2. Hepatitis Viruses
The term ' viral hepatitis ' is
reserved for infection of the liver .
Caused by eight hepatitis
viruses -
3. 1. Hepatitis A virus (HAV)
2. Hepatitis B virus (HBV)
3. Hepatitis C virus
(HCV)
4. Hepatitis D virus (HDV)
5. Hepatitis E virus (HEV)
6. Hepatitis G virus (HGV)
7. SEN virus
8. Transfusion-transmitted virus (TTV)
4. HBV , TTV and SEN virus have DNA
genome.
Other hepatitis viruses have RNA
genome .
.
.
5. Hepatitis A Virus (HAV)
It has RNA
genome.
Morphology
Hepatitis A virus is 27 nm ,
icosahedral , naked ,single_ stranded
RNA virus , the sole member of the
genus Hepatovirus in the family
.
.
6. Pathogenesis
HAV is shed early in the stools of
infected individuals.
1- 2 weeks prior to the onset of
symptoms,
little virus in serum and hardly in other
body fluids which explain the
epidemiology (scientific study of spread
and control of disease) as faecal oral
.
.
.
.
7. Transfusion - associated hepatitis
A is exceedingly rare.
It probably multiplies first in the
intestinal epithelial cells and the
spreads to the liver via the blood.
.
.
8. Clinical
features
It is an acute self limiting
disease.
Incubation period _ 2 - 6
weeks.
The onset is sudden with fever ,
malaise , anorexia , nausea , lethargy
which comprise the prodromal stage
.
It may also produce pain in the right
upper abdominal quadrant.
.
.
.
.
9. Complete recovery occurs in 8-12
weeks.
Only 5%of the children under 3
year of age develop jaundice ,
while more than 50% in adults .
Hepatomegaly, due to cell necrosis ,
causes blockage of the biliary
excretions resulting in jaundice.
.
.
. Fatality rate is also more in
.
10. Laboratory
Diagnosis
Biochemical
tests
Serum levels of both alanine and
aspartate aminotransferase are
markedly raised .
Immunoelectron
Microscopy
Virus particles can be
demonstrated in faecel extracts by
immunoelectron Microscopy.
.
.
11. Serology
Faecal HAV may be detected by
ELISA.
Detection of IgM anti-HAV by ELISA or
RIA is the method of choice for the
diagnosis of HAV infection , detectable
in serum for 2-6 month after onset of
symptoms.
Virus culture
Virus, from the faeces, may be
cultured on continuous lines of
monkey kidney cells or human
.
.
.
14. Hepatitis A vaccine consisting of
formalin inactivated preparation of
virions grown in human fibroblasts or
monkey kidney cell lines, absorbed to
alum as an adjuvant can be used for
active immunization
2 doses injected one month apart with
or without a booster after 6 months
elicit a good immune response in 99%
of vaccines lasting for some years.
.
.
15. Hepatitis B
Hepatitis B virus is an
enveloped partially double
stranded DIVA virus.
Family -
Hepadnaviridae
8 genotypes of HBV ( A-H ) have
been identified.
.
.
.
16.
17. Morphology
HBV or Dane particleis the
complex 45 nm double - shelled
particle.
The outer surface or envelope
contains hepatitis B surface antigen
(HBsAg).
It encloses an inner icosahedral
22 nm nucleocapsid (core).
.
.
.
18. It contains hepatitis B core antigen
(HBcAg).
Inside the core is the genome of HBV
and a DNA - dependent DNA
polymerase.
The HBV genome consists of a 3.2
kilobase pair molecule of circular
double - stranded DNA of most
unusual Structure.
The plus strand is incomplete leaving
15-50%of molecule single stranded.
.
.
.
.
19. The minus strand is
complete.
From the core protein is derived
hepatitis Be antigen (HBeAg).
They normally occur in large (100-
1000 fold) excess over the mature
45nm virions.
.
.
.
20. Pathogenesis
There are three important modesof
transmission of HBV infection -
Parenteral
transmission
Perinatal
transmission
.
21. Parenteral
transmission
HBV is present inthe blood and in body
fluids such as semen , vaginal
secretions , menstrual discharge , saliva
, colostrum and breast milk .
.
. The concentration of HBV in blood and
body fluids is much greater than HIV.
Less than 1 micro.litre of blood
containing a syringe or needle, can
readily transmit hepatitis B from one
.
22. Parenteral
transmission
HBV is present inthe blood and in body
fluids such as semen , vaginal
secretions , menstrual discharge , saliva
, colostrum and breast milk .
.
.The concentration of HBV in blood and
body fluids is much greater than HIV.
Perinatal
transmission
HBV transmitted from carrier mother
to their babies during the perinatal
period.
Transmission probably occurs when
maternal blood contaminates the
mucous membranes of the new
born during birth.
Infection may also result from
haematogenous transplacental
transmission , breast feeding and
close postnatal contact between
.
.
.
23. Sexual
transmission
HBV present in serum and vaginal
secretions , therefore , it can be
transmitted by sexual contact.
Sexually promiscuous individuals
particularly male homosexuals are at ver
high risk .
Most of the HBV infections are
subclinical , particularly in
childhood .
.
.
.
24. Course of acute infection divided into
3 phases -
Preicteric or prodromal
phase
Incubation period - 6 weeks - 6
months
Causes malaise , anorexia ,weakness
,nausea, vomiting and pain in right
upper abdominal quadrant.
.
.
.
25. Icteric phase
Incubation_ 2 days - 2
weeks
Symptoms _ jaundice, pale stool, dark
urine , etc .
Convalescent
phase
Long phase with malaise and
fatigue for several weeks .
.
.
.
27. Prophylaxis or
treatment
Screening of blood donors , use of sterile
disposal syringes and needles by
healthcare workers and parenteral drug
users, reduction of the number of sexua
partner the use of condoms etc
.
.
Wears gloves , gown , eyeglasses, to
prevent exposure to blood and body
fluids in place of work and proper
handwashing after work .
.
Blood spills should be cleaned up with
2% glutaraldehyde or 0.5% sodium
28. Hepatitis C virus
(HCV)
Belongs to the genus Hepacivirus inthe
family Flaviviridae.
HCV particles is 50 _ 60 nm in
diameter .
And consists of an envelope derived
from host cell membrane into which are
inserted encoded glycoproteins(E1_E2)
surrounded a nucleocapsid and positive
sense , single stranded RNA genome of
.
.
.
29. Classified into 6 genotypes and more
than 80 subtypes.
Genotype 1 is main HCV
genotype.
Pathogenesis
HCV transmission occurs by
needlestick injuries or cuts with
sharps , use of contaminated needle
or syringes ,transfusion of
unscreened blood and sexual
.
.
.
30. Also transmitted in utero during
parturition and by breast milk.
Incubation period_ 6-8 weeks and also
several months
.
.
32. Treatment
Prevented by screening of blood
donors, avoidance of use of
unsterile needles for intravenous
drug abuse, tattooing and for
medical and dental procedures.
Prevent transmission of human
health immunodeficiency virus and
HBV and HCV by parenteral routes.
.
.
33. Hepatitis D
(HDV)
Also known as Delta
hepatitis virus.
Detective Satellite virus requiring
HBV as helper virus.
Sole member of the genus
Deltavirus.
Spherical shape
36-38 nm in diameter with
HBsAg coat and HDAg
.
.
.
.
.
34.
35. Pathogenesis
HDV is transmitted by blood and
blood products and also sexual
contact.
Simultaneous coinfection with HBV
and HDV in the same inoculum -
acute infection
Super infection of an HBsAg carrier
by HDV- commoner and more
serious because large nu. Of
hepatocytes are already producing
.
.
.
36. Leads to severe liver damage .
Laboratory diagnosis
HBV - HDV coinfection shortly before
the end of incubation period , HBsAg
appear in the serum .
Towards the end of incubation period
HDAg appears and detected by ELISA.
.
.
.
38. .
.
.
Pathogenes
is
HEV is primarily associated with
ingestion of faecally contaminated
drinking water.
Incubation period of HEV ranges
from 2-9 weeks, with an average
of 5-6 weeks.
Clinically, the disease closely
resembles that of HAV.
. .
39. Incubation period- 2-9
weeks
.
.
.
.
However , bilirubin levels tend to be
higher and jaudice deeper and more
prolonged .
Like HAV , HEV also does not
progress to chronic hepatitis ,
cirrhosis, cancer or carrier state.
.
.
41. Prophylaxis
Prevented by improved standards of
sanitation and provision of
chlorinated water.
No vaccine or effective antiviral
drugs exist.
.
.
42. Hepatitis G virus
(HGV)
Family -
Flaviviridae
Genus-
Hepacivirus
.
The genome of HGV consists of 9.4kb
molecule of ssRNA of positive polarity.
Majority of the individuals with HGV
infection have no detectable evidence
of liver disease
HGV infection is mainly detected by
reverse transcriptase polymerase chain
.
.
.
.