3- Hepatitis A,B,C,D

Question 1

TAXONOMY OF HEP C / HCV

Answer 1

Flaviviridae Hepacivirus

Question 2

morphology HEP C

Answer 2

• spherical
• complex virus
• single stranded RNA (+VE)
• surface antigens:

Question 3

antigenic properties (+ virulence factors) of HEP C

Answer 3

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

Question 4

TAXONOMY OF HEP D / HDV

Answer 4

(Togaviridae) Deltavirus

Question 5

morphology HEP D

Answer 5

• 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)

Question 6

antigenic properties (+ virulence factors) of HEP D

Answer 6

ONLY ONE ANTIGEN:
- Core antigen

BUT for
**virulence (VF):
*its a SATELLITE virus so it uses the antigens and virulence factors of Hep B.

Question 7

TAXONOMY OF HEP B / HBV

Answer 7

Нepadnaviridae OrthoНepadnavirus

Question 8

morphology of HEP B

Answer 8

• small spherical
• complex virus
• circular DOUBLE stranded DNA

Question 9

antigenic properties (+ virulence factors) of HEP B

Answer 9

antigens: (**for Virulence Factor)
*S - surface antigen
E - envelope antigen
C- core antigen
X -

Question 10

cultivation HEP B /C /D

Answer 10

can not be grown in cell culture only in VIVO (-in a living organism) only in CHIMPANZEE

Question 11

pathogenicity of HEP C

Answer 11

• 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

Question 12

clinical manifestations of HEP C

Answer 12

acute:
-general malaise( fatigue, nausea, vomiting, lack of appetite)
-jaundice

chronic:
-INCrease in liver size
-progressed jaundice

Question 13

Pathogenicity of HEP B

Answer 13

• 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)

Question 14

clinical manifestations of HEP B

Answer 14

acute:
-general malaise (fatigue, nausea, vomiting, lack of appetite)
- (choleostasis) = dark urine, pale stools

chronic:
- jaundice, yellow eyes

Question 15

pathogenicity of HEP D

Answer 15

• 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

Question 16

clinical manifestations of HEP D

Answer 16

• general malaise (discomfort)
• choleostasis: dark urine, pale stools
• severe jaundice (yellow eyes)
• hepatic necrosis & liver damage

Question 17

lab diagnosis of HEP A/B/C/D

Answer 17

-PCR
-ELISA

Question 18

treatment of HEP C

Answer 18

a combination of:
antiviral chemotherapy (ribovarin) & alpha-interferon

Question 19

treatment of HEP B

Answer 19

antiviral therapy of chronic
hepatitis B

Question 20

treatment of HEP D

Answer 20

(by controlling hep B infection
so:) antiviral therapy of chronic
hepatitis B

Question 21

prophylaxis of HEP C

Answer 21

no vaccine ;)

Question 22

prophylaxis of HEP B

Answer 22

• Recombinant vaccine

( genetically engineered) containing HBs (surface )antigen

Question 23

prophylaxis of HEP D

Answer 23

-by vaccination against Hep B. using its vaccine
= Recombinant vaccine

( genetically engineered) containing HBs (surface) antigen

Question 24

taxonomy of HEP A

Answer 24

picornaviridae hepatovirus

Question 25

morphology HEP A

Answer 25

• small
• Simple/naked (only nucleocapsid)
• Single stranded RNA (+ve) (unsegmented)

Question 26

antigenic properties + virulence of HEP A

Answer 26

antigens: (* for VF)
*E - envelope antigen
C - core antigen

Question 27

cultivation of HEP A

Answer 27

cell lines of primates/monkeys

Question 28

pathogenesis of HEP A

Answer 28

• 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)

Question 29

CLINICAL MANIFESTATION of HEP A

Answer 29

-jaundice
-dark urine, pale stool

Question 30

treatment of HEP A

Answer 30

• no antiviral drugs
• only symptomatic treatment

Question 31

prophylaxis of HEP A

Answer 31

(inactivated) HARVIX vaccine