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Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Hepatitis B Virus : Hepatitis B Virus History & Introduction : History & Introduction Viral hepatitis is a common infectious disease that kills about 1.5 million people every year. Although hepatitis had been recognized for centuries, doctors had no idea what caused it until the 1940s when they came to suspect that a virus carried in human blood was responsible. Intensive research ensued to isolate the infectious agents causing two types of hepatitis, hepatitis A and hepatitis B. However, the breakthrough came from an independent study in which researchers were looking for immune reactions to foreign proteins in the blood of patients who had received many transfusions. Slide 3: Dr. Blumberg, when studying hemophilia in 1965, found an antibody in two patients which reacted against an antigen from an Australian Aborigine. Subsequent study found the Australian Antigen to be the Hepatitis B surface antigen. Dr. Blumberg was awarded the Nobel Prize for his discovery. DESCRIPTION : DESCRIPTION HBV, small double stranded DNA virus Hepadnaviridae Infection restricted to humans and higher apes High levels in blood (102 to 1010 copies/ml) Causes both acute and chronic hepatitis Parenteral, sexual and maternal-infant spread Marked geographic variation in incidence Common in Asia & Africa, uncommon in the United States and Western Europe Classification : Classification Family: Hepadnaviridae Genus: Orthohepadnavirus Genome: DNA defect Morphology : Morphology Slide 7: Lipid Bilayer HBsAg Protein Core: HBcAg DNA Slide 8: Enveloped virion containing partial double-stranded circular DNA genome Replication occurs through an RNA intermediate Virus encodes and carries a reverse transcriptase Virus encoded several antigenically and clinically predictive important proteins Virus has a strict tissue tropism to the liver Virus infected cells produce and release large amounts of HBsAg particles lacking DNA Viral DNA can integrate into the host chromosome Cultivation : Cultivation Since hepatitis virus has the propensity in vivo to infect human hepatocytes it seemed appropriate to undertake attempts at hepatitis virus cultivation using hepatocyte cultures. Early studies led to technology for the cultivation of fetal hepatocytes with the exclusion of fibroblastic cells. Similar approaches were used to cultivate adult hepatocytes and most recently these recent studies have demonstrated the successful long-term cultivation of adult hepatocytes for periods in excess of 10 weeks. The conditions for growth have been delineated and the methods are now reproducible. The inocula used have been hepatitis B antigen positive sera known to be rich in Dane particles,from liver biopsies obtained from patients with hepatitis B surface antigen positive chronic aggressive hepatitis. Inoculation of cultures with Dane particle-rich hepatitis B sera has not resulted in cytopathogenic change (CPE) in monolayer cultures. Efforts have been devoted at attempts at cultivation of hepatitis B virus by using 'slow virus techniques'. By means of cocultivation, mixed monolayers of normal hepatocytes were co-cultivated with hepatocytes obtained from liver biopsies of patients with hepatitis B surface antigen positive chronic aggressive hepatitis. The cell layers which resulted were maintained and were sub-cultured but did not yield evidence of either CPE or evidence of multiplication of hepatitis B surface antigen HBV Structure & Antigens : HBV Structure & Antigens Dane particle HBsAg = surface (coat) protein ( 4 phenotypes : adw, adr, ayw and ayr) HBcAg = inner core protein (a single serotype) HBeAg = secreted protein; function unknown Transmission : Transmission Hepatitis B is transmitted through: Blood Blood sucking arthropods (mainly in the tropics). Blood transfusions Contaminated drinking water or ice Feces Raw or uncooked shellfish (oysters, clams or mussels) Saliva Seminal fluid Uncooked fruits or vegetables grown with or washed in contaminated water Urine Vaginal secretions Pathogenesis & Immunity : Pathogenesis & Immunity Virus enters hepatocytes via blood Immune response (cytotoxic T cell) to viral antigens expressed on hepatocyte cell surface responsible for clinical syndrome 5 % become chronic carriers (HBsAg> 6 months) Higher rate of hepatocellular ca in chronic carriers, especially those who are “e” antigen positive Hepatitis B surface antibody likely confers lifelong immunity (IgG anti-HBs) Hepatitis B e Ab indicates low transmissibility Slide 13: Incubation period From 2 weeks to 6 months after viral entry to the liver, during which time a person is extremely contagious Symptoms disappear over 6-12 months until complete recovery Hepatitis B symptoms are similar to Hepatitis A but can also include: Muscle/joint aches Pain in the abdomen However, the virus may continue its silent attack on the liver which over a period of years can lead to: Cirrhosis scarring of the liver which slows the blood flow through the liver, causing increased pressure in the vein that transports blood from the stomach and the intestines to the liver Slide 14: Lifelong infection Varicose veins esophageal varicies can develop in the stomach and esophagus and these large veins can break without warning, causing a person to vomit blood or have black, tarry stools Over 5,000 persons die from chronic liver disease caused by the Hepatitis B Virus infection each year including: Liver cancer Liver cell damage Liver failure Scarring of the liver Laboratory Diagnosis : Laboratory Diagnosis Laboratory Diagnosis : Laboratory Diagnosis A battery of serological tests are used for the diagnosis of acute and chronic hepatitis B infection. 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. 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. Current Treatment Options : Current Treatment Options Interferon alfa (Intron A) Response rate is 30 to 40%. Lamivudine (Epivir HBV) (relapse ,drug resistance) Adefovir dipivoxil (Hepsera) Slide 19: Side Effects A number of side effects have been experienced from this treatment including: Depression Diarrhea Fatigue Flu-like symptoms Headache Loss of appetite Nausea Thinning of hair Vomiting Blood tests are needed to monitor levels of Interferon as it can also lower the production of white blood cells, platelets and liver enzymes by depressing the bone marrow Prevention : Prevention Prevention : Prevention Vaccination - highly effective recombinant vaccines Hepatitis B Immunoglobulin (HBIG) -exposed within 48 hours of the incident/ neonates whose mothers are HBsAg and HBeAg positive. Other measures -screening of blood donors, blood and body fluid precautions. Prevention : Prevention HBV: Pre-exposure prophylaxis: Vaccine :months 0,1,6 Booster is not recommended Post-exposure prophylaxis: HBIG:0.06 cc/kg and complete course of vaccine Slide 23: THANK YOU!!! Sahan Mahanama 3rd year Kursk State Medical University Russia You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.