1. Hepatitis B virus
Dr. K. G. Maharjan
Liver unit, Bir hospital

2. Introduction
• Hepatitis is an inflammation of the liver.
• It is usually caused by viral & non viral infections also
due to toxins (alcohol) & drugs (mostly ATT)
• In our setup it maybe due to bacterial infection but
may be an autoimmune response as well.
• It is characterized by anorexia , jaundice, abdominal
pain, liver enlargement and sometimes fever.
• Others , usually bacterial infections leading to HV&IVC
thrombophlebitis, metabolic cause (Wilson disease)
• Congestive causes like ( HVOO,IVC disease , CHF)
• HBV can lead to cirrhosis and liver cancer.

3. Introduction
• Hepatitis is an inflammation of the liver.
• It is usually caused by viral & non viral infections also
due to toxins (alcohol) & drugs (mostly ATT)
• In our setup it maybe due to bacterial infection but
may be an autoimmune response as well.
• It is characterized by anorexia , jaundice, abdominal
pain, liver enlargement and sometimes fever.
• Others , usually bacterial infections leading to HV&IVC
thrombophlebitis, metabolic cause (Wilson disease)
• Congestive causes like ( HVOO,IVC disease , CHF)
• HBV can lead to cirrhosis and liver cancer.

4. Viral hepatitis
• The different types of viral hepatitis A,E,(virus
transmitted through the faces of an infected
person.
• Hepatitis B,C,D are serum hepatitis
• Hepatitis F,G, cryptogenic ( caused by a virus
as not identified)
• More hepatitis viruses are less common
yellow fever, epstien barr virus(EBV),
cytomegalovirus(CMV),

5. Hepatitis B virus
• HBV is a serious disease ,can cause lifelong
infection , liver cirrhosis ,liver cancer , and
liver failure ,death.
• HBV is 100 times more infectious than HIV and
10 times more infectious than HCV.
• HBV is a blood borne transmitted ( body fluids
, semen, saliva,vaginal fluid (high titers in the
blood and lower titer in body fluids)

6. Hepatitis B virus introductions
• HBV is a 42 nm,double-shelled DNA virus of
the class Hepadnaviridae.
• The outer surface membrane contains HBV
surface antigen (HBsAg) which also circulates
in blood as 22 nm spherical and tubular
particles.

7. HBV virus

8. Continu…
• The inner core of the virus contains HBV core
antigen (HBcAg) (HBeAg)
• HBV is a single molecule of partially double –
stranded DNA, and DNA- dependent DNA
polymerase.

9. Continu…

10. Risk groups
• 1, I/V drug users Health workers
• 2, Multiple sex partners
• 3,Homosexuals
• 4,Infant born to HBV infected mothers
• 5,Hemodialysis patients
• 6, Areas with high rates of HBV infections
• 7,Tatooing

11. HBV transmitted
• HBV is transmitted by the exchange of blood
& body fluids ,eg . Blood, semen, breast milk
,saliva and vaginal secretor fluids , tears.

13. Epidemiology
• Globally
• 50 million new cases per year
• 350-400 million chronic carriers 75% in Asia
• 520,000 deaths per year

14. Epidemiology in Nepal
• One epidemiology study in done in nepal
• Group;1, Population No. HBsAg
• a, Soldiers 922 20 (2.2%)
• b, healthy people 232 2 (0.8%)
from districts
• c, pregnant women 81 1 (1.2%)
• d, blood donors 624 5 (0.8%)
• blood donors 168 1 (0.6%)

15. Continu…….
• Group 2,
• Hospital staff 792 7 (0.8%)
• Student nurses 122 0
• Relatives of CLD 388 12 (3.1%)
• Patients
• Group 3,
• Hemophilia 4 1 (25%)
• Drug addicts 72 2(3%)
• Hemodialysis 41 1(2%)
• HBV carriers 49 49(100%)

16. Continu…
• Group 4,
• Chronic liver disease 145 57 (39%)
• Acute hepatitis 150 14 (9.3%)

18. Clinical course of hepatitis B infection
Death Recovery
1% 99%
Transient
Acute 100%
Subclinical
hepatitis
infection
25% 65%
Acute HBV
infection
10%
10-30% Chronic HBV 70-90%
Infection
Chronic Healthy
Hepatitis ?
HBsAg
Carrier
Cirrhosis
Hepatocellular
Carcinoma ?

19. HBsAg
True Positive Negative
ALT Search for other virus
Raised Normal
Anti-HbcIgM Positive HbcAb
Negative F/u after 6 months Positive Negative
F/U
HBeAg HBvDNA F/U
Positive Negative >105ml <105ml
Liver biopsy HBcAb
Rx F/U
HBvDNA Negative Positive
Rx Liver biopsy HBvDNA
HBvDNA
Absent Raised
Search for other causes
of
ALT

20. Infection
• Acute hepatitis B develops in approximately 30% to
50% of adults at the time of initial infection and is
characterized by anorexia, nausea , vomiting and
jaundice.
• SGPT raises 2 ½ times
• The risk of progression to chronic infection varies
with age , being highest among young children and
infants (30%-90%) and lowest among adolescents
and adults (2%-6%).
• Rates of progression to cirrhosis and HCC vary
according to age at acquisition of chronic
infections ,HBeAg status , co infection with
HGV,HIV,HCV, and alcohol abuse.

21. Clinical features
• The first serologic marker to appear following
acute infection is HBsAg, which can be
detected as early as 1 or 2 weeks and as late
as 11 or 12 weeks (mode 30-60 days) after
exposure to HBV
• HBeAg is generally detectable in patients with
acute infections, the presence of HBeAg in
serum correlates with higher titers of HBV and
greater infectivity.

22. Continu….
• A diagnosis of acute HBV infection can be
made on the basis of the detection of IgM
class antibody to HBV core antigen (IgM ,anti-
HBc) in serum ,It is generally detectable at the
time of clinical onset.

23. Serological markers ; HBV
• HBsAg: Marker of infection,presence
>6months=chronic
• HBeAg: active viral replication,
• Anti-HBsAg: indicates recovery and /or
immunity (after vaccine)
• Anti-Hbe: inactive viral replication
• Anti-HBc: infection or immunity

25. HBV genotypes
• HBV classified into 7 genotypes (A-G)
• -a: north america and western europe
• B&C: asia
• D: southern europe and india
• E:&G: africa
• F:central and south america and alaska
• H: central america
• B associated with less HCC, less active and more slowly
progressive liver disease than C
• A&B respond better to Interferon than C&D
• Genotype does not predict response to oral agents

26. HBV infection
• Chronic HBV: chronic necroinflammatory liver
disease >6month,ALT^,HBeAg-postive or –
negative, HBV DNA> 10 x4-5
• Inactive HBsAg carrier : Persistent infection
without necroinflammatory disease, ALT
normal , HBeAg -negative HBV DNA<10 x 4-5
• Resolved HBV: previous infection without
virological ,biochemicalor histological
evidence of active disease.

27. Continu…
• Acute exacerbation HBV: elevated ALT>10 x
ULN or >2 x baseline
• Reactivation of HBV: reappearance of
necroinflammatory disease in person known
to be inactive carrier or resolved HBV

28. Liver histology ≥
Phases of chronic HBV
• Immunotolerant phase: HBeAg- postive; HBV
DNA high (10 x 5-10) ALT normal
-candidates for therapy.
Immunoactive phase: HBeAg-postive or HBeAg –
negative,HBV DNA high (10 x4-10) ,ALT
elevated, symptoms +/-
Non replicative phase :(inactive HBV carrier)
HBeAg –negative HBV DNA low(<10 x4 ) ALT
normal, HBsAg may later become undectable.

29. Routine HBV carriers exam
• Follow-up interval 6 months : Tests : ALT and
AST; AFP. USG,
• Inactive HBsAg carrier: If ALT/AST increase , re
evaluate
• Chronic hepatitis B: CBC,LFT,HBeAg, anti-HBe

30. HBV infected mothers
• Hepatitis B immunoglobulin (HBIG 0.5 ml ,
I/M to new born.
• Hepatitis B vaccination should have been
given 12 hours of birth.

31. Post exposure prophylaxis
• 1, HBIG is required
• 2,the first dose of hepatitis B vaccine
immediately, 0 – 1 – 6 months.

32. Hepatitis B vaccine
• The standard regimen for adult is 10-20mcg
initially ( depending on the formulations ) .
• Schedules; 0 -1 -6 months.
• Alternative schedules have been approved
• 0 -1 -2 -12 months
• 0- 7 and 21 days ,plus 12 months
• Preferred site vaccine deltoid muscles

33. Treatment of chronic HBV
• Nucleoside/nucleotide analogues:
- Entecavir : 0.5-1.0 mg/d
• -Lamivudine : 100 mg/d
• -Adefovir dipivoxil :10mg/d
• -Tenoforvir : 300mg/d
• Interferon: interferon alfa-2b 5MU/d or 10MU tiw x 4
months.
• Peginterferon alfa-2a (Pegasys) 180 mcg/week x 24-48
weeks.
• Liver transplantation ( decompensated chronic HBV
with cirrhosis.

34. Reference
• Davidson principal and practice of medicine
• C.M.D.T
• Oxford hand book of medicine
• Liver unit, Bir hospital

35. Thank you
Thank you