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MIIM30014 Virology > MST2 L11-22 Questions > Flashcards

MST2 L11-22 Questions Flashcards

1
Q

What is false about viral pathogenesis?

a. Many enveloped viruses are stable to low pH and proteases
b. Most viral infections aren’t established to cause illness
c. Many viral particles are sensitive to heat, drying and UV
d. Viruses can still replicate and be transmitted in the absence of symptoms

A

a. Many enveloped viruses are stable to low pH and proteases

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2
Q

What largely determines the course of a viral infection?

a. Specific viral tropism (receptor specificity)
b. The entry route of the virus
c. The immune response of the host
d. The ability for the virus to be passed congenitally

A

c. The immune response of the host

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3
Q

How might a virus enter a host via the skin?

a. Through the bite of an infected animal, like HIV
b. By injection, like rabies
c. By mechanical trauma, like HPV
d. By a mosquito bite, like poxvirus

A

c. By mechanical trauma, like HPV

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4
Q

What is false about entry via the respiratory tract?

a. Defences in healthy people include the muco-cillary escalator, sinus filtering and immune cells
b. Immune responses are largely mediated by IgE
c. Droplets that are larger than 10um often lodge in the nose when inhaled
d. Barriers include alveolar macrophages and a temperature gradient

A

b. Immune responses are largely mediated by IgE

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5
Q

Which virus is unlikely to replicate in the lower respiratory tract?

a. Influenza virus
b. Adenovirus
c. Parainfluenzavirus
d. Rhinovirus

A

d. Rhinovirus

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6
Q

What is a feature of viruses that enter by the alimentary route?

a. Acid stable and resistant to bile salts
b. Envelope for protection in low pH environments
c. Must be able to invade mucosal layer
d. Must not interact with proteolytic enzymes

A

a. Acid stable and resistant to bile salts

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7
Q

Which virus enters via the alimentary route despite having an envelope?

a. Influenza
b. Coronavirus
c. Rhinovirus
d. Hepatitis A

A

b. Coronavirus

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8
Q

Which virus is MOST likely to invade deep tissue?

a. Herpes Simplex Virus
b. Influenza Virus
c. Papillomavirus
d. Rhinovirus

A

a. Herpes Simplex Virus

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9
Q

What leads to secondary viremia?

a. When the virus in present in the blood
b. When the virus multiplies in secondary lymphoid tissue
c. When passive viremia switches to active viremia
d. When viruses become associated with cells of the immune system

A

b. When the virus multiplies in secondary lymphoid tissue

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10
Q

What does not happen at the capillary endothelial cells?

a. Some viruses replicate in the endothelial cells and release progeny into tissue
b. Some viruses cross to tissue using monocytes and lymphocytes
c. Some viruses cross the cells via transcytosis
d. Some viruses activate proteases that degrade tight junctions between the cells, aiding passage

A

d. Some viruses activate proteases that degrade tight junctions between the cells, aiding passage

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11
Q

What can happen during neural spread of viruses?

a. They can only travel within the CNS
b. The uncoated nucleocapsid can passively travel along axons or dendrites
c. Viruses are at risk of CTL attack due to MHC I expression
d. Herpes simplex virus cannot travel back to the epithelium after entering the CNS

A

b. The uncoated nucleocapsid can passively travel along axons or dendrites

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12
Q

How does Rabies virus spread?

a. The virus replicates at the infection site before entering the CNS from the bloodstream
b. It enters peripheral axons by invading the myelin sheath
c. It replicates in myocytes before traveling to the spinal cord through peripheral nerves
d. It has unidirectional movement that allows it to reach the salivary gland

A

c. It replicates in myocytes before traveling to the spinal cord through peripheral nerves
d. Wrong, not uni

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13
Q

What is involved in the infection and spread of Herpes Virus, VZV?

a. VZV utilises viremia before using neural spread to stay latent in the dorsal root ganglia
b. The virus enters the host following an animal bite and replicates in the muscle before utilising neural spread
c. VZV can undergo secondary viremia or spread neuronally and can’t utilise both processes during the same infection
d. Infection is first established in the lower respiratory tract before the viral replicates in the spleen

A

a. VZV utilises viremia before using neural spread to stay latent in the dorsal root ganglia

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14
Q

What is not involved in the shedding and transmission of viruses?

a. Viruses of the respiratory tract are most often spread by aerosols
b. HIV can be spread in semen and milk
c. Viruses are often excreted into the faeces from intestinal epithelial cells or the liver
d. CMV is most likely to be spread by mosquito or in cervical secretions

A

d. CMV is most likely to be spread by mosquito or in cervical secretions

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15
Q

• Virulence refers to the “capacity” to produce disease.

A

T

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16
Q

• Most symptoms of a viral infection are due to our own immune system.

A

T

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17
Q

• Symptoms of Norovirus infection last for four days and the virus is only shed during this period.

A

F

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18
Q

• The most common route of viral entry is via the skin.

A

F (Respiratory)

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19
Q

• Droplets that are 5-10um in size usually lodge in the airways when inhaled.

A

T

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20
Q

• HIV cannot enter the alimentary tract through epithelial cells unless there is a breach in the surface, such as in the rectal route.

A

T

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21
Q

• Measles and dengue can spread in CD4+ T lymphocytes to demonstrate cell-associated viremia.

A

F (monocytes)

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22
Q

• Some viruses can be spread vertically from host to progeny by crossing the placenta or via the birth canal during labour.

A

T

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23
Q

• Viruses that cause acute respiratory disease are spread at a high titre for long periods.

A

F (

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24
Q

• Enveloped Hepatitis B particles can be shed in the faeces and are extremely infectious.

A

F

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25
Q

• Both VZV and Measles can be spread by rash lesions.

A

F (only VZV)

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26
Q

What is not a consideration for viral tropism?

a. Receptors must be expressed ubiquitously
b. Accessibility
c. Permissivity
d. Local factors as preventatives

A

a. Receptors must be expressed ubiquitously

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27
Q

Why is influenza confined to the respiratory tract?

a. NA is cleaved next to a fusion peptide to become infectious
b. When the endosome reaches pH 9, the fusion peptide changes conformation
c. HA is cleaved by tryptase Clara which is unique to the respiratory tract
d. Furin cleaves HA so it cannot exit the respiratory tract

A

c. HA is cleaved by tryptase Clara which is unique to the respiratory tract

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28
Q

Why is H5N1 so virulent?

a. HA cleavage is dependent on the action of tryptase clara
b. There is an insertion of acidic AA residues at the HA cleavage site
c. HA can be cleaved by Furin which is expressed ubuqutiously
d. It doesn’t have a requirement for NA cleavage during virion release

A

c. HA can be cleaved by Furin which is expressed ubuqutiously

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29
Q

How can papillomavirus replicate in the skin?

a. By initially transcribing early genes in the mature, apical layer
b. By first transcribing structural genes to establish infection of the skin
c. By utilising cellular tRNAs in the basal layer that translate structural proteins
d. By starting replication in basal germinal cells which have proteins that block transcription of late structural genes

A

d. By starting replication in basal germinal cells which have proteins that block transcription of late structural genes

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30
Q

Which virus is correctly matched to the way it changes cells?

a. Tumour formation – Epstein-Barr Virus
b. Lytic infection – reovirus
c. Chronic infection – adenovirus
d. Latent Infection – enterovirus

A

b. Lytic infection – reovirus

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31
Q

What is an accurate example of a cytocidal virus?

a. During cytoplasmic replication, Pox virus encodes a DNase to act on host DNA
b. Adenovirus encodes protease 2A which cleaves eIF4g to shutdown host translation
c. Rotavirus inhibits transport of cellular mRNA to the cytoplasm
d. Influenza virus encodes tryptase clara which cleaves cellular glycoproteins

A

a. During cytoplasmic replication, Pox virus encodes a DNase to act on host DNA

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32
Q

What is false about cytopathic effects of viral proteins?

a. Formation of syncytia is common during measles infection
b. Flavivirus and Rotavirus produce cytoplasmic inclusions
c. Accumulated viral proteins are rarely cytotoxic and aid in diagnosis by microscopy
d. Adenovirus can cause nuclear inclusions

A

c. Accumulated viral proteins are rarely cytotoxic and aid in diagnosis by microscopy

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33
Q

What is true about T-cell mediated pathology?

a. Hepatitis B leads to CD4+ mediated responses which leads to a viral rash
b. HCV mediates a CD8+ response that leads to hepatocyte lysis and liver damage
c. Measles can lead to a type IV hypersensitivity reaction and rash due to CD4+ responses
d. CD4+ mediated response of cytokine that recruit eosinophils can clear hepatitis B infection

A

c. Measles can lead to a type IV hypersensitivity reaction and rash due to CD4+ responses

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34
Q

Which correctly describes a virus that causes immunosuppression?

a. HIV replicates in CD4+ cells which leads to their demise
b. Norovirus has a non-productive replicative stage that occurs in T cells and macrophages
c. Measles can replicate in dendritic cells and macrophages
d. Rotavirus produces granzymes that lyse CD4+ T cells

A

a. HIV replicates in CD4+ cells which leads to their demise

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35
Q

• Poliovirus and Rhinovirus are both enteroviruses which are activated by low pH.

A

F (just polio activated)

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36
Q

• Host cells can be damaged by lysis due to the release of non-enveloped viruses and replication cycle of enveloped viruses.

A

T

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37
Q

• LCMV(arenavirus) has a non-lytic persistence in growth hormone producing cells in pituitary gland and specifically reduce the transcription of growth hormone mRNA.

A

T

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38
Q

• Some viruses encode oncogenes whose expression leads to transformation and reduced cell proliferation.

A

F

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39
Q

• Antibody dependent enhancement is when cross reactive antibodies neutralise the virus to such high degrees that tissue is damaged.

A

F

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40
Q

• HCV affects lymphocytes which impacts antibody production and the formation/deposition of immune complexes with rheumatoid factors leading to tissue damage.

A

T

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41
Q

• A CCR5 mutation was selected for during the Black Death and the mutation is associated with HIV resistance.

A

T

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42
Q

What would not be used to quantify virulence?

a. Measurement of the reduction of CD4+ T cells following poliovirus infection
b. Mean time to death
c. Mean time to symptoms appear
d. Measurement of weight loss

A

a. Measurement of the reduction of CD4+ T cells following poliovirus infection

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43
Q

Which is not a class of viral virulence genes?

a. Gene products that alter the ability to replicate
b. Gene products that modify host defence mechanism
c. Genes that prevent spread in host
d. Toxic viral proteins

A

c. Genes that prevent spread in host

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44
Q

What is false about viral gene products that alter a viruses ability to replicate?

a. Mutants can arise that exhibit reduced replication in the host AND cell culture
b. Wildtype viruses only replicate in the host and not cell culture
c. Mutants can arise that exhibit reduced replication in the host but not cell culture
d. An ideal vaccine would be based on a mutant that only replicates in cell culture

A

b. Wildtype viruses only replicate in the host and not cell culture

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45
Q

Which statement about viral gene products that modify host defence mechanisms is false?

a. Virokine and Viroreceptors can interfere with host intrinsic defences
b. The genes affect replication and not virulence
c. Most virokine and virorecpetors are encoded for by DNA viruses
d. Viroreceptors are homologs of host receptors

A

b. The genes affect replication and not virulence

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46
Q

What is not a feature of NSP4?

a. It is produced by Rotavirus and acts as an enterotoxin by increasing calcium in enterocytes
b. It is a non-structural glycoprotein that aids in the formation of the viral envelope
c. It acts as a chaperone during virion assembly
d. It is produced by poliovirus to disassemble the golgi complex

A

d. It is produced by poliovirus to disassemble the golgi complex

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47
Q

What is involved in genome recombination?

a. Mixed RNA segments are packaged during assembly to generate diversity
b. Host DdDp switches between two viral genome templates in the same cell
c. A chimeric viral genome is produced from two different viral strains
d. It cannot occur in viruses that produce sub-genomic RNAs

A

c. A chimeric viral genome is produced from two different viral strains

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48
Q

Which is a correctly described protein essential in poliovirus virulence?

a. 3AB is cleaved to release 3A and 3B (VpG)
b. 2BC impairs the function of GTPases that regulate COP transfer
c. 3A recruits COPII to facilitate formation of the replication complex
d. 2ABC is a NTPase

A

a. 3AB is cleaved to release 3A and 3B (VpG)

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49
Q

Which virus is associated with disassembly of the golgi?

a. Rotavirus
b. Poxvirus
c. Poliovirus
d. Norovirus

A

c. Poliovirus

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50
Q

What is involved in the pathogenesis of poliovirus?

a. It manipulates the host secretory pathway to upregulate MHCII
b. It hijacks the host secretory pathway to aid virion production
c. It causes the Golgi to disassemble and prevents cytokine secretion
d. It causes the Golgi to over-produce viral encoded glycosylated proteins

A

c. It causes the Golgi to disassemble and prevents cytokine secretion

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51
Q

What is false about ebola pathogenesis?

a. Secreted glycoproteins act as decoys to sequester host antibodies and avoid neutralisation
b. VP35 prevents IRF3 activation to block IFN production
c. VP24 prevents STAT1 entering the nucleus to down regulate IFN production
d. Transcriptional editing results in the production of 10 different glycoproteins

A

d. Transcriptional editing results in the production of 10 different glycoproteins

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52
Q

• Poliovirus type 1 won’t infect mouse CNS but poliovirus type 2 is neuro-virulent.

A

T

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53
Q

• Dengue virus is the most neurovirulent Flavivirus.

A

F (Japanese encephalitis virus)

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54
Q

• Viral virulence can be compared between different viruses if the same assay is used.

A

F

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55
Q

• A virus may be neurovirulent if injected to the CNS and not neuroinvasive if injected into the skin.

A

T

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56
Q

• A single nucleotide change in the 5’ NCR of poliovirus can reduce neurovirulence.

A

T

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57
Q

• RNA polymerase efficiently corrects errors during replication.

A

F

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58
Q

• COPII mediates retrograde movement.

A

F

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59
Q

What is not a feature of bats?

a. They have a long life span
b. They have a high rate of tumour formation
c. They show variable thermoregulation
d. They are a reservoir for many viruses

A

b. They have a high rate of tumour formation

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60
Q

What is a feature of the Hendra and Nipah viruses?

a. They have a +ssRNA genome
b. They are in the coronaviridae family
c. They are henipavrisues in the paramyxoviridae family
d. They share identical morphology to measles and mumps viruses

A

c. They are henipavrisues in the paramyxoviridae family

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61
Q

What is not part of the Henipavirus viral protein?

a. The fusion and attachment proteins on the envelope
b. A nucleocapsid with L, N and P proteins
c. A segmented dsRNA genome
d. An 18.2kb genome

A

c. A segmented dsRNA genome

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62
Q

What was a feature of the 2011 Hendra Virus outbreak?

a. Over 200 pet dogs were infected
b. The outbreak location remained localised to Hendra
c. There was a 50% increase in spill over events
d. There was more Hendra virus shed in bat urine

A

d. There was more Hendra virus shed in bat urine

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63
Q

The host range of Nipah virus:

a. Can include bats, cats, dogs and pigs
b. Involves only humans and bats
c. Cannot be shown in cultured cells in vitro
d. Excludes all terrestrial species

A

a. Can include bats, cats, dogs and pigs

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64
Q

What is Ephrin B2?

a. A ligand receptor for Hendra and Nipah virus
b. A fusion receptor found on Coronaviridae
c. A unique receptor of the pig upper respiratory tract that interacts with paramyxoviridae
d. The protein subunit of the spikes found on coronaviruses

A

a. A ligand receptor for Hendra and Nipah virus

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65
Q

What is a feature of SARs-CoV?

a. It causes respiratory, enteric, orphan infection
b. It has an envelope spike which acts as an attachment and fusion protein
c. It has a –ssRNA genome
d. It is part of the paramyxoviridae family

A

b. It has an envelope spike which acts as an attachment and fusion protein

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66
Q

What were the consequences of the SARs outbreak?

a. Over 8000 deaths
b. Nearly 200 infections
c. 774 deaths
d. Nearly 100,000 infections

A

c. 774 deaths

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67
Q

What is a feature of MERS?

a. It uses the same receptor as SARS
b. It is 90% fatal
c. There have been 1368 confirmed cases
d. Camels are the source of infection

A

c. There have been 1368 confirmed cases

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68
Q

Why are bats often reservoirs for viruses?

a. They are less prone to immunopathology and inflammation
b. They have all the receptors that interact with human respiratory viruses
c. They have a short life span and viruses replicate quickly in bat cells
d. They often share habitats with humans who spread viruses to bats

A

a. They are less prone to immunopathology and inflammation

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69
Q

• Zoonosis is an infectious disease that can be transmitted from animals to humans.

A

T

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70
Q

• The henipavirus is smaller than other paramyxoviridae genomes due to having smaller coding regions.

A

F

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71
Q

• Nipah virus can spread from bats to pigs to horses.

A

F (humans)

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72
Q

• Bangladesh Nipah virus can spread from bat to human and human to human only.

A

T

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73
Q

• Melaka virus has a unimolecular –ssRNA genome.

A

F (dsRNA segmented)

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74
Q

• Bat Reovirus can cause severe respiratory disease in humans and human and bat isolates are almost identical.

A

T

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75
Q

• Melaka virus pathogenesis is aided by it’s non-fusogenic ability.

A

F

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76
Q

• The mitochondria is a key organelle when considering cell pathways and bats harbouring viruses.

A

T

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77
Q

How do innate and adaptive immunity compare?

a. Natural killer cells are a second line of defence in innate immunity
b. Skin and lysozymes are a second line of defence in innate immunity
c. Cytokines are only produced during adaptive immunity
d. Antibodies are formed during the second line of defence in innate immunity

A

a. Natural killer cells are a second line of defence in innate immunity

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78
Q

Which endosomal receptor is critical during the innate response to viral infection?

a. TLR5
b. TLR1
c. TLR8
d. TLR11

A

c. TLR8

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79
Q

Which statement is correct?

a. PRRs are a major component of adaptive immunity
b. The innate response to repeat infections is much more rapid than the primary response
c. Innate immunes response are more diverse than adaptive immune responses in terms of specificity
d. Antibodies are a component of the adaptive immune response

A

d. Antibodies are a component of the adaptive immune response

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80
Q

Which is correctly matched?

a. TLR3 recognises flagellin
b. TLR8 recognises ssRNA
c. TLR7 recognises CpG unmethylated dinucleotides
d. TLR9 recognises dsRNA

A

b. TLR8 recognises ssRNA (7,8)

a. TLR5 recognises flagellin
b. TLR7, 8 recognises ssRNA
c. TLR9 recognises CpG unmethylated dinucleotides
d. TLR3 recognises dsRNA

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81
Q

What is special about viral specific TLRs?

a. All are embedded in the ER membrane
b. They are cytoplasmic
c. They are localised to the endosomal membrane
d. They can only be found on the cell membrane

A

c. They are localised to the endosomal membrane

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82
Q

What is not involved in the activation of human TLRs?

a. There is ligand induced dimerization of TLR
b. MYD88 can repress NFKB and IRF7 activation
c. TLRs assemble with adaptor signalling molecules
d. MyD88 and TRIF activate transcription factors and MAP kinases

A

b. MYD88 can repress NFKB and IRF7 activation

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83
Q

What does IRF3 do?

a. It interacts with eIF3 to promote protein synthesis
b. It causes the production of IFN
c. It down regulates production of the antiviral ISG56 protein
d. It induces it’s effects from the cytoplasm

A

b. It causes the production of IFN

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84
Q

What is a feature of MDA5 and RIG-I?

a. MDA5 recognises long dsRNA such as that produced during picornavirus infection
b. RIG-I can only recognise RNA from a segmented viral genome
c. MDA5 recgonises short dsRNA such as that produced during paramyxovirus infection
d. RIG-I and MDA5 are TLRs embedded in the endosome membrane

A

a. MDA5 recognises long dsRNA such as that produced during picornavirus infection

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85
Q

What is MAVS?

a. An IRF that is activated via TRAF3 and TBK1
b. A mitochondrial membrane adaptor protein that is activated by RLR signalling
c. An IFN protein produced following NFKB signalling
d. A RLR that directly binds dsRNA before activated MDA5 or RIG-I

A

b. A mitochondrial membrane adaptor protein that is activated by RLR signalling

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86
Q

What is involved in the early recognition of viral infection via RLRs?

a. dsRNA interacts with RIG-I or MDA5 which interact with MAVS on the ER
b. Interactions between RIG-I/MDA5 and MAVS are facilitated via the helicase domain
c. The NFKB signalling pathway is activated after RIG-I/MDA5 interact with MAVS
d. TRAF6, RIP1 and FADD facilitate the dimerization and activation of IRF3 and IRF7

A

c. The NFKB signalling pathway is activated after RIG-I/MDA5 interact with MAVS

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87
Q

What is cGAS?

a. A viral protein that recognises foreign DNA in the cytoplasm
b. A host protein that can generate cGAMP when cytosolic DNA is detected
c. A monophosphate that binds STING in the ER
d. A ligand for TBK1, IRF3 and NFKB that leads to IFN production

A

b. A host protein that can generate cGAMP when cytosolic DNA is detected

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88
Q

Which antiviral protein is cytosolic, sequesters nucleocapsids and is potent against influenza?

a. OAS
b. RNaseL
c. PKR
d. MxA

A

d. MxA

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89
Q

What is a feature of OAS and RNaseL?

a. OAS and RNaseL production is down regulated by IFN
b. They are antivirals against viral DNA species
c. OAS monomers form tetramers before making a nucleotide that activates RNaseL
d. OAS digests viral RNA when activated by RNaseL

A

c. OAS monomers form tetramers before making a nucleotide that activates RNaseL

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90
Q

What is a feature of Protein Kinase R (PKR)

a. It affects virus production without impacting the host
b. It can phosphorylate host EIF2a to halt host translation
c. It has a viral DNA binding domain
d. When it binds dsRNA, it forms a tetramer and up regulates host cell translation

A

b. It can phosphorylate host EIF2a to halt host translation

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91
Q

How can a virus inhibit IFN signalling?

a. Measles virus can prevent phosphorylation of Tyk2
b. SARS CoV can degrade STAT proteins
c. Mumps can prevent the nuclear import of the STAT1/2 heterodimer
d. West Nile virus prevents the nuclear import of the STAT1 homodimer

A

c. Mumps can prevent the nuclear import of the STAT1/2 heterodimer

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92
Q

What is NOT an example of how viruses can counteract the innate immune response?

a. Upregulate TLR signalling and compromise host cells. i.e. Poxvirus
b. PKR can be inhibited as shown by poxvirus and reoviruses
c. IFN signalling can be inhibited, i.e West Nile Virus
d. RNA recognition and MAVs signalling can be interfered with. i.e. Influenza virus

A

a. Upregulate TLR signalling and compromise host cells. i.e. Poxvirus

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93
Q

How can PKR be inhibited?

a. Poliovirus can phosphorylate EIF2a
b. Reovirus can cleave the inactive PKR monomer
c. Dimerization and phosphorylation can be prevented by poxvirus
d. HSV can produce fake RNAs that lead to PKR degradation

A

c. Dimerization and phosphorylation can be prevented by poxvirus

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94
Q

• NFKB and IRF are key TLRs involved in innate immunity.

A

F (transcription factors)

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95
Q

• RLRs are cytoplasmic helicases that recognise viral nucleic acid.

A

T

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96
Q

• TLR3 activates IRF3.

A

T

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97
Q

• MYD88 and TRIF are important transcription factors activated by TLR activation.

A

F (adaptor molecules)

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98
Q

• Cytoplasmic DNA receptors can detect foreign, cytosolic DNA that results from some viral infections.

A

T

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99
Q

• Interferons only demonstrate paracrine signalling action.

A

F (all 3 types of signalling)

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100
Q

• Interferon can relieve sleepiness, muscle pain and nausea during viral infection.

A

F

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101
Q

• STAT is a signal transducer and transcription factor with a key role in IFN signalling.

A

T

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102
Q

• Type I IFN causes STAT1 and 2 to heterodimerise and Type II IFN causes STAT1 molecules to homodimerise.

A

T

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103
Q

• RNaseL is always active and abundant in cells

A

F

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104
Q

• Influenza virus can interferes with RIG-I signalling via NS1.

A

T

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105
Q

What would NOT be a way for a virus to interact with its host to avoid the immune response?

a. Stop the action of pattern recognition receptors
b. Up-regulate interferon signalling
c. Modulate apoptosis and autophagy
d. Stop host protein expression

A

b. Up-regulate interferon signalling

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106
Q

What is not a feature of viral latency?

a. The viral genome can replicate in conjunction with the host DNA without disrupting the cell cycle
b. The viral genome can persist intact in the host nucleus
c. Expression of productive cycle viral genes is very efficient
d. Immune detection is greatly reduced

A

c. Expression of productive cycle viral genes is very efficient

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107
Q

What is a correct example of viral persistence?

a. Influenza can cause a chronic infection due to producing decoy proteins
b. HPV causes a non-cytopathic infection of an inaccessible site
c. Mesles demonstrates chronic infection due to immune exhaustion
d. HIV can avoid the immune response using antigenic shift

A

b. HPV causes a non-cytopathic infection of an inaccessible site

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108
Q

Which virus can result in Subacute sclerosing panencephalitis due to persistence?

a. HBV
b. HPV
c. Vaccinia
d. Measles

A

d. Measles

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109
Q

What is false about Antigenic Drift of B cell epitopes?

a. In influenza, a diversity of strains usually arises in a single patient
b. The antigenic structure of the virus changes and is selected for
c. Changes can be spontaneous and due to errors in RNA replication
d. Drift occurs when changes are selected for and allow the virus to escape neutralisation by pre-existing antibodies

A

a. In influenza, a diversity of strains usually arises in a single patient

110
Q

What is a feature of Antigenic Drift of T cell epitopes?

a. It is commonly shown by HBV
b. The TCR contact residues can be changed so the epitope is not processed or presented
c. If the epitope anchor residues are altered, it can avoid binding MHC
d. Changing the flanking amino acids of the epitope allow for faster processing by T cells

A

c. If the epitope anchor residues are altered, it can avoid binding MHC

111
Q

What is not an example of how viruses can inhibt T cell priming by dendritic cells?

a. By blocking cytokine induced maturation
b. By blocking signal transduction in immature DCs
c. By clocking T cell stimulation at the receptors
d. By increasing signal transduction in mature DCs

A

d. By increasing signal transduction in mature DCs

112
Q

What is not part of CD8 T cell recognition of viral infected cells?

a. Viral proteins are degraded by the proteasome before the peptides are loaded to the ER through TAP
b. In the ER, Tapasin loads viral peptides into MHCI
c. Viral proteins are modified in the Golgi before being loaded into the ER through TAP
d. Once viral peptides are loaded into MHCI, the complex is transported to the cell surface

A

c. Viral proteins are modified in the Golgi before being loaded into the ER through TAP

113
Q

What is not a method used to evade CD8 T cell recognition?

a. Antigenic variation in the CTL epitope as shown by HIV
b. A HSV protein binds cytosolic side TAP to prevent ER translocation
c. A HCMV protein binds tapasin to inhibit peptide loading in ER
d. Adenovirus can increase the expression of MHCI genes

A

d. Adenovirus can increase the expression of MHCI genes

114
Q

What is not a viral evasion strategy shown by CMV (human or murine)?

a. Using a protein that sequesters NKC activation ligands in the ER
b. Up regulating cellular non classical HLA-E (MHCI) which only binds/presents signal peptides of other MHC molecules
c. Encode a soluble cytokine receptor homologue that binds and inhibits cytokine function
d. Encode a MHCI like molecule that is expressed on infected cells and activates “not kill” signals on NKCs

A

c. Encode a soluble cytokine receptor homologue that binds and inhibits cytokine function

115
Q

How does poxvirus interfere with cytokine function?

a. By encoding soluble cytokine receptor homologues that bind and inhibit IFN
b. By encoding a IL-10 homolog that suppresses the Th1 response and CTL activation
c. By encoding proteins that interfere with the TNFa mediated killing of a cell
d. By promoting the cleavage of IL-1B to decrease inflammation

A

a. By encoding soluble cytokine receptor homologues that bind and inhibit IFN

116
Q

What is not a feature of apoptosis?

a. The intrinsic pathway involves the permeabilisation of mitochondrial and release of cytochrome C
b. Dying cells release apoptotic bodies which contain viral proteins that can be taken up by APCs and presented on MHC molecules
c. The process is mediated by caspases
d. All virus infected cells eventually undergo apoptosis so viral particles can be released

A

d. All virus infected cells eventually undergo apoptosis so viral particles can be released

117
Q

What does a viral FLIP do?

a. It prevents pro-caspase 8 to caspase 8 cleavage
b. It binds to BCL2 to prevent the intrinsic apoptosis pathway
c. It promotes pro-caspase 3 to caspase 3 cleavage
d. It degrades cytC to prevent apoptosis

A

a. It prevents pro-caspase 8 to caspase 8 cleavage

118
Q

How do poxvirus and herpesvirus evade complement?

a. They encourage cells to undergo autophagy and degrade complement proteins
b. They encode control protein homologues which bind to C’ components and prevent the C’ cascade
c. They encode IgG ligand homologues that neutralise IgG antibodies
d. They undergo xenophagy and highjack the host cell lysosome so complement proteins are degraded

A

b. They encode control protein homologues which bind to C’ components and prevent the C’ cascade

119
Q

• Herpes virus grows productively in epithelial cells before becoming latent so evasion is in the context of an existing immune response.

A

T

120
Q

• Viruses that evade CD8 T cells by down regulating MHCI are also successful at evading natural killer cells.

A

F

121
Q

• EBV encodes an IL-10 homolog that suppresses the Th1 response and reduces CD8+ T cells.

A

T

122
Q

• Viruses always evade autophagy by blocking the process.

A

F

123
Q

What is true about the general patterns of infection?

a. Measles SSPE leads to chronic infection
b. During latent, reactivating infection, virus release is always associated with symptoms
c. Slow virus infection involves periodical stages of virus release
d. Herpes simplex virus causes an acute infection

A

c. Slow virus infection involves periodical stages of virus release

124
Q

What can be considered an active evasion mechanism?

a. Non cytopathic infection by DNA integration
b. Cell tropism in non-replicating cells
c. Free passage through skin barrier
d. Tropism in MHC negative cells like neurons

A

a. Non cytopathic infection by DNA integration

125
Q

What can be considered a passive evasion mechanism?

a. Limited expression of viral genes
b. DNA integration
c. Spread by cell fusion
d. Block apoptosis mechanisms

A

c. Spread by cell fusion

126
Q

What is not a reason that persistent viral infections are significant?

a. They can only be eradicated by antiviral chemotherapy
b. Unapparent infections can be reactivated
c. They can lead to immunopathogenic diseases
d. They may be established in vaccinated people

A

a. They can only be eradicated by antiviral chemotherapy

127
Q

Which virus has a 150kb dsDNA genome with inverted repeats and terminal repeats?

a. Hepadna
b. Parvovirus
c. Herpesvirus
d. Papovavirus

A

c. Herpesvirus

128
Q

What is false about herpesviruses?

a. There are 8 human types that all establish lifelong latency
b. VZV, HSV1 and HSV2 are all alphaherpesviruses
c. EBV is a gammaherpesvirus that causes glandular fever
d. Human herpes virus 6 is a betaherpesvirus that causes fever and shingles

A

d. Human herpes virus 6 is a betaherpesvirus that causes fever and shingles

129
Q

What are the sites of persistence for the three major herpesvirus subfamilies?

a. Alphaherpesviruses persist in neurons
b. Betaherpesviruses persist in lymphocytes
c. Gammaherpesviruses persist in monocytes
d. Deltaherpesviruses persist in secretory glands

A

a. Alphaherpesviruses persist in neurons

130
Q

What is a feature of replicating and non-replicating genomes?

a. Ori-P is used when EBV replicates during lytic infection
b. HSV has OriL and OriS for replicating during lytic infection
c. Ori-Lyt is used when EBV replicates during latent infection of B cells
d. EBV has a non-replicating genome

A

b. HSV has OriL and OriS for replicating during lytic infection

131
Q

What is involved in HSV infection of the primary surface?

a. 90% of infected individuals develop lesions
b. Approximately 10% of infections spread to the blood
c. 85-90% of those infected have an unapparent infection
d. Individuals without symptoms are sero-negative

A

c. 85-90% of those infected have an unapparent infection

132
Q

What happens during HSV latent infections?

a. 90% of infections spread to the blood following local multiplication in regional lymph nodes
b. Primary disease can lead to the virus migrating to sensory nerve ganglia
c. Primary disease always leads to inapparent infection and a negative serotype
d. The virus can only travel by retrograde axonal flow

A

b. Primary disease can lead to the virus migrating to sensory nerve ganglia

133
Q

What happens during HSV recurrence?

a. HSV-1 replicates in the sacral ganglion
b. 50% of facial isolates are HSV-2
c. HSV-2 replicates in the trigeminal ganglion
d. 40% of genital isolates are HSV-1

A

d. 40% of genital isolates are HSV-1

134
Q

What occurs during VZV infection?

a. A skin rash appears on day 10
b. Primary viremia occurs roughly a month after exposure
c. Secondary viremia involves B cells and occurs 15 days after exposure
d. Skin vesicles do not contain virus particles

A

a. A skin rash appears on day 10

135
Q

What is not a feature of EBV?

a. It infects and persists in T cells
b. It causes glandular fever and infects the oropharyngeal cavity
c. 90% of humans are latent carriers
d. It contains an Ori-P and Ori-Lyt

A

a. It infects and persists in T cells

136
Q

• The longest period of virus release occurs during infections that are acute.

A

F

137
Q

• Out of all Herpesviruses, only HSV1 and 2 can cause lifelong persistent infection.

A

F

138
Q

• Gene expression is limited during herpesvirus latency.

A

T

139
Q

• Herpesviruses integrate their DNA into host genomes using an episome.

A

F (no integration)

140
Q

• The circular herpesvirus episome acts as a template for the dsDNA linear genome by rolling circle replication.

A

T

141
Q

• HSV-CNS disease is rare in adults and 70% fatal.

A

T

142
Q

• LATs are stably translated in virus infected cells.

A

F

143
Q

• Immediate early gene expression results in latent infection of Herpesvirus.

A

F

144
Q

• Unlike measles infection, the rash vesicles that result from VZV infection contain virus particles.

A

T

145
Q

What is a feature of latent EBV infection?

a. It occurs in CD4+ T cells
b. Viral genes like EBNA1-6 and LMP1,2 are up-regulated
c. EBNA-1 is involved in the replication of the viral genome in dividing B cells
d. It is initiated by interactions between B cell receptors and LMP1

A

c. EBNA-1 is involved in the replication of the viral genome in dividing B cells

146
Q

What kinds of B cells are involved in EBV latency?

a. Type I have no EBV antigen expression
b. Type III only express EBNA-1
c. Type II express 9 latent EBV antigens
d. Circulating B cells express 3 latent EBV antigens

A

b. Type III only express EBNA-1

147
Q

How can EBV be linked with tumorogenesis?

a. Burkitt’s lymphoma can arise when cells express EBV EBNA1 and there is a chromosome translocation of c-myc and Ig
b. Nasopharyngeal carcinoma can arise when cells express EBNA 1 through 6
c. Hodgkin’s disease can arise when cells express EBNA1, LMP1 and LMP2
d. A chromosome translation and expression of LMP1 can lead to adenocarcinoma

A

a. Burkitt’s lymphoma can arise when cells express EBV EBNA1 and there is a chromosome translocation of c-myc and Ig

148
Q

What is a feature of congenital CMV?

a. 90% of primary infections during pregnancy are transmitted to the foetus
b. 85% of foetal infections lead to asymptomatic infection
c. 100% of symptomatic foetal infections lead to long term sequelae
d. 40% of asymptomatic foetal infections lead to hearing loss

A

b. 85% of foetal infections lead to asymptomatic infection

149
Q

Which statement about HIV prevalence in 2012 is incorrect?

a. About 35.3 million people were infected
b. 2.3 million new infections arose
c. 1.6 million people died
d. 25 million infected people resided in Latin America

A

d. 25 million infected people resided in Latin America

150
Q

What is the cause of 70% of HIV cases acquired in Australia?

a. Injecting drug use
b. Male homosexual contact
c. Heterosexual contact
d. Undetermined causes

A

b. Male homosexual contact

151
Q

What is cause of 80% of HIV cases acquired throughout the world?

a. Injecting drug use
b. Male homosexual contact
c. Heterosexual contact
d. Undetermined causes

A

c. Heterosexual contact

152
Q

What does not influence a heterosexually transmitted HIV epidemic?

a. Social factors like large sexual networks
b. Behavioural factors like condom use
c. Social factors like high viral loads
d. Biological factors like low rates of circumcision

A

c. Social factors like high viral loads

153
Q

What is a feature of HIV as a lentivirus?

a. It is enveloped and has helical symmetry
b. It has a diploid linear 9.2kb +ssRNA genome
c. HIV1 is the only human virus
d. The disease progresses rapidly

A

b. It has a diploid linear 9.2kb +ssRNA genome

154
Q

What is a feature of the HIV-1 genome?

a. Pol encodes enzymes like RT, IN and PR
b. Env encodes structural proteins such as MA, CA and NC
c. Gag encodes envelope proteins SU and TM
d. Tat and Rev are spliced from the gag-pol polyprotein

A

a. Pol encodes enzymes like RT, IN and PR

155
Q

What is correct about reverse transcription?

a. It cannot be targeted by antiviral drugs
b. The process has a low error rate
c. It leads to the formation of LTRs in viral cDNA
d. It requires host cell integrase and reverse transcriptase

A

c. It leads to the formation of LTRs in viral cDNA

156
Q

What is a feature of HIV integration?

a. HIV cDNA integrates at OriP in host DNA
b. Integration cannot occur in terminally differentiated cells
c. Viral integrase is resistant to antiviral drugs
d. The 5’ LTR of the provirus acts as the HIV gene promoter

A

d. The 5’ LTR of the provirus acts as the HIV gene promoter

157
Q

What is not a feature of the LTRs in the HIV provirus?

a. U5 at the 5’ end contains a polyadenylation signal
b. U3 at the 5’ end contains enhancer sequences and transcription start signals
c. NfKb can bind to the 5’ LTR
d. The 5’ LTR contains a cap site between U3 and R

A

a. U5 at the 5’ end contains a polyadenylation signal

158
Q

What acts as the HIV gene promoter following integration into host DNA?

a. The 3’ LTR
b. Gag-pol sequence
c. The 5’ LTR
d. The Rev responsive RNA element

A

c. The 5’ LTR

159
Q

What is a feature Tat?

a. It binds to RREs on the 4kb and 9kb HIV RNA transcripts and exports them to the cytoplasm
b. It regulates structural gene expression
c. It represses transcriptional to initiate HIV latency
d. It binds 5’ TAR and activates CDK9 which phosphorylates and activates RNApolII

A

d. It binds 5’ TAR and activates CDK9 which phosphorylates and activates RNApolII

160
Q

What is a feature of Rev?

a. It activates HIV transcription elongation
b. It binds to RREs on the 4kb and 9kb HIV RNA transcripts and exports them to the cytoplasm
c. It binds and activates CDK9 in order to initiate splicing of late HIV RNA transcripts
d. It is expressed from the 9kb un-spliced HIV RNA transcript

A

b. It binds to RREs on the 4kb and 9kb HIV RNA transcripts and exports them to the cytoplasm

161
Q

Which statement about HIV accessory proteins is correct?

a. Vpu promotes infectivity by blocking cell defences and targeting ssCDNA
b. Nef down modulates MHC1 and Cd4
c. Vpr regulates particle release and Env processing and the degradation of MHC1 and CD4
d. Vif aids the nuclear import of cDNA and is involved in cell growth arrest

A

b. Nef down modulates MHC1 and Cd4
a. promotes infectivity by blocking cell defences and targeting ssCDNA (Vif)
c. regulates particle release and Env processing and the degradation of MHC1 and CD4 (Vpu)
d. aids the nuclear import of cDNA and is involved in cell growth arrest (Vpr)

162
Q

What is a feature of the CCR5 co recptor?

a. Highly pathogenic, used late in infection, macrophage tropism
b. Naturally binds SDF1, T cell tropism, moderate pathogenicity
c. No syncytium, used early in infection, macrophage tropism
d. Moderate pathogenicity, induces syncytium, t cell tropism

A

c. No syncytium, used early in infection, macrophage tropism

163
Q

What is not a phase of untreated HIV infection?

a. Primary infection
b. Asymptomatic infection
c. Secondary infection
d. Symptomatic infection

A

c. Secondary infection

164
Q

What occurs during the primary infection of HIV?

a. There is an increase in blood and body CD4 T cells
b. There is a massive loss of memory T cells in the GALT
c. About 40% of mucosal T cells are killed
d. HIV levels rise due to the abundance of CD4

A

b. There is a massive loss of memory T cells in the GALT

165
Q

What can be detected following the sero-conversion window seen in HIV1 infection?

a. A HIV-1 EIA can be used after 5 days
b. A p24 antigen EIA can be used after 28 days
c. vRNA PCR can be used after 50 days
d. A HIV1/HIV2 EIA can be used after 75 days

A

b. A p24 antigen EIA can be used after 28 days

166
Q

What would not be used by HIV1 to avoid the immune response?

a. Sequence variation achieved through the low error rate of reverse transcription
b. Down-regulation of MHCI molecules
c. Variability in env V regions to escape antibody
d. Replication in privileged sites like the brain

A

a. Sequence variation achieved through the low error rate of reverse transcription

167
Q

What is not a way that HIV can cause T cell depletion?

a. By directly destroying infected cells
b. By damaging the GALT, leading to the release of microbial products and an inflammatory response
c. Indirectly destroying uninfected cells by down-regulating CD4 and CD8 T cell activation
d. Chronic immune activation of T lymphocytes

A

c. Indirectly destroying uninfected cells by down-regulating CD4 and CD8 T cell activation

168
Q

• The initial lytic stage of EBV infection occurs in B cells.

A

F

169
Q

• EBV is the leading infectious cause of stillbirth.

A

F (CMV)

170
Q

• HIV has caused 42.5 million deaths and 75,800,000 people have been infected.

A

T

171
Q

• HIV is more prevalent in Australia than other blood borne virus infections such as hepatitis.

A

F (HCV)

172
Q

• There is a high degree of variability for gag and env proteins due to the high error rate during reverse transcription.

A

T

173
Q

• HIV accessory proteins are critical in in vitro replication and in vivo pathogenesis.

A

F

174
Q

• Dendritic cells do not display CXCR4 receptors.

A

T

175
Q

• A Quasi steady state exists when viral production = viral clearance and this is known as the virological set point.

A

T

176
Q

What is not a viral factor that can influence the progression of HIV?

a. Being attenuated
b. Having an r5 phenotype
c. Co-infection with hepatitis G
d. Have a reverse transcriptase mutation

A

d. Have a reverse transcriptase mutation

177
Q

What is not a host factor that determines HIV disease progression?

a. Having a CCR5 mutation
b. Having a high titre of neutralising antibody
c. Down regulation of HIV-1 specific CD8+ T cells
d. HLA type

A

c. Down regulation of HIV-1 specific CD8+ T cells

178
Q

What is not a reservoir for HIV?

a. Proliferating B cells
b. Macrophages in lymph nodes
c. The brain
d. LN germinal centres, trapped on follicular DCs

A

a. Proliferating B cells

179
Q

What is a feature of HIV latency in CD4+ T cells?

a. It is common
b. It is established at the level of translation
c. Latent HIV is successfully treated with HAART therapy
d. The latent provirus sequence doesn’t evolve

A

d. The latent provirus sequence doesn’t evolve

180
Q

What is true about the efficacy of biomedical interventions against HIV?

a. The prime boost HIV vaccine is 90% effective
b. Circumcision is 60% effective
c. Immediate ART for positive partners is only 5% effective
d. Tenofovir gel is 10% effective

A

b. Circumcision is 60% effective

181
Q

Which drug is described correctly?

a. Amantadine is used in HIV infection to block Nef
b. Interferons are used to treat Herpesvirus
c. Fuzeon is a HIV fusion inhibitor
d. Ribavirin is a HIV protease inhibitor

A

c. Fuzeon is a HIV fusion inhibitor

182
Q

What is a feature of using interferons as antivirals?

a. They have no side effects
b. They only work on RNA viruses
c. They specifically prevent viral penetration
d. They are delivered as purified recombinant proteins

A

d. They are delivered as purified recombinant proteins

183
Q

What is amantadine?

a. It prevents entry and un-coating of influenza by inhibiting M2 ion channels
b. It prevents the acidification of neuraminidase during influenza uncoating
c. It binds to beta sheets in the M2 ion channel of influenza
d. It is a neuraminidase blocker used to treat influenza via inhalation

A

a. It prevents entry and un-coating of influenza by inhibiting M2 ion channels

184
Q

What is T20?

a. A fusion inhibitor used to fight HIV
b. A potent nucleoside analogue
c. An inhibitor of HIV GP120
d. A inhaled neuraminidase inhibitor

A

a. A fusion inhibitor used to fight HIV

185
Q

What is not a feature of acyclovir?

a. It is a prodrug
b. It is a guanosine analogue which lacks a 3’ OH group
c. It inhibits cellular DNA polymerase only
d. It is activated by viral HSV-TK

A

c. It inhibits cellular DNA polymerase only

186
Q

Which is a pro-drug?

a. Tamiflu
b. Acyclovir
c. T20
d. Amantadine

A

b. Acyclovir

187
Q

What is not a feature of Ribavirin?

a. The monophosphate form reduces nucleic acid synthesis
b. It can only be used for RNA viruses
c. The tri-phosphate form alters viral mRNA formation
d. It can be used against influenza and viruses that cause haemorrhagic fever

A

b. It can only be used for RNA viruses

188
Q

What is a feature of zidovudine/AZT?

a. Cellular kinase phosphorylates it to AZT-triphosphate
b. It is a thymidine analogue that inhibits integrase activity
c. It promotes chain elongation
d. It has a low affinity for viral reverse transcriptase

A

a. Cellular kinase phosphorylates it to AZT-triphosphate

189
Q

What is a feature of Non-Nucleotide Reverse Transcriptase Inhibitors for HIV-1 (NNRTI)?

a. They bind to the binding site of reverse transcriptase
b. They are RNA analogues
c. They indirectly inhibit reverse transcriptase
d. They do not have a close structural similarity to nucleotides

A

d. They do not have a close structural similarity to nucleotides

190
Q

What is Raltegravir?

a. A HIV protease inhibitor
b. An integrase inhibitor that blocks strand transfer
c. A nucleoside analogue that terminates HIV strand transfer
d. An integrase inhibitor that catalytically processes the 3’ ends of viral DNA

A

b. An integrase inhibitor that blocks strand transfer

191
Q

What is involved in HAART?

a. It requires that HIV patients take 25 pills a day
b. It cures HIV-induced immune dysfunction due to chronic immune activation
c. It can remove latent HIV infection
d. It minimises the chance of drug resistance arising

A

d. It minimises the chance of drug resistance arising

192
Q

• AIDS can lead to the reactivation of EMV or CMV.

A

T

193
Q

• HIV is only active when patients are symptomatic.

A

F

194
Q

• HIV can survive in quiescent T cells from months to years.

A

T

195
Q

• Neuraminidase is enzymatically inactive.

A

F

196
Q

• Relenza is taken orally and Tamiflu is inhaled.

A

F

197
Q

• Tamiflu has a high affinity for the neuraminidase active site due to a hydrophobic group.

A

T

198
Q

• R5 co-receptor anti-HIV drugs are most common due to the abundance of CCR5 and it’s presence on dendritic cells.

A

T

199
Q

• Nucleosides contain phosphate groups.

A

F

200
Q

• Adding a valine chain to acyclovir derivatives can increase passage through the digestive tract and into circulation.

A

T

201
Q

• Nucleoside Reverse Transcriptase Inhibitors contain a 5’ hydroxymethyl and 3’ OH group.

A

F

202
Q

• Protease inhibitors are peptidomimetics that bind tightly to the enzyme active site.

A

T

203
Q

Which hepatitis virus has the longest incubation period?

a. HAV
b. HBV
c. HCV
d. HEV

A

c. HCV

204
Q

Which hepatitis virus has the shortest incubation period?

a. HAV
b. HBV
c. HCV
d. HEV

A

a. HAV

205
Q

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

A

d. Most disease is mediated by the immune system

206
Q

Which are acute viruses?

a. Hepatitis B and D
b. Hepatitis A and E
c. Hepatitis A and B
d. Hepatitis C and E

A

b. Hepatitis A and E

207
Q

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

A

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

208
Q

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

A

b. It has a single serotype across the world

Picorna

209
Q

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 penetrate the intestinal epithelia following ingestion

A

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

210
Q

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.

A

c. Cirrhosis can develop as a chronic sequelae

211
Q

What is the primary method used to prevent HAV?

a. Pre exposure immune globulin
b. Supportive nutrition
c. Sanitation
d. Post exposure immune globulin

A

c. Sanitation

212
Q

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

a. It is a whole virus vaccine inactivated by formalin

213
Q

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

A

c. It has a 7.7kb +ssRNA genome

Hepeviridae

214
Q

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

A

c. Perinatal transmission is possible for HBV

215
Q

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

A

b. Hepatitis B, C and D

216
Q

What is the pre-C region?

a. It is called 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

a. It is called HBeAg and indicates active replication of HBV

217
Q

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

A

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

218
Q

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

A

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

219
Q

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

A

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

220
Q

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 severe acute disease but a low risk of chronic infection
d. It can “piggyback” HCV and lead to superinfection and chronic liver disease

A

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

221
Q

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

A

c. It contains a self-replicating RNA replicon

Flavivirus

222
Q

Which virus is a flavivirus and contains a lipid droplet in its capside?

a. HAV
b. HBV
c. HCV
d. HDV

A

c. HCV

223
Q

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

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

224
Q

• Acute viral hepatitis causes cirrhosis and liver cancer.

A

F

225
Q

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

A

F

226
Q

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

A

T

227
Q

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

A

T

228
Q

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

A

F

229
Q

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

A

T

230
Q

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

A

F

231
Q

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

A

F

232
Q

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

A

F (30%)

233
Q

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

A

T

234
Q

What is involved in transfecting poliovirus RNA into cultured cells?

a. cDNA is cloned into a plasmid with a RNA pol II promoter
b. In vitro RNA synthesis requires cellular RNA pol
c. cDNA is directly transfected into cultured cells
d. Poliovirus cannot directly infect cultured cells

A

a. cDNA is cloned into a plasmid with a RNA pol II promoter

235
Q

A requirement of a viral vector is:

a. Must not be replicative defective
b. Must have the capacity to produce and release new infectious particles
c. The sequences for replication and particle production must not be separated
d. The transgene must be flanked by essential cis-acting sequences and packing signals

A

d. The transgene must be flanked by essential cis-acting sequences and packing signals

236
Q

Which viral vector can not be used on non-dividing cells?

a. Adenovirus
b. AAV
c. Lentivirus
d. Retrovirus

A

d. Retrovirus

237
Q

Which statement is correct?

a. Adenovirus vectors have a lower titre than Adeno-associated vectors
b. Adeno-associated vectors can only carry a small insert of about 4.5kb
c. Retrovirus and Herpes virus can infect non-dividing cells
d. Adenovirus, Lentivirus and Retrovirus show poor tropism

A

b. Adeno-associated vectors can only carry a small insert of about 4.5kb

238
Q

What is true about retro and lentiviral vectors?

a. Both have an insert size of 9.2kb
b. The LTR and packing signal are retained from both viruses
c. Tat is retained and pol is deleted from both viruses
d. Retroviruses are larger vectors than lentiviruses

A

b. The LTR and packing signal are retained from both viruses

239
Q

How can the LTR be modified to preserve reverse transcriptase activity and integration but stop LTR transcription?

a. By duplicating the U3 and U5 sequences in the LTR
b. By silencing att sites found in the vector plasmid
c. By deleting the U3 sequence in the LTR and allowing the expression of a heterologous promoter
d. By silencing all heterologous promoters found in the vector plasmid

A

c. By deleting the U3 sequence in the LTR and allowing the expression of a heterologous promoter

240
Q

What is an issue with retroviral vectors and how is it avoided?

a. A replication competent virus may be regenerated so this is prevented by activating LTR expression
b. Heteroglous gene expression grows over time so this is down-regulated using Tat expression
c. Viral transcriptional elements can have biosafety concerns so this is prevented by removing Tat
d. Structural proteins can only be expressed from the same plasmid and this is aided through the use of packing cells with endogenous retrovirus

A

c. Viral transcriptional elements can have biosafety concerns so this is prevented by removing Tat

241
Q

What is a feature of an application of retro or lenti viral vectors?

a. They can be used in cancer therapy and are expressed transiently and at high levels
b. They can be used in vaccine development and activate the immune response, but expression levels are low
c. They can be used in gene therapy without any risks of insertional mutagenesis
d. They are inefficient in vaccine development as they only activate an innate immune response

A

a. They can be used in cancer therapy and are expressed transiently and at high levels

242
Q

What part of the viral genome needs to be retained when constructing an adenoviral vector?

a. The LTR and E1 protein
b. The ITR and packing signal
c. At least one LTR and an ITR
d. E1, E3 and E4

A

b. The ITR and packing signal

243
Q

What is false about adenovirus expression vectors?

a. They can efficiently transduce mammalian cells and grow to high titres
b. Heterologous genes are cloned in place of E1, E3 and E4
c. They do not elicit a T cell response and are therefore expressed for a long time
d. Pre-existing immunity in about 40% of people can reduce efficiency

A

c. They do not elicit a T cell response and are therefore expressed for a long time

244
Q

What is a feature of the gutless adenovirus expression vector?

a. Cre-recombinase inserts heterologous genes into the ITR
b. LoxP sites are recognised by cre-recombinase to excise adenovirus genes
c. The insert sizes are smaller than normal adenovirus vectors due to the removal of immunogenic genes
d. It can only be used in dividing cells

A

b. LoxP sites are recognised by cre-recombinase to excise adenovirus genes

245
Q

What is not a feature of AAV vectors?

a. They are developed from viruses of the adenoviridae family
b. They infect dividing and non-dividing cell
c. They require a cell line with helper proteins to assist packaging
d. They often integrate into DNA on chromosome 19

A

a. They are developed from viruses of the adenoviridae family

246
Q

Which viruses can be used as +ssRNA vecotrs?

a. Herpesvirus and adenovirus
b. Calicivirus and Reovirus
c. Flavivirus and alphavirus
d. Togavirus and Bunyavirus

A

c. Flavivirus and alphavirus

247
Q

What is a feature of RNA replicons?

a. Replication is host cell dependent
b. Replication occurs in the nucleus
c. They can only be delivered as VLPs
d. They lead to high expression of heterologous genes

A

d. They lead to high expression of heterologous genes

248
Q

What is false about WNV strain Kunjin replicons?

a. They express high levels of heterologous genes in the cytoplasm
b. VLPS are produced following transfection into a packing cell line expressing structural genes
c. The vectors integrate and recombine with the host genome and are therefore noncytopathic
d. The dsRNA intermediate elicits an enhanced immune response that can benefit vaccine development

A

c. The vectors integrate and recombine with the host genome and are therefore noncytopathic

249
Q

• DNA virus promoters can drive a high level of gene expression.

A

T

250
Q

• All retroviruses integrate a provirus into the genome and can only infect non-dividing cells.

A

F

251
Q

• Nearly all of the genes in herpes virus are essential for function and herpes virus vectors can therefore only have small inserts.

A

F

252
Q

• The VSV virus expression system can express ebola glycoproteins to act as a potential ebola vaccine.

A

T

253
Q

A vaccine should:

a. Prime the innate immune response
b. Lead to a primary response when a vaccinee is infected with the pathogen
c. Be safe, effective and stable
d. Cause disease and immunity in the host

A

c. Be safe, effective and stable

254
Q

When does the initial adaptive immune response occur?

a. Within hours of exposure
b. Between 7 and 14 days after exposure
c. 35 days after exposure
d. 21-28 days after exposure

A

b. Between 7 and 14 days after exposure

255
Q

Which vaccine is not produced via a cloning step?

a. DNA vaccine
b. Live Virus vector
c. Virus like particles
d. Non-recombinant purified subunit vaccine

A

d. Non-recombinant purified subunit vaccine

256
Q

Which statement about the history of smallpox vaccine is true?

a. Post Jenner methods used vaccinia
b. Jenner used attenuated human small pox
c. Pre-jenner methods were most successful due to the discovery of viruses in 1892
d. Post Jenner methods involved taking material from smallpox pustles and putting it in a scratch on the arm

A

a. Post Jenner methods used vaccinia

257
Q

What aided in the eradication of smallpox?

a. The virus has a short incubation period
b. The virus had one stable serotype
c. Small pox infection was persistent
d. The infection resulted in short term immunity

A

b. The virus had one stable serotype

258
Q

What is a feature of the poliovirus vaccines?

a. The IPV vaccine was created from 3 different attenuated strains of the virus
b. The OPV vaccine is extremely neurovirulent
c. The Sabin vaccine showed higher levels of nasal and duodenal IgA
d. The OPV vaccine was made after being inactivated with formalin

A

c. The Sabin vaccine showed higher levels of nasal and duodenal IgA

259
Q

What is true about the attenuated strains used to create the Sabin poliovirus vaccine?

a. Strain type 2 was only mutated at the 3’ UTR
b. All strains were mutated at the 5’UTR and in some VP genes
c. Type 1 and 2 have a risk of reverting
d. 1 in 20 vaccinated individuals develop paralysis

A

b. All strains were mutated at the 5’UTR and in some VP genes

260
Q

What happens in SSPE?

a. A measles virus has a mutation that allows persistent survival and brain inflammation
b. A smallpox virus fails to produce infectious particles and survives persistently
c. A measles virus has a mutation that allows up-regulation of structural genes
d. A poliovirus re-assorts and becomes neurovirulent

A

a. A measles virus has a mutation that allows persistent survival and brain inflammation

261
Q

What is a feature of live attenuated viral vaccines?

a. They require many doses
b. They are effective against immunocompromised people
c. The virus may be shed into the environment
d. There is no risk of reversion back to virulence

A

c. The virus may be shed into the environment

262
Q

What is not a feature of using a vaccinia virus vector?

a. The bacterial plasmid contains part of the vaccinia genome encoding TK and this is disrupted by the insertion of an early gene promoter
b. The antigen can be expressed to high levels and delivered by the mucosal route
c. Due to homologous recombination, the mutated gene segment can be inserted into the vaccine virus
d. It is most effective in immunocompromised individuals

A

d. It is most effective in immunocompromised individuals

263
Q

What is a feature of a DNA vaccine?

a. It cannot be delivered via a gene gun due to discrepancies in polarity
b. The plasmid is amplified and purified in yeast
c. The plasmid contains a bacterial ori, eukaryotic promoter and antibiotic resitance marker
d. DNA vaccines are inefficient when delivered to the dermis

A

c. The plasmid contains a bacterial ori, eukaryotic promoter and antibiotic resitance marker

264
Q

VLP vaccines:

a. Cannot be used to prevent hepatitis B
b. Involve the self-assembly or capsid or envelope proteins
c. Are not very immunogenic
d. Cannot be taken up by antigen presenting cells

A

b. Involve the self-assembly or capsid or envelope proteins

265
Q

What is not a feature of the HPV vaccine?

a. It is a whole attenuated virus vaccine that protects against cervical cancer
b. It causes 99.5% seroconversion
c. It is based on the rec L1 capsid protein which can be expressed in yeast
d. It can aid in wart regression and protection against HPV16

A

a. It is a whole attenuated virus vaccine that protects against cervical cancer

266
Q

What is a feature of live attenuated viral vaccines made by genetic reassortment?

a. They can only be used or viruses with non-segmented genomes
b. The Flumist vaccine uses HA and NA of the current influenza strain and 6 genes from a cold-adapted master strain
c. Both parent viruses must be pathogenic
d. The Flumist vaccine reassortant virus can grow in both the URT and lungs

A

b. The Flumist vaccine uses HA and NA of the current influenza strain and 6 genes from a cold-adapted master strain

267
Q

• An example of a natural passive vaccine is maternal IgG.

A

T

268
Q

• The most successful vaccines are live virus vectors because they can replicate.

A

F (live-attenuated)

269
Q

• Polio is only endemic in Nigeria.

A

F

270
Q

• The poliovirus IPV vaccine is more widely used than the OPV vaccine due to reversion risks.

A

T

271
Q

• Vaccination can reduce the rates of encephalitis from measles and mumps infection.

A

T

272
Q

• HPV 6 and 11 cause cancer and HPV 16 and 18 cause genital warts.

A

F

MIIM30014 Virology (23 decks)

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