Hepatitis Viruses (20,23) Flashcards Preview

MIIM30014 Virology > Hepatitis Viruses (20,23) > Flashcards

Flashcards in Hepatitis Viruses (20,23) Deck (54):
1

Which hepatitis virus has the longest incubation period?
a. HAV
b. HBV
c. HCV
d. HEV

c. HCV

2

Which hepatitis virus has the shortest incubation period?
a. HAV
b. HBV
c. HCV
d. HEV

a. HAV

3

What is involved in the pathogenesis of viral hepatitis?
a. Damage is due to cytolytic actions
b. Chronic infections are more common in older individuals
c. The younger someone is exposed to hepatitis, the more severe their acute reaction
d. Most disease is mediated by the immune system

d. Most disease is mediated by the immune system

4

Which are acute viruses?
a. Hepatitis B and D
b. Hepatitis A and E
c. Hepatitis A and B
d. Hepatitis C and E

b. Hepatitis A and E

5

How can acute hepatitis infections be diagnosed?
a. A decrease in IgG titre confirms an acute infection
b. PCR can distinguish acute and chronic infection
c. Rising titre of IgM antibodies can confirm chronic infection
d. An IgM ELISA to viral proteins can demonstrate acute infection

d. An IgM ELISA to viral proteins can demonstrate acute infection

6

What is a feature of the hepatitis A virus?
a. It is a member of the flavivirus family
b. It has a single serotype across the world
c. It is an enveloped –ssRNA virus
d. It is sensitive to stomach acid

b. It has a single serotype across the world

7

What is involved in the lifecycle of hepatitis A and E?
a. After ingestion, the virus replicates in the intestinal epithelia
b. The virus is transmitted percutaneously
c. The viruses have no viremic stage
d. The virus penetrates the intestinal epithelia following ingestion

a. After ingestion, the virus replicates in the intestinal epithelia

8

What is not a clinical feature of hepatitis A?
a. An average incubation period of 30days
b. Symptoms including jaundice and pale faeces
c. Cirrhosis can develop as a chronic sequelae
d.

c. Cirrhosis can develop as a chronic sequelae

9

What is the primary method used to prevent HAV?
a. Pre exposure immune globulin
b. Supportive nutrition
c. Sanitation
d. Post exposure immune globulin

c. Sanitation

10

What makes up the HAV vaccine?
a. It is a whole virus vaccine inactivated by formalin
b. It does not require an adjuvant
c. It is highly effective and cheap to produce
d. It contains sub-viral particles and is cultured by yeast

a. It is a whole virus vaccine inactivated by formalin

11

What is a feature of the hepatitis E virus?
a. It easily passes from person to person
b. It is enveloped with helical symmetry
c. It has a 7.7kb +ssRNA genome
d. It is part of the calicivirdae family

c. It has a 7.7kb +ssRNA genome

12

What is correct about the transmission risk for viral hepatitis?
a. Only HBV and HCV can be transmitted sexually
b. HAV and HEV are only transmitted by intravenous drug use
c. Perinatal transmission is possible for HBV
d. HBV and HCV are transmitted in contaminated food and water

c. Perinatal transmission is possible for HBV

13

Which are chronic viruses?
a. Hepatitis A and B
b. Hepatitis B, C and D
c. Hepatitis A, B and D
d. Hepatitis D and E

b. Hepatitis B, C and D

14

What is the pre-C region?
a. It is added by HBeAg and indicates active replication of HBV
b. It encodes a HBV polymerase that reverse transcribes the preRNA into genomic DNA
c. It is removed by the core protein of HBV to signify the end of the four reading frames
d. It is one of two direct repeats present in the HBV genome

a. It is added by HBeAg and indicates active replication of HBV

15

What is a clinical feature of HBV infection?
a. 90% of those under 5years of age develop a chronic infection
b. Jaundice is observed in 30-50% of those over 5 years of age
c. The incubation period is about 10days
d. The fatality rate is 2-10% in those over 5 years of age

b. Jaundice is observed in 30-50% of those over 5 years of age

16

How does the typical serologic course of HBV differ between acute and chronic infections?
a. HBsAG persists throughout the acute infection
b. There is a steep decrease in total anti-HBc during an acute infection
c. The level of IgM anti-HBc persists during both infections
d. In a chronic infection, the HBeAg phase lasts longer than the anti-HBe phase

d. In a chronic infection, the HBeAg phase lasts longer than the anti-HBe phase

17

What is not a feature of HBV and liver cancer?
a. Hepatocellular carcinoma can develop in 2-10% of those infected with HBV
b. All of those with untreated HBV eventually develop hepatocellular carcinoma
c. It involves a random partial integration of the HBV genome
d. Mutations accumulate due to repeated destruction of regeneration of hepatocytes

b. All of those with untreated HBV eventually develop hepatocellular carcinoma

18

What allows HDV infection to develop?
a. It has a coat with HbsAg antigens and infects in conjunction with HBV
b. It can cause a coinfection with HBV that results in chronic HDV and severe chronic liver disease
c. It can cause a superinfection that results in sever acute disease but a low risk of chronic infection
d. It can “piggyback” HCV and lead to superinfection and chronic liver disease

a. It has a coat with HbsAg antigens and infects in conjunction with HBV

19

What is a feature of hepatitis C virus?
a. It is part of the caliciviridae family
b. It has a low mutation rate
c. It contains a self-replicating RNA replicon
d. It elicits a high immune response and resistance to super-infection

c. It contains a self-replicating RNA replicon

20

Which virus is a flavivirus and contains a lipid droplet in its capside?
a. HAV
b. HBV
c. HCV
d. HDV

c. HCV

21

What is involved in the clinical development and sequelae of HCV?
a. 70-90% of those infected develop a persistent infection
b. The incubation period is often years long
c. Jaundice is evident in 70% of cases
d. Cirrhosis and liver failure are rarely seen as a result of HCV infection

a. 70-90% of those infected develop a persistent infection

22

• Acute viral hepatitis causes cirrhosis and liver cancer.

F

23

• After replication in the hepatocytes, hepatitis particles can only be released into the blood.

F

24

• In Australia, hepatitis virus infections are 18X more prevalent than HIV and chronic HCV is the most common.

T

25

• 50-60% of intravenous drug uses carry a HCV infection.

T

26

• Hepatitis B, C and D replicate in mucosal epithelia whilst Hepatitis A and E penetrate it.

F

27

• During HBV infection, chronic infection decreases as age increases but symptomatic infection increases with age.

T

28

• Anti-HBc IgM marks chronic HBV infection and Anti-HBc IgG marks acute HBV infection.

F

29

• The HBV vaccine is derived from yeast, does not require adjuvants and does not protect from HDV.

F

30

• Only 3% of those with HCV infection can clear the virus.

F (30%)

31

• During HCV replication, NS5B RNA pol mediated replication of viral +ssRNA is very error prone and leads to a high degree of genetic diversity.

T

32

Which is a picornavirus?
a. HAV
b. HBV
c. HCV
d. HEV

a. HAV

33

Which is a hepevirus?
a. HAV
b. HBV
c. HCV
d. HEV

d. HEV

34

Which is a hepdnavirus?
a. HAV
b. HBV
c. HCV
d. HEV

b. HBV

35

Which is a deltavirus?
a. HAV
b. HBV
c. HCV
d. HDV

d. HDV

36

Which is a flavivirus?
a. HAV
b. HBV
c. HCV
d. HEV

c. HCV

37

What cannot be targeted by antiviral drugs against HCV?
a. NS34A protease
b. Reverse Transcriptase
c. NS5A/B and replication
d. Helicase

b. Reverse Transcriptase

38

What is HBsAg?
a. A HBV surface antigen
b. A HBV capsid protein
c. A secreted, short form of HBcAg
d. A general transactivator

a. A HBV surface antigen

39

What is HBxAg?
a. A HBV surface antigen
b. A HBV capsid protein
c. A secreted, short form of HBcAg
d. A general transactivator

d. A general transactivator

40

What is HBcAg?
a. A HBV surface antigen
b. A HBV capsid protein
c. A secreted, short form of HBcAg
d. A general transactivator

b. A HBV capsid protein

41

What is HBeAg?
a. A HBV surface antigen
b. A HBV capsid protein
c. A secreted, short form of HBcAg
d. A general transactivator

c. A secreted, short form of HBcAg

42

• HCV can inhibit PKR and interferon.

T

43

• It is difficult to become re-infected with HCV infection.

F

44

• HBV causes a lytic infection and HCV causes a latent infection and this is why is it more difficult to treat HCV.

F

45

• The current main target of HBV treatment is the reverse transcriptase.

T

46

What can be targeted in the treatment of HCV?
a. RT using nucleoside analogues
b. Post translational processing via NS3-4A protease
c. Viral assembly via cyclophillin B
d. Transcriptional processing via NS5A or NS5B

b. Post translational processing via NS3-4A protease


Cyclophillin B, NS5B, NS5A replication

47

What is sofosbuvir?
a. A nucleotide analogue used to silence cccDNA in HBV infection
b. A pro-drug that can cure HCV genotype 3
c. A nucleotide analogue used in IFN-free DAA against HCV
d. A nucleotide analogue responsible for the growing rate of HCV resistance

c. A nucleotide analogue used in IFN-free DAA against HCV

48

HCV treatment strategies have evolved from PEG-IFN and broad acting Ribavarin to IFN-free direct acting antiviral therapy.

T

49

HBeAg is extracellular and the precursor of HBcAg that indicates active replication of HBV.

T

50

What is NOT a barrier to curing Chronic HBV?
a. The cccDNA reservoir
b. Dysfunctional T cell Responses
c. Insufficient B cell reponses
d. The degradation of monocytes

d. The degradation of monocytes

51

What is a main treatment currently used against HBV?
a. Nucleoside RT inhibitors
b. NS5A and NS5B inhibitors
c. cccDNA agonists and IFN blockers
d. Tenofovir and Telbivudine inhibitors

a. Nucleoside RT inhibitors

52

HCV is more difficult to treat and cure than HBV.

F

53

Once acute HBV has been cured, it cannot arise as a chronic infection, even in the case of immunosupresion.

F

54

HBV has two direct repeats in its genome which define the ends of the genome.

T