viral hepatitis

1. VIRAL HEPATITiS
ANGEL DAS Y.L
ROLL NO: 17

2. What is viral hepatitis?
 Infection of liver caused by hepatotropic viruses
(hepatitis viruses A, B, C, D, and E)
 other viruses that can also cause liver inflammation
include Cytomegalovirus, Epstein–Barr virus, or
Yellow fever.

3. 5 Main varieties of viruses
Hep A –> feco-orally
Hep B-> parenterally
Hep C-> mainly transfusion
Hep D-> associated as super infection with HBV
Hep E-> feco-orally

4. ETIOLOGIC CLASSIFICATION
Viral Hepatitis
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Hepatitis G

6. Benign, self limiting disease
Responsible for 20-25% of clinical acute hepatitis
Incubation period 2-6 weeks
Affected age group 5-14 years
Transmission feco-oral route
Shed in stool 2-3 weeks before & 1 week after the onset of
jaundice

7. Hepatitis A virus
 Small,icosahedral non-enveloped virus
 ss RNA virus
Serological Diagnosis
Anti HAV antibody
IgM-onset of acute hepatitis
IgG- after acute illness & provide life-long
immunity

9. Caused by HBV
Incubation period 4-26 weeks(1-4months)
Transmission:
 exposure to infectious blood or body fluids.
 Possible forms of transmission include:
sexual contact
blood transfusion
reuse of contaminated syringe
vertical transmission

10. Hep B produces
Acute Hepatitis
Chronic Hepatitis
Fulminant Hepatitis
Asymptomatic carrier stage
Role in development of hepatocellular Carcinoma

11. MORPHOLOGY - HBV
 Partially ds DNA virus
a) HBV occurs in 3 morphology form in serum:
o Small particles – 2 forms
22nm diameter
exist as
tubules
spheres
o Large particles – 42 nm diameter
also called as “Dane particles”
double shelled spherical particles

12. HBV evokes
 Humoral immunity
 Cell mediated immunity
 Hepatocyte damage – attack of virus infected cells by CD8+
cytotoxic T cells
HBsAg anti -HBsAg
HBcAg anti -HBcAg
HBeAg anti -HBeAg
Serological Diagnosis

13. HBsAg
before the onset of symptoms
appears after 6 week of infection
declines in 3-6 months
>6 months carrier state
Anti HBs Ab
appears late – 3 months after the onset
HBeAg
soon after HBsAg, present transiently 3-6 weeks
indicator of continued viral replication , infectivity
>10 weeks - development of CLD & carrier state
Anti HBe ab
prognostic sign for resolution of infection
HBc Ag
cannot be detected in blood
demonstrated in nuclei of hepatocyte in
chronic hepatitis & carrier state
Anti –HBc ab
1st ab appears in serum, before the onset of symptoms

16.  Major cause of chronic liver disease(80%)
 Key features-Persistence of infection &
chronic hepatitis
 Late consequence – cirrhosis & hepatocellular
carcinoma
Mode of transmission:
1. Parental: inoculations and blood transfusion
2. Vertical transmission
3. Close personal contact – sexual contact
Type of virus:
 -HCV is a small-enveloped virus
 -ssRNA
 Incubation period : 2 – 26 weeks(mean : 6-12 weeks)

17. Serological Diagnosis
HCV RNA – few days after exposure
Anti HCV ab – within weeks to few months
S. Aminotransferase- 2- 12 weeks

19. 19
HBsAg
RNA
 antigenDefective virus,cause infection only in
presence of HBV
Small, ssRNA particle
Double shelled
outer shell- HBsAg
inner shell-  Ag

22.  Enterically transmitted virus
 By contamination of water supplies
 Usually affects young or middle aged individuals
 High mortality in pregnant women otherwise self limited disease
 Not associated with chronic liver disease