Hepatitis B

Hepatitis B

1. HEPATITIS B

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

3. 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

4. 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)

5. 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 .

6. 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 )

7. 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.

8. 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.

9. 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.

10. 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 ) Core antigen (HBcAg) e antigen (HBeAg

11. STRUCTURE OF HEPATITIS B VIRUS

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

13. 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

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

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

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

17. 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.

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

19. 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 .

20. 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

21. 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 .

22. 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.

23. 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 .

24. 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.

25. 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.

26. 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

27. 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

28. 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

29. 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

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

31. 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.

32. 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.

33. 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

34. 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

35. 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

36. 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

37. 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

38. 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

39. 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

40. 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

41. TREATMENT OF CHRONIC HEPATITIS B

42. 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

43. THANKS TO ALL