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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)

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

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)

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

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

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)

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

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

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

Acute phase with recovery

• 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

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

Test

acute phase Positive Negative Positive

Window phase Negative Negative Positive

HBs Ag Anti-Hbs Anti-Hbc

Complete Chronic recovery carrier state Negative Positive Positive Positive Negative Positive

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

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

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

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

• 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

• 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.

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.

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)

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

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

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

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

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

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

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 nonimmunized infants born to infected mother) • Increased risk of HCC