis B core antigen (typically ordered as [total] anti-HBc and IgM anti-HBc)
●Alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
If acute HBV infection is suspected clinically, initial diagnostic testing is with anti-HBc (total and IgM), as well as ALT, AST, hepatitis B surface antigen (HBsAg), and antibody to hepatitis Bs (anti-HBs) if not already done.
Interpretation — The results are interpreted as follows:
●Acute HBV – The combination of positive HBsAg and IgM anti-HBc is diagnostic of acute HBV infection. HBeAg is positive in the early phase and then converts to negative as anti-HBe appears (figure 1). (See 'Acute hepatitis B virus infection' above.)
●Chronic HBV – The diagnosis of chronic HBV infection is based on persistence of HBsAg for more than six months, with positive (total) anti-HBc and negative IgM anti-HBc.
●Phase of chronic HBV – The phase of chronic HBV infection is determined by the other results, as outlined in the figure (figure 2A) and detailed above. (See 'Phases of chronic hepatitis B virus infection' above.)
Determination of the phase of chronic HBV infection has important implications for treatment:
•Most children with chronic HBV acquired the infection perinatally, and most will be in the immune-tolerant phase (normal or mildly elevated serum aminotransferase activity and high HBV DNA levels). Children in this phase sometimes clear HBeAg and convert to inactive chronic HBV spontaneously and are unlikely to respond to treatment. (See 'Immune-tolerant' above.)
•Children in the immune-active phase (elevated ALT and elevated HBV DNA) may be in the process of spontaneous clearance. They are also the most likely to respond to treatment. Decisions about initiating treatment are discussed in a separate topic review. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Selection of patients for antiviral treatment'.)
Further evaluation — For patients with confirmed chronic HBV infection, further evaluation includes laboratory assessment for severity of liver disease; testing for coinfection with other hepatotropic viruses (hepatitis C and A) and for HIV if any risk factors are present; surveillance for hepatocellular carcinoma (HCC); and, sometimes, liver biopsy (in candidates for antiviral treatment). This evaluation and subsequent treatment decisions are discussed in a separate topic review. (See "Management of hepatitis B virus infection in children and adolescents", section on 'Post-diagnosis evaluation'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diagnosis of hepatitis B" and "Society guideline links: Hepatitis B vaccination" and "Society guideline links: Management of hepatitis B" and "Society guideline links: Benign prostatic hyperplasia".)
SUMMARY AND RECOMMENDATIONS
●Prevalence – In the United States, the majority of children with chronic hepatitis B virus (HBV) infection are immigrants from areas with endemic HBV infection (HBV prevalence map), have immigrant parents, or became exposed through other household contacts. Perinatal transmission of HBV declined sharply after universal hepatitis B vaccination of infants was initiated in 1991. (See 'Epidemiology' above.)
●Natural history – The natural history of chronic HBV infection in children is variable, depending upon age and mode of acquisition, ethnicity, and/or HBV genotype. Children with perinatally acquired HBV usually remain hepatitis B e-antigen (HBeAg)-positive and have high levels of viral replication for prolonged periods, although histologic injury is typically mild (figure 2B). By contrast, children with HBV disease that was not perinatally acquired (ie, horizontal transmission) tend to have higher alanine aminotransferase (ALT) levels and frequently clear HBeAg and HBV DNA from serum during the first two decades of life. (See 'Natural history' above.)
●Acute HBV – If acute HBV infection is suspected clinically, initial diagnostic testing should include hepatitis B core antigen (anti-HBc; total and immunoglobulin M [IgM]) (figure 1).
●Screening for chronic HBV
•Indications – Screening for HBV is recommended for all patients with risk factors (table 3), including internationally adopted children, immigrants from high-prevalence areas and their children, household contacts of individuals with HBV infection, adolescents who engage in high-risk behaviors, and any patient with hepatitis C virus (HCV) or HIV infection (due to common modes of transmission). (See 'Who should be screened' above.)
•Screening tests – Screening is done by serologic testing for hepatitis B surface antigen (HBsAg) and antibody (anti-HBs). Positive HBsAg is diagnostic of chronic HBV infection, and positive anti-HBs indicates immunity (due to immunization or recovery from infection). (See 'Screening tests' above.)
●Further testing for HBsAg-positive patients – Patients with positive HBsAg should be further evaluated with serum ALT and aspartate aminotransferase (AST), HBV DNA, and HBeAg. (See 'Diagnostic evaluation' above and 'Interpretation' above.)
•Children in the immune-tolerant phase of chronic HBV (normal or mildly elevated serum ALT and high HBV DNA, with positive HBeAg) are unlikely to respond to antiviral treatment. This is the most common phase for children, most of whom acquired the infection perinatally. (See 'Immune-tolerant' above.)
•Children in the immune-active phase of chronic HBV (markedly elevated ALT and high HBV DNA) may be in the process of spontaneous clearance. They are also the most likely to respond to treatment. Decisions about initiating treatment are discussed in a separate topic review. (See 'Immune-active, HBeAg-positive (clearance)' above and "Management of hepatitis B virus infection in children and adolescents", section on 'Selection of patients for antiviral treatment'.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Maureen M Jonas, MD, who contributed to earlier versions of this topic review.
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