Virology of hepatitis

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by: Wan Athirah bt Wan Abd Halim

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Virology of hepatitis

  1. 1. Hepatitis A Virus • Picornaviridae family • One serotype- stable(protective for life) • Non-enveloped • Single stranded positive • Stable ( ether, acid, heat: 60 c for 1 hr) • Destroyed (autoclaving, boil 5 min, chlorine)
  2. 2. • Feco-oral route • Crowded: early age, high sanitation: older • Clinical finding • IP: 3-4 weeks • Asymptomatic in children • Life long immunity • No chronicity
  3. 3. Lab investigation • Detect HAV antibodies - IgM: acute phase (most reliable) - IgG: life long protection • Detect HAV antigen in stool (ELISA) • Detect HAV RNA in stool (PCR, nucleic acid hybridization)
  4. 4. Prevention and control • Control food and water • Good hygiene-hand refreshing • Chlorine and proper sewage • Active immunization • Passive immunization
  5. 5. Hepatitis E virus • Unclassified genus • Feco-oral route, water borne • Endemic in tropical countries • IP: 40 days • HIGH MORTALITY RATE IN PREGNANT WOMAN • No chronicity • Detect anti HEV antibodies and HEV-RNA in serum • Same prevention and control as hepatitis A
  6. 6. Hepatitis B virus • Hepadnavirus • Icosahendral nucleocapsid • Partially double-stranded circular DNA genome • Outer shell: HBsAg • Inner core: Hbc Ag • Secreted in soluble form: HBeAg • EM of serum: spherical particles, filamentous particles and complete virions (Dane particle)
  7. 7. Epidemiology and transmission • High titre are present in blood and serum 1. Percutaneous • Blood transfusion • Contaminated syringes and needles • Improperly sterilized instrument • Razor and tooth brush sharing • Needle stick injuries 2. Sexual transmission 3. Perinatal transmission
  8. 8. Clinical features • IP: 10-12 weeks • Many asymptomatic • Outcome: • Adult: 90-95% recover completely • Infected infant: chronic carries • Chronic: can lead to cirrhosis, liver failure and death • CHRONIC: HIGH RISK OF HCC • HBV Vaccine
  9. 9. Virologic and serologic events • First appearance: HBs Ag • Viremic stage: HBV DNA and HBE Ag • HBsAg , appears 2-6 weeks before clinical and biochemical evidence, throughout the course, disappearr by 6 months after exposure • Viral replication: IgM specific anti HBc • Window phase: disappearance of Hbs Ag. After that, antibody to HbsAg is detected • Start of resolution of disease: anti Hbe
  10. 10. Acute phase with recovery
  11. 11. • HBV chronic carriers: Hbs Ag persists for more than 6 months in thepresence of HbeAg or anti-Hbe. • Low titres of IgM anti-Hbc are found in the sera of most chronic carriers. • Lab: • ELISA: HBV antigen and antibodies • PCR: HBV DNA
  12. 12. Interpretation of the result 1. serologic: four phase of HBV infection 2. Immunization: anti-Hbs 3. Transmissibility: HbeAg 4. Infectious virion present: Viral DNA
  13. 13. Test acute phase Window phase Complete recovery Chronic carrier state HBs Ag Positive Negative Negative Positive Anti-Hbs Negative Negative Positive Negative Anti-Hbc Positive Positive Positive Positive
  14. 14. Prevention and control 1. Hepatitis B vaccine - Prevent consequence - Dose: 0,1,6 - Plasma derived HBs Ag - All infant, health care personnel, on transfusion, dialysis 2. Hepatitis B immunoglobulin (simultenously) - Soon after exposure - Infants to HBV positive mother, exposed person
  15. 15. Hepatitis D virus • Defective virus, uses Hbs Ag as envelope (HBV is helper virus) • Blood borne virus Two types: • Coinfection: both at same time • Superinfection: of chronically infected HBV
  16. 16. Outcome: • Coinfected: more severe that HBV alone, but incidence of chronic hepatitis is about the same • Superinfected: much more severe, higher incidence of chronic hepatitis Lab: • ELISA: HD Ag, IgM and anti HD antibodies • PCR: HD-RNA
  17. 17. Hepatitis C vaccine • Flaviviridae • 6 genotypes, not correlated with clinical disease, differ in response to antiviral therepy. • Egypt: 4a • Percutaneous or permucosal
  18. 18. • Appearance of anti-HCV antibodies: 8-9 weeks • HCV RNA: 1-3 weeks after exposure. The means of diagnosis in seronegative patients • Chronic hepatitis: serum ALT fluctuate overtime and maybe intermittently normal. HCV RNA may persists for decades
  19. 19. • Outcome: 70-90% chronic HCV infection • Resembles hepatitis B as regards predisposition to chronic liver disease, cirrhosis and HCC. • End stage liver disease associated with HCV is most common indication for liver transplantation.
  20. 20. Lab diagnosis 1. ELISA: detect antibodies to HCV, consider: - Early seronegative phase: negative result - Positive: acute, chronic, resolved? - False positive can occur. Confirmed by : RIBA. If positive, test for viral RNA for active disease. - Poor serologic response in some patient. Test for HCV RNA.
  21. 21. 2. RT-PCR, for derection of HCV RNA - Active disease - Early seronegative - Poor serologic patients • Acute self limiting: dissappear (resolved) • Measure viral load: response to antiviral therapy (quantitative PCR)
  22. 22. Hepatitis • Diffuse inflammation of parenchyma • Causes: • Infective • Metabolic • Autoimmune • Chemicals • drugs
  23. 23. 1.Hepatotropic - most common form - A, B, C, D, E, G 2. Systemic
  24. 24. Clinicopathological syndromes 1. Subclinical – asymptomatic, any type 2. Acute viral hepatitis – any type 3. Chronic viral hepatitis – HBV, HCV, HDV. NEVER HAV and HEV 4. Carrier state – mainly HBV. NEVER HAV, HEV 5. Fulminant hepatitis – HEV among pregnant females
  25. 25. Clinical course of acute hepatitis 1. HAV - Most undergo complete recovery 2. HBV - Most (>90%) complete recovery - 1-2% chronic hepatitis 3. HCV - >70% progress to chronic hepatitis - <30% undergo recovery - Few develop fulminant
  26. 26. 4. HDV - coinfection: • 90% undergo recovery • 3-4% develop fulminat • Rare progress to chronic hepatitis - Superinfection • 10-15%: recovery • 80%: chronic hepatitis • 7-10%: fulminant 5. HEV - Most undergo complete recovery - Pregnant females: fulminant (20%) - No chronic or carrier state
  27. 27. CHRONIC VIRAL HEPATITIS • Symptomatic, biochemical, serological evidence of inflammatory hepatic disease with histologically documented without improvement, more than 6 months • Mainly: HCV >70%, HDV (80% superinfection) and some HBV
  28. 28. CARRIER STATE • Not manifest symptoms, but persistent antigenemia(circulating infectious virus particles), more than 6 months with normal transaminases and no clinical symptoms. • Mainly: HBV (adults infected by HBV and non- immunized infants born to infected mother) • Increased risk of HCC

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