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OD2 Semester 1 - Applied Clinical Training > M: Virology 2 - Week 11 > Flashcards

M: Virology 2 - Week 11 Flashcards

1
Q

What is the eclipse period?

A

the time between infection by (or induction of) a bacteriophage, or other virus, and the appearance of mature virus within the cell; an interval of time during which viral infectivity cannot be recovered.

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2
Q

What is the latent period?

A

the period between infection with a virus or other microorganism and the onset of symptoms

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3
Q

Define Uncoating

A

The release of viral nucleic acids/genome from the capsid that covers them

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4
Q

What is the one-step growth curve?

A

Describes the production of progeny virus over a period of time following infection under one-step conditions

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5
Q

When do one-step conditions exist?

A

When all cells are infected simultaneously so as to prevent secondary cycles of infection

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6
Q

What is a viral plaque?

A

a visible structure formed within a cell culture, demonstrating a region of cell destruction

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7
Q

What is a plaque forming unit (PFU)?

A

A measure of the number of particles capable of forming plaques per unit volume, such as virus particles

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8
Q

What happens to PFU during the Eclipse Period of viral replication? (in one-step growth curve of the unenveloped virus)

A

No change

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9
Q

What happens to PFU during the Latent Period of viral replication?

A

No change for most of it, then a logarithmic increase near the end

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10
Q

What happens to PFU during the Uncoating Phase of viral replication?

A

No change

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11
Q

What happens to PFU during the Synthetic Phase of viral replication?

A

logarithmic increase

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12
Q

In the one-step growth curve for viral replication, at what times after viral absorption do the following periods/phases occur?

  • Eclipse
  • Uncoating
  • Latent
  • Synthetic
A

Eclipse: 0-12 hours
Uncoating: 0-12 hours
Latent: 0-16 hours
Synthetic: 12-16 hours

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13
Q

In the one-step growth curve: what happens to the virus 16 hours after viral absorption?

A

extracellular bursting out of new viruses (happens for the next 28 hours until hour 44)

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14
Q

Name the 6 steps of viral replication

A 
Attachment/Adsorption
Penetration
Uncoating
Replication
Assembly 
Release
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15
Q

How do viruses attach?

A

Viral attachment protein binds specifically to a receptor on the cell plasma membrane

This interaction defines and limits the host species as well as the type of cell that is infected

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16
Q

What receptors might the cell plasma membrane have for viruses? (2) Provide an example for each

A

Protein (e.g. ICAM-1 for most rhinoviruses)

Carbohydrate (e.g. sialic acid for influenza)

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17
Q

Can viruses use multiple different receptors on the same host cell?

A

Yes. Some viruses do that

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18
Q

What is referred to as the “one-two punch” for viruses to get into the cell

A

Some viruses use 2 different receptors on the same host cell: for initial attachment, then a coreceptor for closer attachment and entry

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19
Q

How do viruses penetrate the cell membrane? (2)

A

The coat of enveloped viruses may fuse with the host cell membrane and release the virus nucleocapsid into the host cytoplams
Alternatively,
other viruses may enter the cell via “endocytosis”

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20
Q

What does viral endocytosis involve?

A

invagination of the cell membrane to form vesicles in the cell cytoplasm which becomes acidified

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21
Q

What is the purpose of viral uncoating?

A

enables the nucleic acid to be transported within the cell and transcribed to form new progeny virions

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22
Q

What is direct fusion?

A

is when viruses initiate fusion and penetration of their core or nucleocapsid directly through the cell’s surface (plasma) membrane at neutral or alkaline pH

Several viruses do this.

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23
Q

Name 2 examples of viruses that undergo direct fusion

A

Paramyxoviruses (e.g. measles)

Retrovirus HIV

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24
Q

How do paramyxoviruses undergo direct fusion?

A

via a fusion (F) glycoprotein on their envelope

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25
Q

How does retrovirus HIV undergo direct fusion?

A

gp120 binds sequentially to 2 receptors: CD4 receptor and CCR5 (chemokine co-receptor)
- this exposes gp41, which drives fusion of envelope and plasma membrane

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26
Q

Describe the steps involved in the entry of HIV-1 by membrane fusion

A
  1. Native trimer: Attachment through non-specific cell receptors
  2. CD4 binding: structural changes in gp120 after binding CD4 receptor
  3. Coreceptor binding: binding to newly exposed chemokine coreceptor sites promotes gp41 fusion peptide insertion
  4. Membrane fusion: structural rearrangement of gp41 trimers drives membrane fusion
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27
Q

In the entry of HIV-1, which chemokine coreceptor sites become exposed? (2) Which chemokine is predominantly used during the process of transmission?

A

CCR5 and CXCR4. CCR5 is the predominantly used on for transmission

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28
Q

What does the entry and uncoating of influenza viruses require? (2) Why?

A

requires endocytosis and acidification - to induce a conformation change in HA that reveals a fusion domain on HA

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29
Q

What is HA? What does it stand for? (in relation to influenza virus)

A

Influenza Haemagglutinin. is a homotrimeric glycoprotein found on the surface of influenza viruses and is integral to its infectivity

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30
Q

Describe the assembly phase of the viral life cycle

A

proteins assemble around the nucleic acids to form new viral particles

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31
Q

Where do DNA viruses replicate? Are there any exceptions?

A

in the nucleus. (poxyviruses are an exception)

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32
Q

Where do RNA viruses replicate?

A

in the cytoplasm

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33
Q

What does mRNA encode?

A

viral proteins that are translated by the host cel

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34
Q

Where is mRNA transcribed from?

A

viral DNA

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35
Q

Where is mRNA formed directly from?

A

some RNA viruses

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36
Q

What is the difference between transcription and translation? (2)

A

Transcription: the synthesis of RNA from a DNA template where the code in the DNA is converted into a complementary RNA code

Translation: the synthesis of a protein from an mRNA template where the code in the mRNA is converted into an amino acid sequence in a protein

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37
Q

Are “early” viral proteins structural or non-structural? What about “late” viral proteins?

A

early: usually non-structural
late: structural

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38
Q

What do “early” viral proteins assist with?

A

replication (e.g. polymerases)

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39
Q

Provide one example for “early” and “late” viral proteins?

A

early: polymerases
late: capsid proteins

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40
Q

Name 3 viruses that can directly translate their genome to proteins. Why can they do this?

A

Picornaviridae
Togaviridae
Flaviviridae

Can do this because their genome is m(+)RNA. This is needed before we can translate but since these viruses already have it there is no need to undergo transcription to get it.

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41
Q

Can negative sense viral RNA act as mRNA?

A

No. Only positive-sense do that (i.e. only positive sense can act as mRNA to be translated into protein in the host cell)

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42
Q

What does RDRP stand for? What does it do?

A

RNA-dependent RNA polymerases. Enzyme that produces complementary strands from the template

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43
Q

Which of the following contains a RNA-dependent RNA polymerase in its capsid?
- Positive sense ssRNA or Negative sense ssRNA?

A

Negative-sense

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44
Q

How do (+)ssRNA viruses overcome their inherent lack of RNA-dependent RNA polymerase?

A

they use their genome as an mRNA to make an RNA-dependent RNA polymerase (or REPLICASE) upon infection

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45
Q

How does replication of ssRNA work when starting with (+)ssRNA? What if we start with (-)ssRNA?

A

Minus strands are copied form plus strands, then more plus strands from the minus strand template

(vice-versa if starting with (-)ssRNA)

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46
Q

What is the replicative intermediate?

A

refers to the complex formed when RNA-dependent RNA polymerase produces the complementary strand for ssRNA

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47
Q

How do (-)ssRNAs make mRNA?

A

They use their replicase (i.e. rna-dependent rna polymerase) to make mRNA using the -ve sense genome as a template

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48
Q

Can DNA viruses make DNA?

A

Yes. They have a DNA genome so they can just transcribe and make RNA

49
Q

True/False: Most dsDNA viruses have viral enzymes within them

A

False. They make viral enzymes when they arrive from the copy of DNA genome

50
Q

ds DNA viruses use cellular enzymes in the nucleus for what purpose? (2)

A

to express mRNA

to replicate DNA

51
Q

What do DNA viral proteins modulate?

A

normal cellular control mechanisms to favor virus replication

i.e. DNA viruses will have proteins that greatly favour the replication of viral proteins

52
Q

Name 4 DNA viruses

A

Adenovirus
Herpes virus
Pox virus
Papo virus

53
Q

What do ssDNA viruses need to do to further their genome replication?

A

They need to make a copy of the second strand

54
Q

How and where is translation of structural and non-structural proteins carried out?

A

Carried out by ribosomes in the host cell cytoplasm

55
Q

Once translated, what do the translated proteins almost invariably undergo?

A

Post-translational cleavage of polyproteins or trimming of structural proteins

56
Q

What does post-translational cleavage of polyproteins or trimming of structural proteins require?

A

virus-coded proteases

57
Q

Where does glycosylation of envelope glycoproteins occur? (2)

A

RER and Golgi vesicles

58
Q

What are viral structural proteins designed to assemble into?

A

Capsids

59
Q

What might the virus particle require to induce the final capsid conformation?

A

Proteolytic cleavage

60
Q

Where do virions accumulate following assembly? (2) and where are they released? (1)

A

Accumulate in the cytoplasm or nucleus and are released by lysis

61
Q

How may virus particles be released following assembly? (3)

A

Particles may be released from the cell by:
movement through the ER (exocytosis),
breakdown of the cell,
or by budding

62
Q

Which method of viral release from the cell is the main method for enveloped viruses?

A

By budding

63
Q

What is viral budding?

A

Nucleocapsids assembled or in the process of being built induce formation of a membrane curvature in the host cell membrane and wrap up in the forming bud which is eventually pinched off by membrane scission to release the enveloped particle

64
Q

Are enveloped or non-enveloped viruses released by exocytosis after assembly?

A

Can be either. However most often tends to be non-enveloped viruses

65
Q

What is viral exocytosis?

A

Viral progeny are synthesized within the cell and the host cell’s transport system is used to enclose them in vesicles; the vesicles of virus progeny are carried to the cell membrane and then released into the extracellular space.

66
Q

Does viral exocytosis (via movement through ER) kill the infected cell?

A

No

67
Q

What is the primary mode of viral exit from the cell for non-enveloped viruses?

A

cell lysis (to violate the integrity of the bilayer). This kills and ruptures the cell obviously

68
Q

Name 2 drugs that target the attachment of viruses

A

Maraviroc

Fuzeon

69
Q

Name 1 drug that targets the uncoating of viruses

A

Amantadine

70
Q

Name 2 drugs that target the genome replication of viruses

A

Acyclovir herpesviruses

Zidovudine (AZT)

71
Q

Name 2 drugs that target the RNA synthesis of viruses

A

Ribavirin

Interferons

72
Q

Name 3 drugs that target the protein synthesis of viruses

A

Interferons
Saquinavir
Darunavir

73
Q

Name 2 drugs that target the release of viruses from the cell

A

Tamiflu

Relenza

74
Q

Name the 3 classes of Interferons

A

IFN-alpha
IFN-beta
IFN-gamma

75
Q

What is the role of interferons?

A

induce proteins (IRPs) that inhibit viral replication or modify immune responses

76
Q

Describe the antiviral actions of interferons

A

Wide variety of antiviral actions - block viral protein synthesis

77
Q

Are interferons active against DNA viruses?

A

No. Not very active

78
Q

Do Interferons cause side effects? If so, how broad?

A

Yes. Wide ranging effects

79
Q

How many phosphate groups do nucleosides have? What about nucleoside analogues

A

none for both

80
Q

What is the substrate for DNA polymerisation?

A

Nucleoside triphosphate

81
Q

What is Acyclovir?

A

A guanosine analogue used to treat herpesviruses

82
Q

Why aren’t nucleoside analogues able to form a DNA polymer?

A

they lack the 3’ hydroxyl group required

83
Q

What does the synthesis of acyclovir monophosphate require? (1)

A

thymidine kinase (which adds a phosphate group to acyclovir)

84
Q

What is Ribavirin?

A

Guanosine analogue

85
Q

What is the function of Ribavirin?

A

Inhibits replication of many DNA and RNA viruses in vitro

86
Q

How does Ribavirin work? Describe its forms and what function each have (3 + 2)

A

Intracellular phosophorylation gives it mono-, di- and tri-phosphate forms.
Mono-phosphate form: reduces nucleic acid synthesis
Tri-phosphate form: alters viral mRNA formation

87
Q

Name 4 conditions you can use Ribavirin for

A 
Use for:
respiratory syncitial virus bronchiolitis + pneumoniae
influenza
haemorrhagic fevers
hepatitis C
88
Q

How do you administer Ribavirin for treatment of influenza and respiratory syncitial virus bronchiolitis and pneumoniae?

A

Aerosolised, IV (intravenous)

89
Q

How do you administer Ribavirin for treatment of hemorrhagic fevers? (2)

A

oral or IV

90
Q

How do you administer Ribavirin for treatment of hepatitis C?

A

oral; in combination with interferon

91
Q

Describe the HIV replication cycle (3)

A

HIV is an RNA virus
HIV consists of an enzyme inside the particle – the enzyme converts the 2 copies of (+) viral RNA and reverse transcribes them into a double-stranded copy of DNA
The double-stranded DNA is taken into the nucleus and gets stitched into the host cell DNA to form pro-virus DNA

92
Q

Name 4 targets in the HIV replication cycle for anti-retroviral therapy

A

Fusion/Entry inhibitors
Reverse Transcriptase inhibitors
Integrase inhibitors
Protease inhibitors

93
Q

What is Zidovudine?

A

A reverse transcriptase inhibitor

94
Q

What are reverse transcriptase inhibitors (RTIs)? What can they be used to treat? (3) What is reverse transcriptase required for? (2)

A

are a class of antiretroviral drugs used to treat HIV infection or AIDS, and in some cases hepatitis B. RTIs inhibit activity of reverse transcriptase, a viral DNA polymerase that is required for replication of HIV and other retroviruses.

95
Q

What does NRTI (or NARTI) stand for? Name one example

A

Nucleoside analogue reverse-transcriptase inhibitors; a type of reverse-transcriptase inhibitor

e.g. Zidovudine

96
Q

What type of nucleoside analogues can NRTIs be? (3)

A

Analogues of:
Thymidine
Cytidine
Guanine

97
Q

How are NRTIs incorporated into the viral DNA? (so that they can inhibit reverse-transcriptase)

A

In order to be incorporated into the viral DNA, NRTIs must be activated in the cell by the addition of 3 phosphate groups to form NRTI triphosphates

98
Q

How are NRTIs phosphorylated?

A

via intra-cellular kinase enzymes

99
Q

Can reverse-transcriptase inhibitors eliminate HIV virus completely?

A

No. They can reduce the infection of new cells but cannot eliminate the virus completely

100
Q

When might you use combination therapy with reverse-transcriptase inhibitors?

A

When you have drug resistant mutant viruses

101
Q

What nucleoside analogue is Zidovidine?

A

a Thymidine analogue

102
Q

What does NNRTI stand for? Do NNRTIs have close structural similarity to nucleosides?

A

Non-nucleoside reverse-transcriptase inhibitors. No they do not!

103
Q

What type of anti-HIV drugs have a close structural similarity to the amino acid recognition sequence?

A

Protease inhibitors

104
Q

What features of a virus in general help confer drug resistance? (2)

A

High replication rate

High mutation rate (RNA>DNA)

105
Q

How does viral drug resistance typically emerge? How can we overcome this?

A

by “selective pressure”. Overcome by using combination therapy

106
Q

What is a “pre-existing” viral mutant

A

is a viral resistance mutation that exists before the patient has had any kind of treatment

107
Q

How often do “pre-existing” viral mutations occur? (in comparison to non-pre-existing)

A

often

108
Q

What is HAART?

A

Refers to any HIV treatment that uses a combination of 2 or more drugs

109
Q

What are the advantages of HAART? (3)

A

Synergistic potency
Durable anti-viral response
Minimise development of drug resistance

110
Q

Define Viral hepatitis

A

“inflammation of the liver”. a viral infection that causes liver inflammation and damage.

111
Q

Is viral hepatitis acute or chronic?

A

Can be either (Acute = weeks to months) (Chronic = years to lifetime)

112
Q

How does acute viral hepatitis present? [symptoms] (3)

A

non-specific, flu-like symptoms
jaundice
dark urine

113
Q

How does chronic viral hepatitis present? [symptoms] (3)

A

general malaise
cirrhosis
liver cancer

114
Q

In what body fluids is the concentration of blood born viruses high? (3)

A

blood (obviously)
serum
wound exudates

115
Q

In what body fluids is the concentration of blood born viruses moderate? (3)

A

semen
vaginal fluid
saliva

116
Q

In what body fluids is the concentration of blood born viruses low? (5)

A 
urine
faeces
sweat
tears
breastmilk
117
Q

What proteins were used in HIV treatment a few years ago and are being phased out? Why are they being phased out?

A

Interferons (IFNs). They are being phased out because they made the treatment unpallatable.

Now we have IFN-free DAA combination treatment

118
Q

What does DAA stand for?

A

Direct acting antivirals

OD2 Semester 1 - Applied Clinical Training (47 decks)

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