This document summarizes several types of hepatitis viruses. It discusses hepatitis viruses A through E, which are the confirmed types. Hepatitis viruses are named hepatitis A, B, C, D, and E. They differ in their structure, modes of transmission and replication, and clinical course. Hepatitis B and C viruses are responsible for many cases of hepatocellular carcinoma. The document describes the morphology, antigenic structure, transmission routes, clinical features, diagnosis, and prophylaxis measures for each of the hepatitis A, B, C, D, and E viruses.
2. HEPATITIS VIRUSES
HEPATITIS - inflammation & damage to
liver
7 diff types - viruses causing hepatitis –
called HEPATITIS viruses - A to G
A TO E – confirmed
F & G - awaiting confirmation
Type F - proved to be mutant of type B
virus & not a separate entity - deleted
3. Target organ- liver
Differ in
structure
Mode of transmission/ replication
Course of the disease
• Taxonomically unrelated
HBV - DNA V – A , C , D , E , G - RNA genome
• Common feature-
hepatotropism
to cause similar icteric illness
Inf caused - HBV – most severe / fatal
HBV & HCV – responsible -many cases of
HEPATOCELLULAR carcinoma
4. HEPATITIS VIRUSES
HEPATITIS - may also be caused by
other viruses Yellow fever v , Lassa v
, EBV , CMV , HSV , VZV , Measles v
, Rubella v -- not included category of -
hepatitis viruses - becoz – can cause
hepatitis as a part of disease syndrome /
incidentally during course of infection -
no primary involvement of LIVER
5. Types of viral hepatitis
By epidemiological & clinical criteria 2 types
1) Infective / Infectious hepatitis
occurred sporadically or as an epidemics
affecting mainly children / young adults
transmitted – fecal-oral route
Type A hepatitis
2)Serum /Transfusion hepatitis /
Homologus serum jaundice
Transmitted mainly by inoculation (serum
inoculation , blood transfusion)
Type B hepatitis
3) NANBH
Type C- transfusion associated
Type D /defective /delta
TypeE – fecal- oral
6. HAV -- infectious hepatitis
Morphology - 27 nm / non enveloped / SS RNA V
/ icosahedral symmetry
FAMILY – Picornaviridae –
Originally designated as Enterovirus 72
now- recognized – prototype of new genus-
Hepatovirus.
Affecting mainly children & young adults
7. HAV
MODE OF TRANSMISSION - Fecal oral route
ingestion - multiplies – intestinal epithelium -
through haematogenous spread - reaches to
LIVER
Shed in feces- late I.P./Prodromal phase
Once jaundice develops - rarely detectable in feces
Carrier stage- nil
Oncogenicity- nil
8. Clinical course
I. P. – 2 – 6 Wks – brief viremia –preicteric -
ceases with onset of jaundice
no chronic viremia- parental transmission rare
Transplacental infection- not documented
Majority of Inf - asymptomatic
Clinically 2 stages –
1 ) preicteric / prodromal–
2) icteric
Fever , nausea , vomiting , liver tenderness -
subside -on set of jaundice
V rarely – fulminant / fatal
MORTALITY - 0. 1- 1 %
9. HAV - LAB DIAGNOSIS
LAB DIAGNOSIS –
1) DEMONSTRATION OF VIRUS - BY
IEM –in feces - late I P & preicteric phase
ELISA – HAV- FAECES
2) Ab DETECTION - Anti HAV Ab - serum IgM
/IgG
IgM – recent inf , appears during late I. P. ,
detectable in serum for 2 - 6 mts - after onset of
symptoms
IgG - past inf , persist for many years
ELISA available
3) BIOCHEMICAL TESTS – LFT / bilirubin
10.
11. Prophylaxis --vaccine
Safe / effective – formalin inactivated , alum
conjugated v - containing HAV – grown - human
diploid cell culture
Course - 2 IM injections – protection begins 4
wks after injection / lasts for 10 – 20 years
Natural inf – clinical / subclinical - lifelong
immunity
No cross immunity between HAV & other
hepatitis viruses
Prophylaxis- improved sanitation/ prevention of
faecal contamination of food & water
12. Type B hepatitis
Most IMP type of viral hepatitis
2- 7% or quarter of them –HBV carriers
A quarter – serous liver disease-
chronic hepatitis
cirrhosis
primary hepatic ca
Effective vaccine available
Hepatocellular Ca- only human ca- vaccine
preventable
15. HBV– SERUM HEPATITIS/ TRANSFUSION
MORPHOLOGY – Has 3 morphological forms
1) DANE PARTICLE –fewer in number—double
walled spherical - 42 nm dia DNA virus with outer
Envelop & inner Core -- 27 nm in dia , enclosing
viral genome & DNA polymerase– complete HBV
2) Numerous spherical particles of 22 dia
3) Tubular OR Filamentous --22nm in dia --
Antigenically identical -- are surface components
of HBV-- HBs Ag
16.
17. HBV
FAMILY – Hepadnaviridae – hepatotropic DNA virus
ANTIGENIC STRUCTURE
1) HBs Ag – Australia Ag - surface / envelop Ag
indicate Active Infection
Exhibits antigenic diversity.
Has several sub types/2 different Ag components.
Group reactive – a , Type sp – d- y , w -r
HBs Ag – divided in to 4 major Ag subtypes –
adw , adr , ayw & ayr
sub type – adr - common in india
18. Ag structure
2) HBcAg – core / nucleocapsid Ag - not detected
in blood – can be shown in liver cell- IF
3) Hbe Ag – soluble , non-particulate nucleocapsid
protein
hidden antigenic component of core
HBeAg & HBcAg - immunologically distinct ,
coded by same gene
Viral Genome – 2 linear strands of DNA - in
circular configuration -- along with DNA
polymerase
21. HBV Genes & Gene product– genome has compact
structure with 4 overlapping genes
22.
23. GENES CODING FOR Ags OF HBV
GENES REGIONS GENE PRODUCT
S- 3 regions S , pre
S1 & pre S2
S
S + Pre S2
S + Pre S1
&S2
MAJOR PROTEIN - S} HBsAg
MIDDLE PROTEIN – M } HBsAg
LARGE PROTEIN – L }Virion
C- 2 regions C &
PreC
C
C+ Pre C
HBcAg
HBeAg
P DNA polymerase
X HBxAg – non particulate Ag-
leads to enhanced replication of
HBV
24. MODES OF TRANSMISSION
HBV- Blood borne virus
3 IMP modes of transmission
1) PARENTERAL – blood of carriers / patients
– most IMP source of infection -- largely
been eliminated – donor screening strictly
enforced
Now – other therapeutic , diagnostic ,
prophylactic , non medical procedures -- main
modes of infection
25. HBV – highly infectious , far more than HIV
– as little as 0. 00001 ml – blood – transmit
Shared syringes, needles , sharp items
Practices- acupuncture, tattooing , ritual
circumcision , ear/ nose- piercing
Professionals- sharp articles- barbers, dentists & drs
– may unwittingly transmit
Direct contact with- open skin lesions-
pyoderma, eczema, cuts , scratches
Survive in mosquitoes & bugs-2 wks after blood meal
- no virus multiplication occurs- do not appear to
transmit the infection
26. MODES OF TRANSMISSION
2) PERINATAL / CONGENITAL / VERTICAL --
Quite common – carrier mothers
Risk to Baby -
high if mother HBeAg + ve – 60 – 90 %
low if mother - ve – 5 – 15 %
True congenital inf ( in Utero , Transplacental )
rare - acquired during birth – by contact of
maternal blood with skin & mucosa of foetus
27. MODES OF TRANSMISSION
3) SEXUAL TRANSMISSION -
HBV -present in body fluids -
semen , Vg. Secretions, hence -
transmitted by sexual contact
Male homosexuals- at higher risk
Other secretions – saliva , breast milk
,bile , faeces
28. CLINICAL FEATURES
Onset - slow , I . P.-6wks - 6 mts
COURSE - 3 phages
1) Preicteric
2) Icteric
3) Convalescent
Clinical picture- similar to that of type A
more severe
29. HEPATITIS B CARRIERS
Natural inf occurs only in humans , no
animal reservoir
V – maintained in large pool of carriers
CARRRIER – person with detectable
HBsAg in blood - more than 6 mts
Following inf --
5- 10 % Adults
30% Children
90% neonates -- carriers
30. TWO CATEGORIES OF CARRIERS
1) SUPER CARRIER -
a)have HBeAg in blood
b)blood – high titre of HBsAg , DNA polymerase
c) HBV - present in circulation
d) highly infectious -
2) SIMPLE CARRIER – common type of
carriers
a) have no HBeAg & low HBsAg -- in blood
b) HBV , DNA polymerase absent
c) transmit inf - large volumes of blood –
transferred – low infectivity
31. LABORATORY DIAGNOSIS
1) By detection of hepatitis B Ags
2) By detection of Abs - ELISA & RIA
Sequence of appearance of Viral markers
– HB Ags & Abs -- in blood is IMP in
diagnosis
1)DETECTION OF MARKERS –
HBsAg
HBeAg
HBcAg
32.
33. LAB DIAGNOSIS
2) VIRAL DNA POLYMERASE –
Appears in serum - preicteric phase
3) PCR – For detection of HBV DNA
Indicator of viral replication in
liver-- helps to assess progress of pt
– antivial
4) BIOCHEMICAL TESTS
Transaminase / serum bilirubin
34.
35. PROPHYLAXIS
1) PASSIVE – HBIG - 300 – 500 I.U. - Soon after
exposure – may not prevent inf – gives protection
against illness/ development of carrier state
ACTIVE -- Vaccines
1) Plasma derived – source- healthy human
carrier Unacceptable – limited availability, not
free from unknown pathogen
2) Recombinant yeast HBV vaccine --
cloning S genes of HBV in bakers yeast –
sacromyces cervisiae-- HBsAg particles produced
extracted / purified – used as vaccine
36. PROPHYLAXIS
For nonimmune person - combined immunisation
For babies born - carrier mother - 0.5 ml HBIG –
IM - immediately after birth - full course
37. Characteristics of Hepatitis C, D , E Viruses
FEATURE HEPATITIS C HEPATITIS D HEPATITIS E
Common name Non A non B Delta hepatitis Enteric Non A non B
Family Flavi Unclassified Calci
Virion 30 – 60 nm
spherical
35 nm spherical 30 – 32 nm
icosahedral
Envelop enveloped Enveloped - HBsAg nonenveloped
Genome SS RNA SS RNA SS RNA
Transmission Parenteral , vertical
, sexual-
post transfusion
hepatitis
Parenteral , sexual Feco - oral
Severity Usually subclinical Coinf- HBV-
occasionally severe
super inf – HBV
often severe
Mild - N person
Severe - pregnancy
38. FEATURE HCV HDV HEV
Chronicity / carrier
state
Present- 50- 80 % -
develop
Present – with HBV Nil
Associated disease 1) Pri hepatocellular
ca 2) cirrhosis
IMP cause of chr
liver disease - S,
india
Cirrhosis &
fulminant hepatitis
No association
noted between HDV
& hepatocellular ca
Nil
Mortality 0.5 - 1 % moderate High to very high N- 1 – 2 %
pregnant - 20%
Lab diagnosis Detection - Anti
HCV Ab by ELISA
PCR – HCV RNA
Detection - Anti
delta Ab by ELISA
HD –Ag detected in
liver cells -- IF
HDV RNA –
DETECTED BY
Hybridisation
HEV – IN Feces by
IEM ( early stage)
Anti HEV Ab IgM
by ELISA
PCR - detection of
HEV RNA
