3- Hepatitis A,B,C,D Flashcards
TAXONOMY OF HEP C / HCV
Flaviviridae Hepacivirus
morphology HEP C
- spherical
- complex virus
- single stranded RNA (+VE)
- surface antigens:
antigenic properties (+ virulence factors) of HEP C
antigens:
-E1 and E2
-C Ag (core antigen) =nucleocapsid
-NS-proteins (non-structural proteins) – factors of aggression
**virulence (VF)
**E1 and E2 (envelope antigens) = adhesion and penetration factors
TAXONOMY OF HEP D / HDV
(Togaviridae) Deltavirus
morphology HEP D
- spherical
- simple/naked (no supracapsid)
- single stranded RNA (-VE)
- has only C=Core antigen
- it is a satellite virus (= uses the antigens and virulence factors of HBV)
therefore:
**It causes symptoms only in people who also have hepatitis B infection. (either as co-infection or superinfection)
antigenic properties (+ virulence factors) of HEP D
ONLY ONE ANTIGEN:
- Core antigen
BUT for
**virulence (VF):
*its a SATELLITE virus so it uses the antigens and virulence factors of Hep B.
TAXONOMY OF HEP B / HBV
Нepadnaviridae OrthoНepadnavirus
morphology of HEP B
- small spherical
- complex virus
- circular DOUBLE stranded DNA
antigenic properties (+ virulence factors) of HEP B
antigens: (**for Virulence Factor)
*S - surface antigen
E - envelope antigen
C- core antigen
X -
cultivation HEP B /C /D
can not be grown in cell culture only in VIVO (-in a living organism) only in CHIMPANZEE
pathogenicity of HEP C
- source = sick person
- trans. method =
1)parenteral : (contact with infected blood)
2)sexual transmission
3) vertical transplacental - gate = hepatocytes
pathogenesis:
(cytopathogenic)
- virus adheres to
hepatocytes and penetrates them Using envelope 2 antigens E1,E2, replicates inside.
- thus, disrupts hepatocytes functions.
-new mature virus spreads to other hepatocytes, causing *progressive liver damage.
- can spread to other tissues (bone marrow, glands)
- *usually develops into chronic disease
clinical manifestations of HEP C
acute:
-general malaise( fatigue, nausea, vomiting, lack of appetite)
-jaundice
chronic:
-INCrease in liver size
-progressed jaundice
Pathogenicity of HEP B
- source = sick person OR carrier
- trans. method =
1) parenteral : (contact with infected blood)
2)sexual transmission
3) vertical transplacental - gate = hepatocytes
pathogenesis:
(cytopathogenic)
- After adhesion, penetration, is *replication of VIRAL DNA in hepatocytes - without showing symptoms for 45 days
- *viral DNA integrates in hepatocytes with *minimal cytopathic effects
- *infection prolongs for a very long time before starting to cause liver damage (which may be symptomatic or asymptomatic)
clinical manifestations of HEP B
acute:
-general malaise (fatigue, nausea, vomiting, lack of appetite)
- (choleostasis) = dark urine, pale stools
chronic:
- jaundice, yellow eyes
pathogenicity of HEP D
- source = sick person
- trans. method =
1) parenteral : (contact with infected blood)
2)sexual transmission
**occurs only in people who also have hepatitis B infection) either:
1) by coinfection of HDV & HBV at the same time
2)by superinfection of HDV for a patient with chronic HBV
- gate = hepatocytes
pathogenesis:
(cytopathogenic)
- Upon infecting a cell, the virus begins
to exhibit a *strong cytopathic effect
on the cell. Which leads to increased
symptoms.
- symptoms are the same as hepatitis
B, *but more severe.
- *leads to liver damage
clinical manifestations of HEP D
- general malaise (discomfort)
- choleostasis: dark urine, pale stools
- severe jaundice (yellow eyes)
- hepatic necrosis & liver damage
lab diagnosis of HEP A/B/C/D
-PCR
-ELISA
treatment of HEP C
a combination of:
antiviral chemotherapy (ribovarin) & alpha-interferon
treatment of HEP B
antiviral therapy of chronic
hepatitis B
treatment of HEP D
(by controlling hep B infection
so:) antiviral therapy of chronic
hepatitis B
prophylaxis of HEP C
no vaccine ;)
prophylaxis of HEP B
- Recombinant vaccine
( genetically engineered) containing HBs (surface )antigen
prophylaxis of HEP D
-by vaccination against Hep B. using its vaccine
= Recombinant vaccine
( genetically engineered) containing HBs (surface) antigen
taxonomy of HEP A
picornaviridae hepatovirus
morphology HEP A
- small
- Simple/naked (only nucleocapsid)
- Single stranded RNA (+ve) (unsegmented)
antigenic properties + virulence of HEP A
antigens: (* for VF)
*E - envelope antigen
C - core antigen
cultivation of HEP A
cell lines of primates/monkeys
pathogenesis of HEP A
- source = sick person
- trans. method=
1)faecal-oral (food and water)
2)contact - gate = hepatocytes
- pathogenesis = (not cytopathogenic)
-virus enters by ingestion and moves from bloodstream to liver - it replicates in cytoplasm of hepatocytes
-causes cell necrosis and INCrease in liver size - blocks biliary tract - causing jaundice
- however it is not cytopathic and exits cell by exocytosis (not cytolytic - so cell doesn’t rupture)
CLINICAL MANIFESTATION of HEP A
-jaundice
-dark urine, pale stool
treatment of HEP A
- no antiviral drugs
- only symptomatic treatment
prophylaxis of HEP A
(inactivated) HARVIX vaccine
