Hepatitis A, B, C, D, and E viruses can cause acute or chronic viral hepatitis in humans. Hepatitis A and E viruses do not result in chronic infections or carriers. Hepatitis B, C, and D can develop into chronic hepatitis in some cases. Diagnosis involves detecting viral antigens, antibodies, RNA, and liver enzymes. Prevention strategies include vaccination, hygiene, and food/water safety.

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. • Feco-oral route
• Crowded: early age, high sanitation: older
• Clinical finding
• IP: 3-4 weeks
• Asymptomatic in children
• Life long immunity
• No chronicity

4. 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)

5. Prevention and control
• Control food and water
• Good hygiene-hand refreshing
• Chlorine and proper sewage
• Active immunization
• Passive immunization

6. 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

7. 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)

8. 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

9. 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

10. 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

12. Acute phase with recovery

14. • 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

16. Interpretation of the result
1. serologic: four phase of HBV infection
2. Immunization: anti-Hbs
3. Transmissibility: HbeAg
4. Infectious virion present: Viral DNA

17. 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

18. 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

19. 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

20. 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

21. Hepatitis C vaccine
• Flaviviridae
• 6 genotypes, not correlated with clinical
disease, differ in response to antiviral therepy.
• Egypt: 4a
• Percutaneous or permucosal

22. • 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

24. • 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.

25. 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.

26. 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)

27. Hepatitis
• Diffuse inflammation of parenchyma
• Causes:
• Infective
• Metabolic
• Autoimmune
• Chemicals
• drugs

28. 1.Hepatotropic
- most common form
- A, B, C, D, E, G
2. Systemic

29. 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

30. 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

31. 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

32. 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

33. 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