1. Viral Hepatitis
Prodromal symptoms of nausea and
anorexia, presence of pain in upper
abdomen together with characteristic
laboratory features (elevated bilirubin,
elevated SGOT and SGPT > 500 with
SGPT > SGOT and elevated alkaline
phosphates to < 3 times normal ) suggest
the diagnosis of Viral Hepatits.

2. Virus Genome Replication
Defective
DNA
Polymerase
in Virion
HBsAg in
Envelope
Virus
Family
HAV ssRNA No No No Picornavirus
HBV dsDNA1
No Yes Yes Hepadnavirus
HCV ssRNA No No No Flavivirus
HDV ssRNA2
Yes No Yes Deltavirus
HEV ssRNA No No No Calicivirus

3. Features HAV HBV HCV HDV HEV
INCUBATION
(DAYS)
AGE
15-45 Days
Children ,
young adults
30-180 Days
Young adults
15-160 Days
Any age but >
in adults
30-180 Days
Any age
14-60 Days
Young adults
TRANSMISION
•Fecal –oral
•P.C
•Perinatal
•Sexual
+++
unusual
---
+
---
+++
+++
++
---
+++
+
+
---
+++
+
++
+++
---
---
---
CLINICAL
•Severity
•Fulminant
•Progression
to chronicity
•Carrier
•Cancer
•Prognosis
Mild
0.1%
None
None
None
Excellent
Occasionally
severe
0.1- 1.0%
Occasional (1-
10%)
0.1-%-30%
+ nt
Worse with ag
e
Moderate
0.1%
Common (50-
70%)
1.5 to 3.2%
+nt
Moderate
Occasionally
severe
5-20%
Common
variable
variable
Acute : good
Chronic:poor
Mild
1-2%
None
None
None
Good
PROPHYLAXIS IgG vaccine HBIG None - Unknown

4. Hepatitis “A” Virus
CLINICAL CAPSULE:
HAV is a non enveloped RNA Virus.
It is classified in genus Hepatovirus
under family Picornavirus.
Originally called as enterovirus 72.
It is the only human hepatitis virus
which can be cultivated in vitro.
M/C of hepatits in children.
transmission by feco-oral route.
Virus is shed in feces during the
late Incubation period & prodromal
phase of illness.

5. LABORATORY DIAGNOSIS OF
HAV
• “Detection of IgM-specific
anti HAV in the blood of an
acutely infected patient
confirm the diagnosis of
hepatitis A.”
• IgM appears in acute phase,
peaking about 2 weeks after
elevation of live enzymes and
becomes undetectable
withins 3-6 months.
• ELISA is the method of choice
for measuring antibodies.
CLINICAL ASPECTS
• Fever, anorexia, and jaundice
are common.
• ROT: is greatest 2 weeks
before to 1 week after the
onset of jaundice.
• HAV is excreted in clay-
colored feces and dark urine
for about 2 weeks before the
onset of jaundice.
• Blood and serum are infective
during the brief period of
viremia.

6. • DIAGNOSIS
IgM-specific antibody
denotes acute infection.
• TREATMENT And
PREVENTION
 No specific tx
 Passive immunization:
 Immune serum globulin
provides temporary about
80% to 90% protection.
 Active immunization:
Formalin-killed HAV, which
is grown in human cell
culture, is almost 100%
protective

8. HEPATITIS B VIRUS

9. • HBV belongs to hepadna
viridae.
• HBV is the only has DNA
viruses.
• Partial double strand DNA.
• HBV contains both DNA-
dependent DNA polymerase
and RNA-dependent
reverse transcriptase.
• Found in cytoplasm of
infected hepatocytes
Structure of HBV:
• Serum form pt. of HBV shows 3
types of particle:
1. Dane particle
• Double walled spherical
structure,42 in diameter.
• Complete HBV.
• It contains:
I. HBcAg
II. HBsAg
III.HBeAg
2.Spherical particle(MC)
• 22nm
• HBsAg
3. Filamentous or tubular particle:
• 22nm
• Identical to spherical is HBs Ag.

10. Worldwide distribution of hepatitis B infection. Areas with high prevalence (>8% of population)
are in black, and areas with moderate prevalence (2% to 7%) are in gray.

12. Antigen
HBs Ag
Actions :
•1st
virological marker
•Elevation of SGOT/SGPT
•Become undetectable 1-2 months
after the onset of jaundice.
•In chronic HBV infetcion HBsAg
remain detectable beyond 6
months.
Antibodes :
Anti HBsAg
Impact:
•It become detectable
in blood when HBsAg
disappears.
•Protective AB.
•Only marker present
after immunization.
HBc Ag •It is not detectable because it is
enclosed within HBsAg coat.
Anti HBcAg
•IgM
•IgG
•IgM: acute or recent
infection.
•IgG: remote or
chronic infection.
HBe Ag •Appears shortly after HBsAg.
•Indicator of active intraheptic
replication and infectivity.
Anti HBeAg •Disappearance of
HBeAg followed by
anti HBe Ag.
•It pesence indicates
low infectivity & virus
infection.
HBxAg HCC No A/B
Serologic and Virologic Markers of HBV

16. Management
• High carbohydrate diet.
• Domperidome
• Silymarin
• i.v ornithine (it is amino acid reduced the swelling)
• f/u 6 months
Anti HBsAg =0
• Liver start regressing --- fulminant hepatic failure(0.1-1%).
• Bleeding
• Amonia >> in blood >hepatic encephalopathy>coma
Tx : Orthoptic liver transplantation.
Anti HBsAg +
<10 5 copies/ml then wait and watch.
>10 5 copies/ml Tx:alfa interferone+lamividine

17. Hepatitis “C” Virus
• Classified as a new genus Hepacivirus in
the family flaviviridae.
• The virus can’t be cultured.
• Positive-sense RNA genome that
encodes three structural and five
nonstructural proteins .
• Highly heterogeneous virus,
hypervariable regions in E2.
• Eleven genotypes with multiple
subtypes have different geographic
distribution.
• Genotypes important for therapy
response.
• HCV replicates in the cytoplasm via
negative-sense RNA intermediates
• It is the commonest cause of post
transfusion hepatitis and chronic
hepatitis.

18. Laboratory diagnosis of HCV:
• The most sensitive and gold
standard test in establishing
diagnosis is assay for HCV RNA.
• HCV-RNA can be detected within
a few days of exposure of HCV
well before the appearance of
A/B ( IgG class)
Test for HCV-RNA assays are:
• PCR
• TMA
• B DNA hybridization.
• A/B detection by ELISA.
The type of A/B are detected:
Anti NS-5 (TGA)
Anti C22/C33( SGA)
Anti C100(FGA)
• Hepatitis C is the MCC of Chronic
Hepatitis.
• 50-80% patients.
• Long term prognosis is benign.
• Fatigue is the MC symptom.
• Immune complex mediated extra
hepatic complication are less common
than chronic hepatitis B with the
exception of essential mixed
cryoglobulinemia which is more common
in chronic hepatitis C.
• Autoimmune play a role in the
pathogenesis of chronic hepatitis c.
• Lab findings:
Characteristics episodic pattern of
Aminotransferase activity>aminotransferase
level tend to fluctuate.
ALT> AST ( after cirrhosis AST>ALT)
Presence of Anti LKM1 anti body against
p450 2 D6.( HCV microsomal A/B).
Anti LKM2 --- (Drug induced A/B)
Anti LKM3---(Chronic Hepatits D)

20. Inflammation in chronic hepatitis C virus (HCV) infection. Chronic inflammation of
the portal area with a lymphoid aggregate in the center can be seen. At the edges of
the portal area, the interface between the parenchyma and portal connective tissue,
inflammation spreads outward, destroying hepatocytes and expanding the portal tract
by piecemeal necrosis.

21. TREATMENT:
• Pegulated IFN-a + ribavirin
• Chronic hepatits is the most common indication for liver
transplantation.
• MCC of chronic carrier state is HCV. About 50-70% of patients
progress to chronic hepatitis.
• Chronicity----HCV>HDV>HBV
Remember---in HBV infection there are two types of carriers:
1.Super carriers
-high titre of HBsAg, HBeAg DNA polymerase and HBV in the circulation.
-highly infective.
2.Simple carriers
-low titre of HBsAg with negative HBeAg DNA polymerase and HBV.
-have low infectivity.
HOWEVER
• HCV may cause co infection with HBV and co-infection of HCV with
HBV increases the rate of development of cirrhosis and the risk of
HCC compared with infection. With either virus alone.
• HCV can cause liver carcinoma.

22. Hepatitis E
• Also known as enterically transmitted
non-A non-B(NANB) virus or
epidemic NANB.
• Classified in the genus HERPES virus
under the family CALIVIRIDAE.
• Single stranded +sense RNA virus.
• The viral particles in stool are
spherical, 27 to 34 nm in diameter
with icosahedral symmetry, and
unenveloped, and they exhibit spikes
on their surface.
• A unique feature is the clinical
severity and high case fatality rate of
20-40% in pregnant women,
especially in the last trimester of
pregnancy.
• Characteristically associated with
SIMILARITIES IN HAV & HEV:
Both have acute onset with mild
illness.
Both are transmitted by feco-oral
route.
DIFFERENCES IN HAV & HEV:
HAV is more common in children.
While
HEV is more common in young adult.
HEV can cause fulminant hepatitis in
pregnant women ( not HAV).
Secondary attack rate of HEV is very
low (2-3%) as against 10-20% in
HAV.

23. Hepatitis D or Delta virus
• It has been classified in genus Delta
virus.
• Delta core of HDV is encapsulated by
an outer envelope of HBsAg, so
require co-operative function of HBV.
• Intracellular replication of HDV RNA
can occur without HBV but liver injury
requires the presence of HBV.
• It is defective RNA virus depend on the
helper function of HBV for its
replication and expression.
• It contains defective ssRNA.
• It has no independent existence and
can survive and replicate only as long
as HBV infection persists in the host .

24. HDV infection
Superinfection
• Infected with HBV
• Has grave course with more
chances of fulminant
hepatitis & chronic
infection.
• IgM anti HDV (+)ve & IgM
anti HBc(+)ve
Coinfection
• Infection occurs
simultaneously with HBV.
• Comparatively mild course.
• IgM anti HDV(+)ve & IgG anti
HBc(+)ve.

25. • There is no association between HDV and
hepatocellular carcinoma
• HDV antigen ( Delta antigen) is primarily
expressed in liver cell nuclei, where it can be
demonstrated by immunofluroscence.

26. Distribution of hepatitis E virus infection, among countries in which outbreaks have
been identified (shown in black).

27. HEPATITIS G
• Blood born virus.
• It resembles HCV.
• Also k/s GB virus C.
HGV RNA has been found in patients with:
• Acute hepatitis
• Chronic hepatitis
• Fulminant hepatitis
• Hemodialysis
• i.v drug addicts.
• Blood donor.
• Its genome resembles HCV genome except, it lacks a protein
corresponding to the core protein of HCV that forms the
nucleocapsid.
• HGV infection occur independently, it does not require co-infection
of HCV.

28. Treatment of Hepatitis
• Treatment of patients with hepatitis is supportive and directed at allowing
hepatocellular damage to resolve and repair itself.
• Only HBV and HCV have specific treatments, and those are only partially effective.
• Recombinant interferon- and pegylated interferon- are currently the therapy of
proven benefit in the treatment of patients chronically infected with HBV or HCV.
• With nucleoside and nucleotide analogs, such as lamivudine, HBV DNA levels are
reduced, but the virus is rarely eliminated and viral replication resumes in the
majority of patients when treatment is stopped. The emergence of drug-resistant
virus mutants in long-term therapy is a major problem.
• Combination therapy ofinterferon- and ribavirin against chronic hepatitis C gives a
sustained response rate of up to 50%, though that therapy is less successful in
patients with genotype 1.
• Orthotopic liver transplantation is a treatment for chronic hepatitis B and C end-
stage liver damage. However, the risk of reinfection on the graft is at least 80%
with HBV and 50% with HCV, presumably from extrahepatic reservoirs in the body.

29. Drug Nucleoside analogue MOA Viral Spectrum
Entecavir Yes Reverse transcriptase
inhibitor
HBV
Foscarnet No Viral polymerase
inhibitor
HBV
Ribavirin Yes Perhaps blocks capping
of viral mRNA
Respiratory syncytial
virus, influenza A and B,
Lassa fever, hepatitis C,
other
Lamivudine (3TC) Yes Reverse transcriptase
inhibitor
HIV-1, HIV-2, HBV
Zalcitabine (ddC) Yes Reverse transcriptase
inhibitor
HIV-1, HIV-2, HBV
Examples of Antiviral Compounds Used for Treatment of Viral Infections

30. Clinical and Laboratory Features of Chronic Hepatitis
Type of hepatitis Diagnostic test(s) Autoantibodies Therapy
Chronic hepatitis B HBsAg, IgG anti-HBc,
HBeAg, HBV DNA
Uncommon IFN- , PEG;IFN-
lamivudine ;adefovir
entecavir ;telbivudine
;tenofovir
Chronic hepatitis C Anti-HCV, HCV RNA Anti-LKM1a
PEG IFN- plus;
ribavirin;Telaprevir;
Boceprevird
Chronic hepatitis D Anti-HDV, HDV RNA,
HBsAg, IgG anti-HBc
Anti-LKM3 IFN- , PEG ; IFN- c
Autoimmune
hepatitis
ANAb
(homogeneous)
, anti-LKM1 (±)
Hyperglobulinemia
ANA, anti-LKM1
anti-SLAe
Prednisone,
azathioprine
Drug-associated — Uncommon Withdraw drug
Cryptogenic All negative None Prednisone (?),
azathioprine (?)

31. Will be grateful for advice.