The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
3. Hepatitis B
Hepatitis B infection is caused by the hepatitis B
virus (HBV), an enveloped DNA virus that infects
the liver, causing hepatocellular necrosis and
inflammation
HBV infection can be either acute or chronic
Associated illness ranges in severity from
asymptomatic to symptomatic, progressive
disease
Chronic hepatitis B (CHB) – defined as
persistence of hepatitis B surface antigen
(HBsAg) for six months or more – is a major
public health problem
4. Structure of Hepatitis B Virus –
wild type (HBeAg Positive)
HBs Protein
( HBsAg)
HBc Protein
(HBcAg)
Partially double
stranded DNA
(HBV DNA)
HBV DNA
Polymerase
HBe Protein
(HBeAg)
5. Mutant viruses
Clinically relevant mutants are :
Precore mutants: abolishes HBeAg production
Core mutants: down regulation of HBeAg
production
They do not produce HBeAg, but are capable of
multiplication.
This type of hepatitis is referred to as HBeAg
negative hepatitis B.
Mutants are also formed during treatment.eg. YMDD
mutant with continued treatment using lamivudine &
is believed to be defective in terms of replication.
6. Hepatitis B viral replication cycle
The hepatitis B virus virion enters the hepatocyte via endocytosis. Viral nucleocapsids are uncoated
and transported into the nucleus, where viral DNA is transformed into covalently closed circular DNA (cccDNA).
Replication subsequently occurs through reverse transcription. The mature nucleocapsids are responsible for
mediating viral persistence, and may be released to infect neighbouring hepatocytes. HBsAg: Hepatitis B
surface antigen.
World J Gastroenterol 2014; 20(20): 6262-6278
7. Risk groups for Hepatitis B
Children of immigrants from areas where there is
high prevalence of hepatitis B.
Injection drug abuse.
Infants born to infected mothers.
History of sexually transmitted diseases, multiple sex
partners, homosexual relations
Sexual contacts of infected persons.
Household contacts of chronically infected
individuals.
Healthcare & public safety workers.
Hemodialysis patients.
8. Epidemiology and burden
2 billion people have evidence of past or present
infection with HBV
240 million are chronic carriers of HBV surface
antigen (HBsAg)
Hepatitis B infection
Acute hepatitis B Chronic hepatitis B
•Case fatality rate of 0.5–1%
•650 000 people die each year
from the complications of CHB
•Accounts for around 45% of
cases of HCC and 30% of
cirrhosis
9. Global HBV prevalence
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10. Modes of transmission
HBV is transmitted via exposure to blood or mucous membranes
with infectious bodily fluids
In children :vertically at birth, or through iatrogenic events; folk
remedies, such as acupuncture, or exposure to infected bodily fluids
via person-to-person contact
In adults: sexual exposure or percutaneous/mucosal exposure to
infectious blood/bodily fluids (horizontal transmission), such as
through needle sharing in injection drug users or exposure to
infected blood or needles in the healthcare setting
Direct percutaneous exposure of susceptible individuals to virus
during blood transfusion or organ transplant
Person-to-person transmission of HBV can also occur in settings
involving close interpersonal contact over an extended period of
time, such as in household contacts or developmentally disabled
persons living in long-term care facilities
MMWR Morb Mortal Wkly Rep. 2008;57(RR-8):1-20.
12. Clinical presentation
Acute symptomatic disease :typically begins 2-3 months after
exposure and generally lasts 2-4 months
Symptoms of acute HBV : fatigue, loss of appetite, nausea,
arthralgias, vomiting, abdominal pain, low-grade fever, jaundice,
dark urine, and light-colored stools
Acute hepatitis B becomes chronic in > 90% of infants, in 25% to
50% of children aged 1-5 years, and in <5% of older children and
adults
Patients who are immunosuppressed, including those infected
with HIV or on hemodialysis, are at increased risk of developing
chronic infection
0.5% of infected patients who acquire disease early in life
spontaneously resolve the infection annually
Of those patients who develop chronic HBV infection as children,
25% will die from the consequences of hepatitis B, such as
cirrhosis or liver cancer 1. Hepatology. 2007;45:507-539.
2. J Infect Dis. 1985;151:599-603.
13. • LIVER
FUNCTION TETS
• LIVER BIOPSY
• FIBROSCAN
• NON INVASIVE
MARKERS
• VIRUS
ANTIGENS
• ANTIBODIES
• PRESENCE OF
HBV DNA
• GENOTYPE OF
VIRUS
VIROLOGICALSEROLOGICAL
BIOCHEMICAL
Markers of Infection
HISTOLOGICAL
14. Interpretation of Serologic Test Results
for Hepatitis B
Serologic Marker
Interpretation
HBsA
g
Total
HBcAb
IgM
HBcAb HBsAb
- - - - Never infected
+ - - - Early acute infection; transient (up to
18 days) after vaccination
+ + + - Acute infection
- + + + or - Acute resolving infection
- + - + Recovered from past infection and
immune
+ + - - Chronic infection
- + - - Past infection; false positive (ie,
susceptible); occult infection; or
passive transfer of HBcAb to infant
born to HBsAg-positive mother
- - - + Immune if concentration is > 10
mIU/mL after vaccination series
complete; passive transfer afterHBsAg = hepatitis B surface antigen; total HBcAb = total hepatitis B core antibody; IgM HBcAb = immunoglobulin M hepatitis B core antibody; HBsAb = hepatitis B
surface antibody; + = positive test result; - = negative test result
15. Virologic Markers
Viral load: HBV DNA: correlates with active replication;
quantification of serum HBV DNA has become a pivotal tool to guide
the management of the HBV carriers, to select candidates for
antiviral therapy and to guide treatment with nucleoside/nucleotide
analogues (NAs), which have potent direct antiviral activity
HBV Genotypes
Worldwide, at least nine genotypes of HBV (A through I) on basis
of more than 8% difference in their genome sequences
Higher rates of HCC have been found in genotypes C and F
(compared with genotypes B or D),
Antiviral therapy is equally effective, and the HBV vaccine
protective against all HBV genotypes
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16. Liver function tests /Histological markers
Liver enzymes :
One of the most important liver enzymes to look for is alanine
aminotransferase (ALT).
ALT levels fluctuate in persons with chronic hepatitis B and
require longitudinal monitoring to determine the trend. Upper
limits for normal ALT have been defined as below 30 U/L for
men and 19 U/L for women
During acute hepatitis B infection, ALT levels can be
temporarily elevated, but this rarely leads to long-term liver
problems
In chronic hepatitis B, ALT levels can be either periodically or
consistently increased, indicating a higher risk of long-term
liver damage
Serum albumin
Prothrombin time
Serum bilirubin
17. Histological markers
Liver biopsy : invasive procedure, which is indicated only when
a specific diagnosis of CHB cannot be posed or excluded using
non-invasive procedures
Transient elastometry (FibroScan®)- rapid, easy to perform,
reproducible, non-invasive technique for the evaluation of liver
stiffness
The combination of serum markers has been shown to predict
liver fibrosis and activity in a number of studies
;aminotransferases and indices including α(2)-macroglobulin,
apolipoprotein A1, haptoglobin, γ-glutamyl transpeptidase, total
bilirubin (FibroTest®) and ALT (Actitest) have been shown to be
accurate markers of HBV-related activity
18. Non-invasive assessment of liver
disease stage
Presence of cirrhosis
APRI (aspartate aminotransferase [AST]-to-platelet
ratio index) is recommended as the preferred non-
invasive test (NIT)
Transient elastography (e.g. FibroScan) or
FibroTest preferred when available and cost not a
constraint
19. Others
Quantification of HBsAg
Significantly improved recently by the introduction
of new automated assays
Potential role for quantitative serum HBsAg in on-
treatment prediction of virological response to
CHB therapy
20. Natural history of chronic hepatitis B
CHB is dynamic and complex, and progresses
non-linearly through several recognizable phases
The phases are of variable duration, are not
necessarily sequential, and do not always relate
directly to criteria and indications for antiviral
therapy.
21. Natural history of chronic hepatitis B
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a Not all persons after HBeAg seroconversion enter the inactive phase. Up to 20% may progress directly from HBeAg immune active to anti-HBe immune escape phase
22. Natural history of chronic hepatitis
B
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23. Natural history of chronic hepatitis
B
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28. Initial evaluation of patients
History and physical examination
Family History of liver disease, HCC
Laboratory tests to assess liver disease
Tests for HBV replication—HBeAg/anti-HBe, HBV
DNA.
Tests to rule out viral co-infections—anti-HCV,
anti-HDV, and anti-HIV in those at risk.
Tests to screen for HCC–AFP at baseline and, in
high risk patients-Ultrasound (USG).
Consider liver biopsy to grade and stage liver
disease - for patients who meet criteria for chronic
hepatitis
29. Recommendations: Who to treat and who not to
treat in persons with chronic hepatitis B
Who to treat
As a priority, all adults, adolescents and children with CHB and clinical
evidence of compensated or decompensated cirrhosis (or cirrhosis
based on APRI score >2 in adults) should be treated, regardless of ALT
levels, HBeAg status or HBV DNA levels
Treatment is recommended for adults with CHB who do not have
clinical evidence of cirrhosis (or based on APRI score ≤2 in adults), but
are aged more than 30 years (in particular), and have persistently
abnormal ALT levels and evidence of high-level HBV replication (HBV
DNA >20 000 IU/mL), regardless of HBeAg status
Existing recommendation for HBV/HIV-coinfected persons1:
In HBV/HIV-coinfected individuals, ART should be initiated in all
those with evidence of severe chronic liver disease, regardless of CD4
count; and in all those with a CD4 count ≤500 cells/mm3, regardless of
stage of liver disease
30. Who not to treat but continue to monitor
Antiviral therapy is not recommended and can be deferred in
persons without clinical evidence of cirrhosis (or based on APRI
score ≤2 in adults), and with persistently normal ALT levels and
low levels of HBV replication (HBV DNA <2000 IU/mL),
regardless of HBeAg status or age
Continued monitoring is necessary in all persons with CHB, but
in particular those who do not currently meet the above-
recommended criteria for who to treat or not treat, to determine if
antiviral therapy may be indicated in the future to prevent
progressive liver disease. These include:
persons without cirrhosis aged 30 years or less, with HBV
DNA levels >20 000 IU/ mL but persistently normal ALT;
HBeAg-negative persons without cirrhosis aged 30 years or
less, with HBV DNA levels that fluctuate between 2000 and 20
000 IU/mL, or who have intermittently abnormal ALT levels
31. Suppression of HBV replication to undetectable
levels
Decrease hepatic necroinflammation and fibrosis
Prevent progression to cirrhosis, liver failure and
HCC
Goals of treatment
Chronic Hepatitis B
32. Treatment Options
Currently, seven antiviral agents (lamivudine,
adefovir, entecavir, telbivudine, tenofovir,
emtricitabine, standard and PEG-IFN) are
approved for the treatment of CHB
33. Injectables in HBV treatment
● Immunomodulators
Mode of Action
• Enhances phagocytic activity of macrophages
• Inhibits viral replication in virus-infected cells
• Increases cytotoxicity of lymphocytes for target cells
Interferon alpha 2b
Peg- interferon
alpha 2a/2b
IFN
PEG IFN
34. Oral drugs: Nucleoside/nucleotide
Analogues
Mode of Action
•Mainly act by inhibition of HBV DNA polymerase enzyme
activity resulting in decrease of viral replication
Lamivudine
Adefovir
Entecavir
Telbivudine
Tenofovir
3TC/LAM
ADV
TDF
ETV
LdT
35. Antiviral agents active against hepatitis B
virus infection (in order of potency and
barrier to developing resistance)
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36. Orals vs. IFN
The advantage of NA therapy over IFN includes few side-effects
and a one-pill-a-day oral administration.
The main advantages of IFN over NAs -absence of resistance,
and achievement of higher rates of HBeAg and HBsAg loss
However, the disadvantages of IFN are that less than 50% of
persons treated will respond, its high cost, administration by
injection and common side-effects, which precludes its use in
many persons, particularly in resource-limited settings.
A number of relative and absolute contraindications to IFN -
presence of decompensated cirrhosis and hypersplenism,
thyroid disease, autoimmune diseases, severe coronary artery
disease, renal transplant disease, pregnancy, seizures and
psychiatric illness, concomitant use of certain drugs, retinopathy,
thrombocytopenia and leucopenia
IFN also cannot be used in infants less than 1 year and in
pregnant women
37. WHO Recommendations: first-line antiviral
therapies for chronic hepatitis B
In all adults, adolescents and children aged 12 years or older in whom
antiviral therapy is indicated, the nucleos(t)ide analogues (NAs) which
have a high barrier to drug resistance (tenofovir or entecavir) are
recommended. Entecavir is recommended in children aged 2–11 years
NAs with a low barrier to resistance (lamivudine, adefovir or
telbivudine) can lead to drug resistance and are not recommended
Existing recommendation for HBV/HIV coinfected persons (including
pregnant women and adults with tuberculosis (TB) and HBV
coinfection):
In HBV/HIV-coinfected adults, adolescents and children aged 3 years
or older, tenofovir + lamivudine (or emtricitabine) + efavirenz as a
fixed-dose combination is recommended as the preferred option to
initiate ART
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38. National Institute for Health and
Care Excellence - treatment
guidelines
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39. Drug doses
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40. Comparison of antiviral agents for chronic
hepatitis B
World J Gastroenterol 2014; 20(20): 6262-6278
41. What is response to treatment ?
Virologic
• Decrease in HBV
DNA levels
Biochemical
• Normalization of
ALT levels
Histologic
• Improvement in
Histology
Serologic
• HBsAg
seroconversion
• HBeAg
Seroconversion
42. HBV Resistance
The primary limitation of all oral antiviral agents is development
of viral resistance because of mutations in the viral DNA during
replication
Lamivudine and telbivudine are most likely to fail because of
resistance
If resistance develops to one agent, the effectiveness of a
second agent with the same site of action is reduced
The risk of resistance increases whenever patients have
persistent detectable HBV DNA levels
The addition of a second agent with a different site of action or
switch to a potent drug is vital in patients with detectable serum
HBV DNA levels after six to 12 months of therapy
44. WHO Recommendations: Second-line Antiviral
therapies for management of treatment failure
In persons with confirmed or suspected antiviral
resistance (i.e. history of prior exposure or
primary non-response) to lamivudine, entecavir,
adefovir or telbivudine, a switch to tenofovir is
recommended
Primary non-response (defined as less than 1 log
decrease in HBV DNA level after 3 months of
treatment) is rare in persons initiating and
adherent to entecavir or tenofovir treatment, but
can occur in persons treated with lamivudine,
adefovir or telbivudine
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45. WHO Recommendations: when to stop treatment
Lifelong NA therapy
All persons with cirrhosis based on clinical evidence (or APRI score >2
in adults) require lifelong treatment with nucleos(t)ide analogues (NAs),
and should not discontinue antiviral therapy because of the risk of
reactivation, which can cause severe acute-on-chronic liver injury
Discontinuation
Discontinuation of NA therapy may be considered exceptionally in:
persons without clinical evidence of cirrhosis (or based on APRI
score ≤2 in adults);
and who can be followed carefully long term for reactivation;
and if there is evidence of HBeAg loss and seroconversion to anti-
HBe (in persons initially HBeAg-positive) and after completion of at
least one additional year of treatment;
and in association with persistently normal ALT levels and
persistently undetectable HBV DNA levels.
Retreatment
Relapse may occur after stopping therapy with NAs. Retreatment is
recommended if there are consistent signs of reactivation (HBsAg or
HBeAg becomes positive, ALT levels increase, or HBV DNA becomes
detectable again)
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46. WHO Recommendations : Monitoring for disease
progression and treatment response
It is recommended that the following be
monitored at least annually:
ALT levels (and AST for APRI), HBsAg, HBeAg,
and HBV DNA levels
Non-invasive tests (APRI score or FibroScan) to
assess for the presence of cirrhosis, in those
without cirrhosis at baseline
If on treatment, adherence should be monitored
regularly and at each visit
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47. WHO Recommendations :Monitoring for disease
progression and treatment response
More frequent monitoring
In persons who do not yet meet the criteria for antiviral
therapy: persons who have intermittently abnormal ALT levels
or HBV DNA levels that fluctuate between 2000 IU/mL -20 000
IU/mL and in HIV-coinfected
In persons on treatment or following treatment
discontinuation: More frequent on-treatment monitoring (at
least every 3 months for the first year) is indicated in:
persons with more advanced disease (compensated or
decompensated cirrhosis)
during the first year of treatment to assess treatment response and
adherence
where treatment adherence is a concern
in HIV-coinfected persons; and in persons after discontinuation of
treatment
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48. WHO Recommendations :Monitoring for
hepatocellular carcinoma (HCC)
Routine surveillance for HCC with abdominal
ultrasound and alpha-fetoprotein testing every six
months is recommended for:
persons with cirrhosis, regardless of age or other risk
factors
persons with a family history of HCC
persons aged over 40 years without clinical evidence
of cirrhosis, and with HBV DNA level >2000 IU/mL
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49. WHO Recommendations :Monitoring
for tenofovir and entecavir toxicity
Measurement of baseline renal function and
assessment of baseline risk for renal dysfunction
should be considered in all persons prior to
initiation of antiviral therapy.
Renal function should be monitored annually in
persons on long-term tenofovir or entecavir
therapy, and growth monitored carefully in
children
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52. Specific populations
HBV/HDV coinfection
There are limited data to inform definitive guidance on
the management of persons with HDV infection
Persistent HDV replication is the most important
predictor of mortality and the need for antiviral therapy.
PEG-IFN is the only drug effective against HDV; antiviral
NAs have no or limited effect on HDV replication
optimal duration of therapy is not well defined
more than 1 year of therapy may be necessary
most patients relapse after discontinuation of therapy
New therapeutic agents and strategies are needed
53. Specific populations
HBV/HCV coinfection
HBV DNA levels are usually low or undetectable and as
HCV is responsible for the activity of chronic hepatitis in
most persons
Patients should generally receive initial treatment for HCV
infection
The optimal regimens are uncertain, and more treatment
studies are required in coinfected persons.
PEG-IFN and ribavirin can be effective
HBV DNA monitoring is necessary as there is a potential
risk of HBV reactivation during treatment or after
clearance of HCV, which can be treated with NAs
54. Specific populations
HBV/Tuberculosis
Groups at increased risk of infection with HBV are
also at risk of infection with TB
In the absence of a cough, weight loss, fever and
night sweats, active TB can be confidently ruled out.
Drug-induced liver injury with elevation of
aminotransferases is three- to sixfold higher in
persons coinfected with HBV, HCV or HIV who are
receiving antituberculosis drugs, due to
hepatotoxicity with isoniazid, rifampicin and
pyrazinamide
55. Specific populations
Extrahepatic manifestations
Comparative trials of antiviral therapy are lacking,
and the efficacy reported in case reports is variable.
Lamivudine has been the most widely used, and
entecavir and tenofovir would be expected to have
enhanced efficacy in this group.
PEG-IFN may worsen some immune-mediated
extrahepatic manifestations and it is advisable to
avoid its use.
56. Specific populations
Acute hepatitis B
Antiviral therapy is not necessary for uncomplicated
symptomatic acute hepatitis B, as >95% of
immunocompetent adults will spontaneously clear HBV
infection
Persons with fulminant or severe acute hepatitis may
benefit from NA therapy with entecavir or tenofovir, to
improve survival and reduce the risk of recurrent
hepatitis B
Duration of treatment is not established, but continuation
of antiviral therapy for at least 3 months after
seroconversion to anti-HBs or at least 12 months after
anti-HBe seroconversion without HBsAg loss is generally
advised
57. Specific populations
Children and adolescents
majority of children will not require antiviral therapy
early identification and monitoring of children at risk for
progression of liver disease guided by liver histology and
a family history of HCC remains important
Only conventional IFN, lamivudine and adefovir have
been evaluated for safety and efficacy, but children
generally have a similar response as adults
IFN cannot be used in infants aged less than 1 year
in adolescents and children above the age of 12 years
tenofovir is approved for use
Entecavir is approved for use in children with CHB
above 2 years of age
58. Specific populations
Pregnant women
Indications for treatment in adults with CHB also
apply to pregnant women.
Tenofovir is the preferred antiviral, because it has a
better resistance profile and more extensive safety
data in pregnant HBV-positive women.
Safety of entecavir in pregnancy is not known, and
IFN-based therapy is contraindicated
Prevention of mother-to-child HBV transmission
deliver the first dose of hepatitis B vaccine as soon as
possible after birth, preferably within 24 hours followed by at
least two timely subsequent doses
59. Specific populations
Dialysis and renal transplant patients
persons with end-stage renal disease, including renal
transplant recipients, who should be screened for HBV
infection, and HBV-seronegative persons vaccinated
Renal function should be monitored during antiviral therapy
All Nas require dose adjustment and should be used with
caution in persons with renal impairment or in renal
transplant recipients
Unexpected deterioration of renal function during antiviral
therapy may necessitate a change of treatment or further
dose adjustment.
HBsAg-positive persons undergoing renal transplantation
should receive prophylactic NA therapy to prevent HBV
reactivation
IFN-based therapy is not recommended in renal transplant
recipients because of the risk of graft rejection
62. Prevention: Hepatitis B Vaccines
Vaccination of infants and, in particular, delivery of
hepatitis B vaccine within 24 hours of birth is 90–95%
effective in preventing infection with HBV as well as
decreasing HBV transmission if followed by at least two
other doses
WHO recommends universal hepatitis B vaccination for all
infants, and that the first dose should be given as soon as
possible after birth 3 doses: month 0, 1, 6.
Sero-protection requires: anti HBs titer>=10 mIU/ml
Factors associated with poor response: older age, chronic
medical illness (cirrhosis, kidney failure, diabetes),
decreased immune response, smoking, obesity, genetics
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63. Indications for HBV Vaccines
Hepatitis B immune globulin and HB vaccine to
infants of HBsAg+ mothers(90% efficacy)
All infants, children and adolescents who were
not vaccinated at birth
Vaccination of adults at risk of infection:
Occupational
Sexual / household contacts
Injection drug users
Long-term residence in high prevalence areas
64. Conclusion
Chronic hepatitis B (CHB) virus infection is a global
public health problem
Wide clinical spectrum ranging from a subclinical
inactive carrier state, to progressive chronic hepatitis,
cirrhosis, decompensation, and hepatocellular
carcinoma
Current international guidelines recommend first-line
treatment of CHB infection with pegylated interferon,
entecavir, or tenofovir
Future research will focus on identifying patients who
can successfully stop oral therapy as well as on novel
therapies or combinations of therapies that can target
the HBV at various levels