Hepatitis B

2. HEPATITIS B

3. HEPATITIS B
• PREPARED BY :-
DR ABDUL SAMI
MPHIL EASTERN MEDICINE

4. HEPATITIS
• The term hepatitis describes inflammation of the liver. Hepatitis may be
caused by alcohols, drugs, autoimmune diseases, metabolic diseases, and
viruses. Viral infections accounts for more than half the cases of acute
hepatitis.
• Viral hepatitis is a systemic infection affecting the liver predominately
with primary inflammation of the liver

5. TYPES OF HEPATITIS
There are different types of Hepatitis viruses :-
• Hepatitis A (HAV)
• Hepatitis B (HBV)
• Hepatitis C (HCV)
• Hepatitis D (HDV)
• Hepatitis E (HEV)
• Hepatitis F – Not separate entity – Mutant of B Virus.
• Hepatitis G (HGV)

6. HEPATITIS B
• Hepatitis B is a serious and common infectious diseases of the liver,
affecting millions of people throughout the world.
• The severe pathological consequences of persistent HBV infections
include the development of chronic hepatic insufficiency, cirrhosis
and hepatocellular carcinoma (HCC).
• All of these are RNA viruses except HBV which is a DNA viruses.

7. CLASSIFICATION OF VIRAL HEAPTITIS
The viral hepatitis is classified as:
• Acute hepatitis (self-limited liver injury of less than 6 months)
• Chronic hepatitis ( hepatic inflammation more than 6 months)

8. PREVALENCE OF HEPATITIS B
• More than 2,000 million people alive today have been infected with
HBV at some time in their lives. Of these, about 350 million remain
infected chronically and become carriers of virtues. Three quarters of
the world’s population live where there are high levels of infection.

9. HEPATITIS B VIRUS
• Hepatitis B is caused by the hepatitis B virus
(HBV), an enveloped virus containing a
partially double stranded, circular DNA
genome, and classified within the family of
hepadnavirus.
• The virus interferes with the functions of liver
while replicating in hepatocytes. The immune
system is then activated to produce a specific
reaction to combat and possibly eradicate the
infectious agents. As a consequence of
pathological damage, the liver becomes
inflamed.

10. STRUCTURE OF HEPATITIS B VIRUS
• Hepatitis virus is a DNA virus with a remarkably compact genomic
structure.
• It have circular partially double-stranded DNA viruses.
• Replication occurs by reverse transcriptase.
• It is small, circular, 3200 base- pair size, HBV DNA codes for four
sets of viral products and has a complex, multi particle structure.

11. STRUCTURE OF HEPATITIS B VIRUS
• The hepatitis B virus is 42nm in diameter and composed of 27 nm
nucleocapsid core (HBcAG), surrounded by outer lipo protein coat (also
called envelope) containing the surface antigen (HBsAG)
• Virion also referred to as Dane particle (ds-tranded DNA)
• Core antigens located in the center (nucleocapsid)
1. Core antigen (HBcAg)
2. e antigen (HBeAg

12. STRUCTURE OF HEPATITIS B VIRUS

13. STRUCTURE OF HEPATITIS B VIRUS
• HBsAg = surface (coat) protein
• HBcAg = inner core protein
• HBeAg = secreted protein

14. REPLICATION OF HEPATITIS B VIRUS
• The HBV virion binds to a receptor at the surface of the hepatocyte.
• Viral nucleocaspids enter the cell and reach the nucleus, where the viral
genome is delivered.
• Reverse transcription: one of the mRNAs is replicated with a reverse
transcriptase making the DNA that will eventually be the core of the progeny
virion
• RNA intermediate: HBV replicates through an RNA intermediate and
produces and release antigenic decoy particles.
• Integration: Some DNA integrates into host genome causing carrier state

15. HOW VIRUS REPRODUCE
• First the virus attached to a liver cell membrane

16. HOW VIRUS REPRODUCE
• The virus is then transported into the liver cell.

17. HOW VIRUS REPRODUCE
• The core particle then releases it’s contents of DNA and DNA
polymerase into the liver cell nucleus.

18. HOW VIRUS REPRODUCE
• Once within the cell nucleus the
hepatitis B DNA causes the liver cell to
produce, via messenger RNA ; HBs
protein , HBc protein , DNA
polymerase, the HBe protein, and other
undetected protein and enzymes.
• DNA polymerase causes the liver cell to
make copies of hepatitis B DNA from
messenger RNA.

19. HOW VIRUS REPRODUCE
• The cell then assembles “live” copies of virus.

20. HOW VIRUS REPRODUCE
• However because of the excess numbers
of surface proteins produced many of
these stick together to form small spheres
and chains. These can give a
characteristic “ground glass” appearance
to blood samples seen under microscope.

21. HOW VIRUS REPRODUCE
• The copies of the virus and excess surface antigen are released from
the liver cell membrane into blood stream and from there can infect
other liver cells

23. MODE OF TRANSMISSION
• Sexual - sex workers and homosexuals are particular at risk.
• Parenteral –(Blood, syringes etc.) Health Workers are at increased risk.
• Perinatal - Mothers who are HBeAg positive are much more likely to
transmit to their offspring than those who are not.

24. STAGES OF DISEASE
FIRST STAGE
• The duration of this stage for healthy adults is approximately 2-4
weeks and coincide with the incubation period. For newborns, the
duration of this period often is decades.
• Active viral replication is known to continue despite little or no
elevation in the aminotransferase levels and no symptoms of illness.

25. STAGES OF DISEASE
SECOND STAGE
• In the second stage, an inflammatory reaction with a cytopathic effect
occurs.
• HBeAg can be identified in the sera and a decline of the levels of HBV DNA
is seen.
• The duration of this stage for patients with acute infection is approximately
3-4 weeks (symptomatic period).
• For patients with chronic infection, 10 years or more may elapse before
cirrhosis develops.

26. STAGES OF DISEASE
THIRD STAGE
• In the third stage, the host can target the infected hepatocytes
and the HBV Viral replication no longer occurs.
• HBeAb can be detected. The HBV DNA levels are lower or
undetectable, and aminotransferase levels are within the
reference range.
• In this stage, an integration of the viral genome into the host's
hepatocyte genome takes place.
• HBsAg still is present.

27. STAGES OF DISEASE
FOURTH STAGE
• In the fourth stage, the virus cannot be detected and antibodies to
various viral antigens have been produced.
• Different factors have been postulated to influence the evolution of
these stages, including age, sex, immunosuppression, and co-infection
with other viruses.

28. PATHOLOGY
• There are three antigen-antibody system
1) HBsAg-- anti-HBs system:
• HBsAg appears 1-2 weeks (late up to 11-12 weeks) after exposure, persists for 1-6 weeks(
even 5 months) in acute hepatitis B.
• In chronic patients or carrier, HBsAg persist many years
• HBsAg is the marker of infectivity
• HBsAg can be found in blood and secretions: saliva,urine, semen, tears, sweat and breast
milk
• Anti-HBs appear after HBsAg disappear several weeks (or months) anti-HBs is
protective antibody, can persist for many years

29. PATHOLOGY
2) HBcAg—anti-HBc system
• HBcAg can be found in the nuclei of liver cells, no free HBcAg in serum
• HBcAg is the marker of replication of HBV
• The stage called window phase
• Anti-HBc IgM is a marker of acute infection and acute attack of chronic
infection of HBV. Anti-HBc IgG is the marker of past infection, high titer
means low level replication of HBV

30. PATHOLOGY
3) HBeAg—anti-HBe system
• HBeAg is a soluable antigen
• HBeAg is a reliable indicator of active replication of HBV
• Anti-HBe is a marker of reduced infectivity. If exist long may be a
marker of integration of HBV into liver cell

31. PATHOGENESIS
• HBV invades into the human body by skin and mucosa, Via blood flow
enters the liver and other organs such as pancreas, bile ducts, vessels, WBC,
bone marrow, glomerular basement membrane.
• HBcAg, HBsAg, HBeAg and HLA-Ⅰ appear on the liver cells infected with
are recognized by CTL simultaneously and lead to the cytolysis of liver cells.
• Helper T cell are activated by the receptor of HLA- on its surface combing
with HBsAg, HBcAg and HLAantigen on the B cells promote B cell to
release antiHBs and clear HBV
• The representation of HBcAg on the liver cells may cause cytopathy

32. SIGN & SYMPTOMS
• Fever
• Fatigue
• Loss of appetite
• Nausea
• Vomiting
• Abdominal pain
• Dark urine
• Clay-colored bowel movements
• Joint pain
• Jaundice
• Hepatomegaly

33. DIAGNOSIS
• HBsAg - used as a general marker of infection.
• HBsAb - used to document recovery and/or immunity to HBV
• infection.
• anti-HBc IgM - marker of acute infection.
• anti-HBcIgG - past or chronic infection.
• HBeAg - indicates active replication of virus and therefore
• infectiveness.

34. DIAGNOSIS
• Anti-Hbe - virus no longer replicating. However, the patient can still
be positive for HBsAg which is made by integrated HBV.
• HBV-DNA - indicates active replication of virus, more accurate than
HBeAg especially in cases of escape mutants. Used mainly for
monitoring response to therapy.

35. HEPATITIS B VACCINATION
DISCOVERIES
• 1965 Discovery of Australian antigen
• 1973 Successful HBV infection of chimpanzees
• 1981 Licensure of plasma-derived vaccine
• 1986 Licensure of recombinant vaccine
• 1991 Universal infant vaccination
• 1996 Universal adolescent vaccination

36. HEPATITIS B VACCINE
immune globulin (BayHep B, Nabi-HB)
• given along with the hepatitis B vaccine to unvaccinated people who
have been exposed to hepatitis B
Engerix-B, Recombivax HB
• safe and works well to prevent the disease
• a total of 3 doses of the vaccine are given over several months
• recommended for all children younger than 19 years

37. RECOMMENDATIONS FOR VACCINATION
• All children younger than 18 years, including newborns--especially
those born to mothers who are infected with HBV.
• All health care and public safety workers who may be exposed to blood
• People who have hemophilia or other blood clotting disorders and
receive transfusions of human clotting factors
• People who require hemodialysis for kidney disease

38. RECOMMENDATIONS FOR VACCINATION
• Travelers to countries where HBV infection is common - This includes
most areas of Africa, Southeast Asia, China and central Asia, Eastern
Europe, the Middle East, the Pacific Islands, and the Amazon River
basin of South America.
• People who are in prison
• People who live in residential facilities for developmentally disabled
persons

39. RECOMMENDATIONS FOR VACCINATION
• People who inject illegal drugs
• People with chronic liver disease such as hepatitis C
• People who have multiple sex partners or have ever had a sexually
transmitted disease
• Men who have sex with men

40. TREATMENT OF ACUTE HEPATITIS B
Acute hepatitis B infection
• If dehydration occurs, IV fluids are being prescribed to help the patient feel better.
• Medicines are being prescribed by the physician to control nausea and vomiting.
• People whose symptoms are well-controlled can be cared for at home. If dehydration
or other symptoms are severe, then the patient is managed at the hospital
• NOTE: No treatment can prevent acute HBV infection from becoming chronic

41. TREATMENT OF CHRONIC HEPATITIS B
Chronic hepatitis B infection
• Regularly measuring the amount of HBV DNA in the blood gives a
good idea of how fast the virus is multiplying
• Treatment: antiviral drugs

42. TREATMENT OF CHRONIC HEPATITIS B
• Interferon alfa-2b (Intron A) - was the standard treatment of chronic
hepatitis B for several years
• Lamivudine (Epivir) - an alternative for people who cannot or do not
want to take interferon
• Adefovir dipivoxil (Hepsera) - works well even in people whose disease
is resistant to lamivudine
• Entecavir (Baraclude) - newest medication approved for chronic
hepatitis B

43. TREATMENT OF CHRONIC HEPATITIS B

44. PREVENTIONS
• Safe Sex
• Don't share needles or other sharp equipment's such as razors
• Health care workers should follow standard precautions and handle
needles and sharps safely
• Think about the health risks if you are planning to get a tattoo or body
piercing

45. THANKS TO ALL