The document summarizes various hepatitis viruses including Hepatitis A, B, C, D and E viruses. It discusses the clinical features, transmission, diagnosis and treatment of these viruses. It also briefly describes other viruses that can cause hepatitis such as cytomegalovirus, Epstein Barr virus and yellow fever virus.

2.  Hepatitis viruses: Hepatitis virus A,B, C, D,E
 Other Viruses:
Cytomegalovirus Echo virus
EBV Rubella virus
HSV Coxsackie-B
Yellow fever virus Marburg virus
VZV Lassa fever virus
Paramyxovirus Adeno virus
Enterovirus Rift valley fever virus

3. Source of
virus
feces blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
feces
Route of
transmission
fecal-oral percutaneous
permucosal
percutaneous
permucosal
percutaneous
permucosal
fecal-oral
Chronic
infection
no yes yes yes no
Prevention pre/post-
exposure
immunization
pre/post-
exposure
immunization
blood donor
screening;
risk behavior
modification
pre/post-
exposure
immunization;
risk behavior
modification
ensure safe
drinking
water
Type of Hepatitis
A B C D E

4.  Feco-oral contamination of food, water
(e.g., infected food handlers, raw shellfish,
travel to endemic area)
 Close personal contact
(e.g., household contact, sex contact,child day
care centers)
Blood exposure (rare)
 (e.g., injecting drug use, transfusion)
Hepatitis A & E Virus
Transmission

5.  Fulminant hepatitis (<1%)
Cholestatic hepatitis
Relapsing hepatitis
 Chronic sequelae: None
 Case fatality rate : 0.1% - 2.7%.

6. Fecal
HAV
Symptoms
0 1 2 3 4 5 6 12 24
Hepatitis A Infection
Total anti-
HAV
Titre ALT
IgM anti-HAV
Months after
Typical Serological Course

7. Symptoms
ALT IgG anti-HEV
IgM anti-HEV
Virus in stool
0 1 2 3 4 5 6 7 8 9 1
0
1
1
1
2
1
3
Hepatitis E Virus Infection
Titer
Weeks after Exposure

8. Presence of virus:
Blood -2 weeks before to < 1 week after jaundice
Stool -2 weeks before to 2 weeks after jaundice
Urine -Rare
Saliva, semen –Rare
Prevention
HAV Vaccine:
Available: contains inactivated HAV.
Dose: 2 doses, an initial dose followed by a
Booster dose at 6-12 months.
Immune globulin must be administered within 2 weeks after
exposure for maximum protection.
 HEV Vaccine :
Clinical trial in progress

9. Hepatitis B

11. Replication of Hepatitis B Virus

12. 1. Chronic Persistent Hepatitis -
asymptomatic
2. Chronic Active Hepatitis - symptomatic
exacerbations of hepatitis
3. Cirrhosis of Liver
4. Hepato cellular Carcinoma

13. Clinical outcomes of Hepatitis B infections

14. High Moderate
Low/Not
Detectable
blood semen urine
serum vaginal fluid feces
wound exudates saliva sweat
tears
Breast milk
Concentration of Hepatitis B
Virus in Various Body Fluids

15. Household, 3%
Other, 23%
IDU, 20%Multiple sex
partners, 24%
Sex
contact, 23%
MSM, 23%
Centers for Disease Control and Prevention. Hepatitis B.
In: Atkinson W et al, eds. Epidemiology & Prevention of
Vaccine-Preventable Diseases. 8th ed Washington DC:
Public Health Foundation; 2005:191-212.
Many patients do not reveal IDU as source of infection

16.  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.

18. Symptoms
HBeAg anti-HBe
Total anti-HBc
IgM anti-HBc anti-HBsHBsAg
0 4 8 12 16 20 24 28 32 36 52 100
Acute Hepatitis B Virus Infection with Recovery
Typical Serologic Course
Weeks after Exposure
Titre

19. IgM anti-HBc
Total anti-HBc
HBsAg
Acute
(6 months)
HBeAg
Chronic
(Years)
anti-HBe
0 4 8 12 16 20 24 28 32 36 52 Years
Weeks after Exposure
Titre
Progression to Chronic Hepatitis B Virus Infection
Typical Serologic Course

21.  Aim is to halt the progression of liver damage by
› Suppressing viral replication
› Eliminating the infection
› Successful response to treatment will result in
the disappearance of HBsAg, HBV-DNA, and
seroconversion to HBeAg.

22.  Interferon alpha-2b
 Lamivudine - a nucleoside analogue reverse
transcriptase inhibitor. Well tolerated, most patients
will respond favorably. However, tendency to relapse
on cessation of treatment. Another problem is the
rapid emergence of drug resistance.
 Hepsera (Adefovir Diivoxil) : nucleotide analogue
that inhibit HBV DNA polymerase (RT)

23.  Vaccination
 Hepatitis B Immunoglobulin - HBIG may be used
to protect persons who are exposed to hepatitis B. It
is particular efficacious within 48 hours of the
incident. It may also be given to neonates who are at
increased risk of contracting hepatitis B i.e. whose
mothers are HBsAg and HBeAg positive.
 Other measures - screening of blood donors, blood
and body fluid precautions.

24. CDC, 2006

25. Immune tolerance phase
HBeAg positive; high HBV DNA (105-10 copies/mL)
normal ALT
HBeAg-positive chronic hepatitis (immune clearance)
High HBV DNA (105-10 copies/mL)
high or fluctuating ALT; active inflammation on liver biopsy
Inactive HBsAg carrier (non-replication)
HBeAg negative; low HBV DNA (<104 copies/mL)
normal ALT
HBeAg-negative chronic hepatitis
Intermediate to high HBV DNA (104-8 copies/mL)
high or fluctuating ALT; active inflammation on liver biopsy
4 Phases of Chronic HBV Infection

26. Virology
 HCV is a member of flavi virus family, Genus:
Hepacivirus
 Enveloped.
 HCV genome is a single stranded positive-sense RNA
and contains 9.4kb.
 Genotype: Six genotype and more than 100 serotypes.

27. 1.
• Acute Hepatitis C
2.
• Chronic Infection C 60-85%
3.
• Chronic Hepatitis 70%
4.
• Cirrhosis 20%
5. • HCC • Decompensation
Resolved

28. Symptoms
anti-HCV
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Hepatitis C Virus Infection
Typical Serologic Course
Titre
Months Years
Time after
Exposure

29.  Transfusion or transplant from infected donor
 Injecting drug use
 Hemodialysis (yrs on treatment)
 Accidental injuries with needles/sharps
 Sexual/household exposure to anti-HCV-
positive contact
 Multiple sex partners
 Birth to HCV-infected mother
Risk Factors Associated
with Transmission of HCV

30.  Transfusion or transplant from infected donor
 Sexual/household exposure to anti-HCV-
positive contact
 Multiple sex partners
 Needle stick injury

31.  Hepatitis C virus Antibody test
 HCV-RNA Test ( Qualitative & Quantitative)
 Genotyping
 1,4 - 48weeks
 2,3- 12 weeks
.

32.  Does not distinguish between IgG & IgM or between
acute, chronic or resolved infection.
 Since false positive results can occur in ELISA, a
Recombinant Immunoblot Assay (RIBA) should be
performed as a confirmatory test.
 If RIBA is positive, a PCR based test that detects viral
RNA in serum should be done to determine active
disease.

33. HCV-RNA may be detected from blood or liver tissue, it’s
the direct evidence of infectivity
 Confirms diagnosis of HCV infection.
 Useful in the early diagnosis of acute hepatitis –C.
 Demonstrates the presence of active infection.
 Gold standard- For documenting response to treatment.

34.  Interferon
 Pegylated IFN (alpha interferon) conjugated to
polyethylene glycol is used to treatment of
chronic Hepatitis C.
 Ribavirin - recent studies suggest that a
combination of interferon and ribavirin is more
effective than interferon alone.
 New Drug-Protease Inhibitor(Simeprivir),
Polymerase Inhibitor(Sofosbuvir)from 2013 for all
genotype.

35.  Screening of blood, organ, tissue donors
 High-risk behavior modification
 Blood and body fluid precautions
 Infection control practices in health care and other
settings.
 Counsel person with high risk, drug or sexual practice.
Prevention of Hepatitis C

36. HBsAg
RNA
 antigen
Hepatitis D (Delta) Virus

37.  Percutaneous exposures
injecting drug use
 Permucosal exposures
sex contact
Hepatitis D Virus Modes of
Transmission

38.  Coinfection
 Infection with both HDV and HBV at the same time.
› severe acute disease.
› low risk of chronic infection.
 Superinfection
 Previous infection with HBV and then superinfected with
HDV.
› usually develop chronic HDV infection.
› high risk of severe chronic liver disease.
› may present as an acute hepatitis.

39. anti-HBs
Symptoms
ALT Elevated
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV - HDV
Coinfection
Typical Serologic Course
Time after Exposure
Titre

40. Jaundice
Symptoms
ALT
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV - HDV Superinfection
Typical Serologic Course
Time after
Titre

41.  Anti-HDV can be detected by RIA or ELISA in serum
 HDV RNA may be detected from liver cells, blood.
Treatment
 There is no specific anti viral therapy against HDV.
 There is no vaccine against HDV, persons immunised
with HBV will be protected against HDV as surface
antigen is same.

42.  Member of flavi virus family.
 Isolated from pt with post transfusion hepatitis in 1996.
 Transmission: via sexual and parenteral route.
 Patients coinfected with HIV and HGV have a lower
mortality rate and have less HIV in their blood than
those infected with HIV alone. It is hypothesized that
HGV may interfere with the replication of HIV.