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Virology > Quiz3 > Flashcards

Quiz3 Flashcards

1
Q

Which mechanism do the maximum viral mRNAs use to get translated?

A

5’-end dependent mechanism

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2
Q

What happens to ribosomes in 5’ end independent mechanisms?

A

They bind to the IRES

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3
Q

For ribosomes to bind to IRES, what do the IRES need?

A

RNA-binding proteins

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4
Q

What do the + strand RNA genomes that lack caps and polyA tail need for protein synthesis?

A

Cap independent 3’ translational enhancer

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5
Q

What do unusual translational mechanisms do?

A

Expand coding capacity of viral genomes and allow the synthesis of multiple polypeptides from a single genome

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6
Q

What is common in virus-infected cells?

A

Alterations in the cellular-translational apparatus

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7
Q

To which NT of the mRNA is the 5’-7-methylguanosine added and how?

A

2nd NT of the mRNA by 5’-5’ phosphodiester linkage

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8
Q

What is the advantage of capping?

A

Directs pre-mRNA to processing and transport pathways

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9
Q

What regulates mRNA turnover?

A

5’ capping

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10
Q

What determines the mRNA turnover?

A

Rate of mRNA synthesis and degradation

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11
Q

Parts of an eukaryotic mRNA

A

5’ cap
5’ UTR
Initiation codon AUG
Open reading frame
Stop codon
3’ UTR
Poly A tail

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12
Q

What is the typical length of 5’ UTR?

A

50-70 NT; Some over 1000

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13
Q

What aspects of the mRNA structure influences translational efficiency?

A

Length of 5’ UTR and secondary structures, poly (A) tail, 3’ UTR

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14
Q

What can 3’ UTR regulate?

A

Translation initiation, mRNA stability, translation efficiency

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15
Q

What is the eukaryotic ribosome?

A

80s

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16
Q

What are the subunits of the 80s ribosome?

A

60s+ 40s

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17
Q

What rRNA and proteins is the 60s subunit of the 80s ribosome composed of?

A

28S, 5.8S, 5S rRNA
50 proteins

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18
Q

What rRNA and proteins is the 40s subunit of the 80s ribosome composed of?

A

18s rRNA
30 proteins

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19
Q

What are the kinds of proteins involved in translational machinery?

A

Initiation eIF
Elongation eEF
Termination eRF

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20
Q

Which mRNAs are translated by the 5’ end dependent initiation?

A

Intact mRNAs with 5’ cap and poly (A) tail

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21
Q

What is the first step in the 5’-end dependent initiation pathway?

A

Recognition of the m7G cap by the cap binding protein eIF4E.

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22
Q

Why is the preinitiation complex formed?

A

For scanning

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23
Q

Where does the preinitiation complex reach?

A

AUG start codon

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24
Q

What is the multifunction binding protein of the preinitiation complex?

A

eIF4G

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25
Q

What is the helicase of the preinitiation complex?

A

eIF4A

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26
Q

Why are hairpin structures not inhibitory in some RNAs?

A

Ribosomes bypass them by ribosome shunting

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27
Q

Is ribosome shunting dependent on viral proteins?

A

May be dependent/ independent of viral proteins

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28
Q

How does ribosome shunting start?

A

40S subunit binds to the mRNA by a cap dependent mechanism

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29
Q

How does ribosome shunting work?

A

40S subunit bypass regions of mRNA with secondary structures to reach the AUG start codon

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30
Q

What can direct ribosome movement in ribosome shunting?

A

Shunting elements such as viral or cellular proteins

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31
Q

What are the shunting elements?

A

Loops, viral or cellular proteins

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32
Q

What is shunting predicted to decrease dependence on?

A

Dependence on the EIF4F of mRNAs during initiation is reduced by reducing the need for unwinding

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33
Q

Which viruses use ribosome shunting?

A

Plant pararetroviruses
Adenovirus mRNAs
Sendai virus

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34
Q

What is an internal ribosome entry site?

A

RNA element that allows for translation initiation in a cap-independent manner, as part of the greater process of protein synthesis

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35
Q

Why are IRES sequences used?

A

To express two proteins from a single promoter in an expression construct or a transgenic construct

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36
Q

How many RNAs are produced with IRES?

A

A single RNA, but a second translational start on the same mRNA

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37
Q

What is the organization of plasmids for the expression of two genes?

A

Promoter -> First gene -> IRES -> Second gene

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38
Q

What mechanism is used by the first gene translated in a two-gene-expression plasmid?

A

5’-end dependent mechanism

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39
Q

How is the second gene translated in a two-gene-expression plasmid?

A

Internal ribosome entry

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40
Q

What is initiation on IRES type I and II dependent on?

A

C terminal fragment of EIF4G to recruit the 40S ribosomal subunit via its interaction with the eIF3.

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41
Q

How does EIF4G bind to the IRES?

A

Directly

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42
Q

What is IRES initiation not dependent on?

A

The presence of a cap structure

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43
Q

What is the hepatitis C virus IRES dependent on for the initiation of translation?

A

The 40s ribosomal subunit is not dependent on translation initiation proteins. eIF3 binds to the IRES, necessary for the recruitment of 60S ribosomal subunit.

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44
Q

How many tRNA binding sites are are on the ribosome and what are they?

A

Three tRNA binding sites:
1. Peptidyl (P site)
2. Aminoacyl/acceptor (A site)
3. Exit (E site)

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45
Q

How does the processing map of protein encoded by picornavirus/poliovirus genome look like?

A

One long precursor polyprotein from a mRNA; processed by viral proteases 2Apro and 3Cpro to form viral proteins

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46
Q

How does the processing/cleavage map of protein encoded by flavivirus genome look like?

A

Flavivirus precursor polyprotein cleaved by Host signal peptidase and/or viral serine protease NS3.

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47
Q

How many start sites are there in the Sendai virus C protein?

A

Four

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48
Q

How many proteins can be formed from the P open reading frame of sendai virus and what are they?

A
  1. P, V, W, X.
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49
Q

How are the different proteins formed from the P open reading frame in sendai virus?

A

mRNA editing.

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50
Q

How many proteins are formed from a single mRNA of sendai virus P/C gene/ paramyxoviridae

A

8

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51
Q

What is the process of different proteins being formed from the C open reading frame of Sendai virus?

A

Leaky scanning

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52
Q

What are the translation termination proteins?

A

eRF1 and eRF3

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53
Q

What do the translation termination proteins recognize?

A

They recognize all three stop codons, UGA, UAA, UAG

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54
Q

What other than the translation terminations proteins can recognize the stop codons?

A

Charged-tRNA misreading, charged suppressor tRNA (e.g. selenocysteine for UGA)

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55
Q

What does normal translation and termination produce in retroviruses like rous sarcoma virus in ORFs that have gag and pol proteins in reading frames that overlap by -1?

A

Only the gag proteins are produced

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56
Q

How is the gag-pol fusion protein made in rous sarcoma virus?

A

Ribosomal frameshifting to the -1 frame

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57
Q

When does the slippage of the two tRNAs occur?

A

After the aminoacyl-tRNA enters the A site but before peptidyl transfer

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58
Q

What does slippage allow the tRNA to do?

A

Form only two base pairs with the mRNA

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59
Q

What are miRNAs?

A

They are small, non-coding RNAs found within the viral/cellular genome

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60
Q

How is the miRNA transcribed?

A

By either pol-II or pol-III as 60-70 nt pre-miRNA

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61
Q

How is the pre-miRNA processed?

A

To a ~21-NT miRNA

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62
Q

How many miRNAs are found so far?

A

> 1000

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63
Q

What does miRNA regulate

A

~60% of the protein coding genes

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64
Q

How do miRNA control gene expression?

A

mRNA degradation, repression of translation

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65
Q

Where of the 3’-UTRs do the miRNA bind?

A

About 15-NT after the ORF

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66
Q

What determines whether the mRNA is degraded or translated?

A

Complementarity to the 3’-UTR

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67
Q

What structure do miRNA form while binding to mRNA?

A

Bulge

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68
Q

What does miRNA complex with to function?

A

AGO, Dicer, TRBP to form miRNP

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69
Q

What are the two ways that miRNA regulate translation?

A

Initiation block and elongation block

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70
Q

How does miRNP block initiation of translation?

A

It inhibits cap recognition by eIF4E, or it inhibits the joining of 60S subunit

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71
Q

How does miRNP block elongation of translation?

A

Slowed translation, causing ribosome drop off

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72
Q

What is an example of a liver specific miRNA?

A

miR-122

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73
Q

Why is miR-122 necessary?

A

HCV replication

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74
Q

What do miRNAs target?

A

Viral or cellular genes needed for viral replication

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75
Q

What miRNA is induced during enterovirus infection?

A

miR-141

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76
Q

What does miR-141 inhibit?

A

Translation of eIF4E mRNA

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77
Q

Four functions of viral miRNAs

A
  1. Block apoptosis
  2. Facilitate immune escape
  3. Prevent cell cycle arrest
  4. Promote latency
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78
Q

How many viral encoded miRNA in herpesviridae

A

> 200

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79
Q

How many viral encoded miRNA in polyomaviridae

A

> 4

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80
Q

How many viral encoded miRNA in baculoviridae

A

4

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81
Q

How many viral encoded miRNA in adenoviridae

A

2

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82
Q

How many viral encoded miRNA in ascoviridae

A

1

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83
Q

How many viral encoded miRNA in retroviridae

A

?

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84
Q

What are the three host defenses?

A

Intrinsic, Innate, Acquired

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85
Q

What are some physical and chemical defenses of the host?

A

Skin, low pH, tears, mucus, surface cleansing

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86
Q

What are examples of some intrinsic immune defenses?

A

Autophagy, apoptosis, RNA silencing, antiviral proteins

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87
Q

When is the intrinsic immune defense present?

A

Always in the uninfected cell

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88
Q

How does innate immune system start?

A

Induced by infection

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89
Q

Property of adaptive immune system

A

Tailored to pathogen

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90
Q

Where is RNAi against viral genomes present?

A

Plants and invertebrates.
RNAi present in mammals, but not sure if it’s against viruses

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91
Q

Which of the APOBEC3 proteins can encapsidate into HIV virions?

A

APOBEC3D, APOBEC3F, APOBEC3G, APOBEC3H

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92
Q

What is the function APOBEC3 proteins?

A

Deamination of cytosine to Uracil upon reverse transcription of the viral RNA in target cells.

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93
Q

What kind of mutations happen due to the deamination activity of APOBEC3 proteins?

A

Guanine-to-Adenine mutation

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94
Q

What leads to the Guanine-to-Adenine mutation through the activity of APOBEC3 proteins?

A

Cytosine deaminated to Uracil, which was previously going to template Guanines. But since deaminated to Uracils, they template Adenine.

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95
Q

What is the ultimate fate of the proviral cDNAs with guanine-to-adenine mutation?

A

Degradation

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96
Q

What is the example of a protein that restricts the immune defense by APOBEC3 proteins for HIV-1 infections?

A

Vif proteins

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97
Q

What is the mechanism of action of the Vif proteins for overcoming the APOBEC3 restriction block?

A

Vif binds CBF proteins recruiting E3 ubiquitin ligase complex.
E3 ubiquitin ligase complex polyubiquitylates APOBEC3 proteins and target them for degradation by 26S proteasome.

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98
Q

Among the producer and target cell, where does Vif proteins overcome the APOBEC3 restriction block?

A

Producer cell

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99
Q

What is autophagy?

A

The process of self-digestion by a cell through the action of enzymes originating within the same cell

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100
Q

What are the different steps of autophagy?

A

Phagophore -> Autophagosome -> Fuse to lysosome -> Degradation

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101
Q

What is apoptosis?

A

A type of cell death where the cell uses specialized cellular machinery to kill itself

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102
Q

What does apoptosis (a cell suicide mechanism) allow the animals to do?

A

Control cell number and eliminate cells that threaten the animal’s survival

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103
Q

What are the steps of apoptosis?

A

Apoptosis begins -> Apoptotic bodies are formed -> Taken up by macrophages

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104
Q

What are examples of some innate immune defenses?

A

Sentinel cells (Dendritic cells, NK cells, macrophages), cytokines, complement

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105
Q

When is the innate immune system activated?

A

Minutes to hours after infection

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106
Q

What happens when the Pattern recognition receptors cannot recognize the pathogen?

A

No innate immune response

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107
Q

What happens in adaptive immune response?

A
  1. Pathogen structure evaluation
  2. Fine tuning response
  3. Clonal expansion of B and T cells
  4. Memory
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108
Q

Who identified the toll gene and when?

A

1980, Nusslein-Volhard and Wieschaus

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109
Q

What does the toll gene do in drosophila embryos?

A

Establish the dorsal-ventral axis

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110
Q

What was found out about the toll gene related to flies in 1996

A

Toll have role in immunity of fly to fungal infections

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111
Q

When did Nusslein-Volhard and Wieschaus get the nobel prize

A

1995

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112
Q

When was toll-like receptors identified in mammals?

A

1997

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113
Q

What are the parts of a Toll-like receptor, TLR?

A

Leucine rich repeats and the TIR (Toll/Interleukin-1 receptor) domain

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114
Q

What binds the drosophila toll ectodomain?

A

spaetezie

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115
Q

What are the TLRs concerned to viruses?

A

Tlr3, Tlr7, Tlr8, Tlr9

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116
Q

What pattern does Tlr3 recognize?

A

DSRNA

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117
Q

What pattern does Tlr7 recognize?

A

SSRNA

118
Q

What pattern does Tlr8 recognize?

A

SSRNA

119
Q

What pattern does Tlr9 recognize?

A

CpG DNA; unmethylated CpG oligonucleotides

120
Q

What are the helicases that recognize RNA viruses?

A

MDA-5 and RIG-1

121
Q

What kind of RNA genomes do the helicases MDA-5 and RIG-1 recognize?

A

DSRNA

122
Q

What do the helicases MDA-5 and RIG-1 bind to start the signaling cascade?

A

Mitochondrial CARD, through the MAVS/IPS1/VISA/CARDIF proteins

123
Q

What does the RNA helicase signaling cascade activate transcription factors for?

A

Inflammatory cytokines

124
Q

What happens in sensing DNA?

A

DNA is recognized in the cytoplasm by
- “IFI16” and “DDX41”, that would activate cGAS. cGAS would utilize ATP and GTP to produce cGAMP, which would bind to STING, and start the signaling pathway of many phosphorylations, nfkb activated, they will go to the nucleus, and stimulate transcription of inflammatory and immune genes

125
Q

What is sensing DNA mechanism similar to?

A

GPCRs and their signaling pathways through recognition of hormones

126
Q

What are examples of cytosolic multiprotein oligomers of the innate immune system?

A

Inflammosomes

127
Q

What are the roles of inflammosomes?

A

To produce caspace-1

128
Q

What are two examples of inflammosomes?

A

AIM2 and NLRP3

129
Q

Which inflammosome detects DSDNA?

A

AIM2

130
Q

What do the caspaces produced by inflammsomes activate?

A

Inflammatory interleukins 1beta and 18.

131
Q

Who discovered interferons and when?

A

Issac and Lindenmann; 1957

132
Q

How were interferons discovered?

A

Chicken cells exposed to non-infectious influenza produce substance that interfered with infection of other cells

133
Q

Which cells produce interferons and what triggers its release

A

Virus-infected cells and uninfected sentinel cells produce interferons in response to products released from the cell (i.e. viral nucleic acid)

134
Q

Who are the producer cells of IFN-alpha and IFN-beta

A

Most if not all nucleated cells

135
Q

What induces the production IFN-alpha and IFN-beta

A

Viral infection

136
Q

Who are the producers cells of IFN-gamma

A

T cells, NK cells, epithelial cells

137
Q

What induces the production IFN-gamma

A

T cell activation, IL-2 and IL-12

138
Q

What are the receptors of Type I interferons?

A

IFNAR1 and IFNAR2

139
Q

What are the receptors of Type II interferons?

A

IFNgR1 and IFNgR2

140
Q

What kind of pathway does IFN binding to its receptors activate?

A

JAK-STAT signaling pathway

141
Q

What does IFN binding to its receptors stimulate the synthesis of?

A

ISGs, >1000 cell proteins

142
Q

When does IFNalpha/beta decline?

A

Within 10 hours

143
Q

When is IFNalpha/beta produced?

A

Within hours of infection

144
Q

What physiological consequences do large quantities of IFN have?

A

Fever, chills, nausea, malaise

145
Q

What are the sentinel cells?

A

Macrophages, dendritic cells, NK cells

146
Q

What do the sentinel cells do?

A

They patrol all our tissues looking for signs of change.

147
Q

What causes the common flu-like symptoms?

A

Interferon production

148
Q

How does the classical cascade begin?

A

When a pathogen is detected by C1q

149
Q

How many classical detector systems are there?

A

Two except the detection by C1q.
C1r, C1s

150
Q

Explain the classical complement system

A

C1q detects the virus particle, opsonizes/binds to the antigen antibody complex -> C3 convertase takes the b subunit of C4 and a subunit of C2 and form C4b2a (bound to cell surface) -> Activates C3 -> C3B subunit bound to C4b2a (C4b2a3b) ; a subunit (mediator of inflammation) -> C5 targeted, C5a (mediator of inflammation), C5b bound to membrane -> C6, C7 bound to C5b (C5b67) -> Activates C8 and C9 and they form the membrane attack complex

151
Q

What is the membrane attack complex?

A

C5b6789

152
Q

Which subunits are mediators of inflammation?

A

C3a and C5a

153
Q

How many functions of complement and what are they?

A

Four functions:
1. Opsonization
2. Cytolysis
3. Inflammation
4. Solubilization

154
Q

What is cytolysis?

A

Make holes in the infected cells if they have bound antibody or have unusual proteins on their surface

155
Q

What is inflammation

A

Activation by cytokines

156
Q

What is opsonization

A

Coat virus particles to facilitate uptake by macrophages

157
Q

What is solubilization

A

Solubilization of the immune complexes (antigen antibody complexes)/ breaking them up which can damage the organs

158
Q

How does infection lead to inflammatory response?

A

Infection -> Cytokines produced -> Inflammation -> Increased capillary permeability, increased blood flow, influx of phagocytic cells, Tissue damage -> Redness, heat, swelling, pain (Four classic signs of inflammation)

159
Q

What are the four classic signs of inflammation?

A

Redness, heat, swelling, pain

160
Q

What are the three classes of cytokines?

A

Proinflammatory, anti-inflammatory, chemokines

161
Q

What is the activity of proinflammatory cytokines?

A

Promote leukocyte activation

162
Q

What is the activity of anti-inflammatory cytokines?

A

Suppress activity of proinflammatory cytokines, return system to “circulate and wait” state

163
Q

What is the activity of chemokines?

A

Recruit immune cells during early stages of immune response

164
Q

Examples of proinflammatory cytokines

A

IL-1, TNF, IL-6, IL-12

165
Q

Examples of anti-inflammatory cytokines

A

IL-4, IL-10, TGF-B

166
Q

Example of chemokine

A

IL-8

167
Q

How do the cytokines function initially?

A

Locally in antiviral defense

168
Q

How can cytokines enter circulation and what can they do?

A

In large quantities cytokines can enter circulation and have global effects (sleepiness, lethargy, muscle pain, nausea, no appetite)

169
Q

Which viruses do not effectively activate the adaptive immune response

A

Non-cytopathic viruses

170
Q

How do non-cytopathic viruses work?

A

Do not stimulate inflammatory response, cells are not damaged, no apoptosis/no necrosis -> Low/ineffective innate immune response

171
Q

What are persistent infections?

A

Rarely/inefficiently cleared

172
Q

Which viruses cause persistent infections?

A

Non-cytopathic viruses

173
Q

What does the classic inflammatory response reflect?

A

Communication between innate and adaptive immune system

174
Q

When is inflammation-stimulating adjuvants used?

A

For non-infectious vaccines

175
Q

What is the workflow from innate to adaptive immunity?

A

Virus binds to epithelial cells -> Replication and local spread of infection -> Cytokines released -> Immature dendritic cells mature -> Travel to lymph node -> Then the circulatory system -> Adaptive immunity takes over

176
Q

What can packaging of the genome be coordinated with?

A

It can be coordinated with the assembly of the capsid/nucleocapsid

177
Q

What can the coordinated in enveloped viruses?

A

Acquisition of the envelope can be coordinated with assembly of the internal components (i.e. retroviruses)

178
Q

What are the common steps of assembly reactions?

A

Structural units formed -> Assembly of the protein shell by appropriate and sometimes variable interactions among structural units -> Selective packaging of the viral genome and virion components -> Acquisition of envelope -> Release from host cell -> Maturation of the virion

179
Q

What determines how a virus is formed?

A

The structure of a virus particle

180
Q

What host cell machinery is assembly dependent on?

A

Nuclear import and export machinery, transports, secretory pathway, cellular chaperones

181
Q

What are the concentrated viral components called?

A

Viral components factories or inclusions

182
Q

Where does poliovirus concentrate proteins?

A

Internal membranes

183
Q

What are the concentrated components of rabies virus called?

A

Negri bodies

184
Q

What are the built in structures for membrane targeting?

A

Signal sequences and fatty acid modifications

185
Q

What kind of localization signal does SV40 T antigen have?

A

Simple (Hydrophobic- Basic - Hydrophobic)

186
Q

What kind of localization signal does nucleoplasmin have?

A

Bipartite (Basic -X10 - Basic)

187
Q

How many strategies are there to make sub-assemblies of viral structural units?

A

Three

188
Q

What are the strategies of sub-assembling viral structural units?

A
  1. Assembly from individual protein molecules
  2. Assembly from a polyprotein precursor
  3. Chaperone-assisted assembly
189
Q

Which virus sub-assembles from individual protein molecules?

A

Simian virus 40

190
Q

What does the simian virus 40 sub-assembly look like?

A

SV40 pentamer from VP proteins

191
Q

Which virus sub-assembles from polyprotein precursor?

A

Poliovirus

192
Q

What is the poliovirus sub-assembly called and how is it formed?

A

5S structural unit. It is formed from the processing of folded P1 protein by 3CDPro

193
Q

Which virus sub-assembles using chaperone proteins?

A

Adenovirus type 2

194
Q

What chaperone protein does adenovirus type 2 use?

A

L4 100-kDa protein

195
Q

What does the L4 100-kDa chaperone protein form?

A

AD2 hexon trimer

196
Q

In the poliovirus assembly, when does the transition from provirion to virion occur?

A

Due to the cleavage of Vp0 to Vp2 and Vp4

197
Q

What are the different structures formed sequentially during poliovirus assembly?

A

3CDpro cuts the folded P1 -> 5S structural unit -> 5 of 5S structural unit come together to form the 14S capsid pentamers -> 75S empty capsid -> 150S Provirion -> Cleavage of Vp0 to Vp2 and Vp4 -> 150S Virion

198
Q

When does the 135S structure happen in poliovirus life cycle?

A

When it’s on the membrane/receptor of a new cell -> undergoing conformational change and uncoating

199
Q

What are the late steps in T4 assembly?

A

Head -> Tail -> Tail fiber

200
Q

What does assembly line concept ensure?

A

Orderly formation viral particles and virion subunits. Formation of discrete intermediate structures. Can’t proceed unless the previous structure is formed.

201
Q

Examples of self-assembled virus particles

A

gag - retrovirus
HA - influenza
VLP - HBV

202
Q

Example of a virus undergoing concerted/sequential assembly

A

Influenza A virus

203
Q

Where does the assembly of influenza A virus take place

A

The membrane during budding

204
Q

What happens in influenza A assembly?

A

It’s a -SSRNA. Gets to the nucleus. Gets replicated. mRNA is transcribed. mRNA leaves nucleus, translates M1 and NEP proteins, they get inside nucleus, they bind to the -SSRNA replicated genome, they transport to the membrane. Some other mRNA gets translated in the ribosomes attached to the ERs (HA, NA, M2), through golgi they reach membrane, assemble, bud

205
Q

How is cellular DNA/RNA distinguished from viral DNA/RNA during packaging?

A

Packaging signals in the viral genome

206
Q

Where is the adenovirus (AD5) packaging signal located?

A

Near left inverted repeat and origin of replication and E1A transcription unit

207
Q

What is the adenovirus packaging signal?

A

Set of repeated sequences overlapping with the enhancers that stimulate late transcription

208
Q

Who recognizes the adenovirus packaging signal?

A

Viral protein IVA2 (also a transcriptional activator)

209
Q

Where is the simian virus packaging signal located?

A

After the enhancer, in the SP1 binding sites, before the origin of replication and early transcription unit

210
Q

If the packaging mechanism was random, what would be the particle to pfu ratio of segmented genomes?

A

1 infectious particle per 400 assembled

211
Q

Where are the signals for influenza virus RNA packaging located?

A

Signals at the coding and non-coding sequences at the 5’ and 3’ ends.

212
Q

What does the structure of the RNPs look like during budding for influenza?

A

A distinct pattern, perpendicular to the membrane

213
Q

How does the packaging of the φ6 virus look like?

A

Serial dependence of packaging, 3 DSRNA, first the small (S) goes in, medium goes in if (S) is present, and large (L) goes in if (M) is present

214
Q

What is the particle to pfu ratio of φ6 virus

A

~1

215
Q

When do most enveloped viruses gather envelop?

A

After assembly of internal structures

216
Q

How many budding strategies are there?

A

Four

217
Q

What are the budding strategies

A
  1. Envelope glycoproteins + capsid proteins
  2. Capsid proteins + matrix proteins
  3. Envelope proteins
  4. Matrix proteins drive budding but additional components (glycoproteins, RNP) needed for efficiency
218
Q

What is an example of a virus that uses the envelope glycoproteins and capsid proteins for budding?

A

Alphaviruses

219
Q

What is an example of a virus that uses the internal matrix proteins and capsid proteins for budding?

A

Retroviruses

220
Q

What is an example of a virus that uses the glycoproteins for budding?

A

Coronaviruses

221
Q

How do viruses leave infected cells?

A
  1. Release from the cell by budding or lysis
  2. Move from cell to cell
222
Q

What does the assembly of some large icosahedral proteins require?

A

Scaffolding or chaperone proteins

223
Q

What is an assembly line mechanism well suited for?

A

Orderly formation of some virus particles

224
Q

What must the virus genome do to survive?

A

It must establish itself in a host population

225
Q

What is virus infection with no obvious disease called

A

Inapparent

226
Q

In how many years did West Nile Virus spread?

A

4, From 1999 to October 2004, 1 million cases in US (Antibody positive)

227
Q

How many of the infected people had febrile illness for WNV?

A

20%

228
Q

How many had neuro-invasive disease for WNV?

A

1%

229
Q

Why can’t a WNV epidemic be stopped?

A

It can’t be recognized early

230
Q

What is pathogenesis

A

Process of producing a disease
Chain events leading to that disease
The development of a disease

231
Q

What are the two components of viral disease?

A

Effects of viral replication on the host
Effects of host response on the virus and the host

232
Q

What are thee requirements of a successful infection?

A

Enough virus, cells should be accessible, susceptible, permissible, local antiviral defense absent or overcome

233
Q

How do the viruses that are sensitive to heat, drying, sunlight (UV) overcome this restriction?

A

By producing large number of virions

234
Q

What are the properties of viruses that are stable in low pH or stable to proteases?

A

They survive in gut, they spread by fecal-oral transmission (water borne)

235
Q

Which viruses never experience the environment?

A

Insect and arachnid vectors

236
Q

How do the infections spread by physical contact?

A

Bodily fluids, those viruses are not stable outside for long

237
Q

How many sites of entry are there for viral infection in human body?

A

A limited spectrum

238
Q

How are the virions that land on skin are inactivated?

A

By desiccation, acids, low pH - 5.5, or by other inhibitors formed by our cells or by commensal micoorganism (Antimicrobial peptide)

239
Q

How much mucus does a normal individual produce per day in nasal cavity, lungs

A

20-200ml

240
Q

How much liquid is transferred from lungs to esophagus through muco-ciliary escalator

A

1cm/minute

241
Q

How is the virus swept to esophagus and what happens to it

A

Through ciliary action, where it is swallowed 30 times per hour

242
Q

Where are virus particles filtered?

A

Sinuses

243
Q

What do the lower regions of respiratory tract have?

A

Immune cells, antibodies

244
Q

What kind of barrier does the small intestine have?

A

Selectively permeable

245
Q

What kind of epithelial cells do the small intestine have?

A

Polarized, enterocytes and M cells

246
Q

What is the small intestine in direct contact with

A

Outside world and also the nervous system and the immune system

247
Q

What part of eyes are most vulnerable to viral infections?

A

Bulbar conjunctiva and sclera

248
Q

What is one viral infection of the eye?

A

Subconjunctival bleed

249
Q

What is disseminated viral spread?

A

When it spreads beyond the primary site

250
Q

What is systemic viral spread?

A

If many organs are infected

251
Q

What is a localized virus?

A

Spreads within the epithelium, contained by tissue structure and immune system

252
Q

Example of a neurotropic virus

A

West nile virus

253
Q

What can west nile virus do?

A

Can cause encephalitis or paralysis

254
Q

Example of a virus with tropism for CD4 T cells

A

HIV

255
Q

What can HIV do

A

Immunodeficiency

256
Q

What is tropism

A

The capacity of a virus to infect/damage specific cells/tissues/species

257
Q

What is the capacity to induce disease dependent on for viruses?

A

Dependent on the cell and tissue infected

258
Q

Tissue tropism

A

The tissues where the viruses like to replicate

259
Q

Three tissue tropism examples

A

Enterotropic (Intestine)
Neurotropic (Nervous system)
Hepatotropic (Liver)

260
Q

What is a pantropic virus?

A

It has tropism for multiple organs

261
Q

What are the determinants of tissue tropism?

A

Susceptibility, permissibility, accessibility, defense

262
Q

What is virus shedding

A

Process that occurs when a virus is present in bodily fluids or open wounds and thus can be transmitted to another person

263
Q

What are the exceptions to virus shedding?

A

Germline
Blood supply
Vectors

264
Q

What are examples of virus shedding

A

Respiratory secretions, nasal secretions, urine, semen, blood, skin lesions

265
Q

What are respiratory secretions?

A

Aerosol produced by coughing, speaking, sneezing

266
Q

What are the three kinds of aerosols and how far do they spread

A

Large infectious droplets (1-3 ft)
Small infectious droplets (3-5 ft)
Infectious droplet nuclei (5-160+ ft)

267
Q

What is required to maintain the chain of infection?

A

Spread of infection from one susceptible host to another

268
Q

How many general patterns are there for transmission of infection and what are they?

A

Direct, human - human
Indirect, through a vector

269
Q

What is transovarial transmission

A

The transmission of an infectious agent from parent to offspring via infection of the developing egg which subsequently results in infectious adult arthropods

270
Q

How are non-enveloped virions spread

A

Fomites, fecal-oral routes, transmitted respiratory

271
Q

How are enveloped virions spread

A

Aerosols or secretions, vectors, injections, organ transplantation

272
Q

What is the transmission type when activity of the healthcare worker leads to infection of patient

A

Iatrogenic

273
Q

What is the transmission type when individual is infected in hospital or healthcare facility

A

Nosocomial

274
Q

What is the transmission type when infection is transferred from parent to offspring

A

Vertical

275
Q

What is germline transmission

A

Agent is transferred as part of the genome (Proviral DNA)

276
Q

Chikungunya virus classification

A

Family (Togoviridae)
Genus (Alphavirus)

277
Q

How is chikungunya virus spread

A

Through Aedes aegypti

278
Q

Symptoms of chikungunya virus infection

A

Rash, joint pains

279
Q

Where was chikungunya virus first identified

A

Tanzania

280
Q

When did chikungunya virus spread from Kenya to India

A

2004

281
Q

When and where, the first case of chikungunya in europe

A

2007, Italy

282
Q

What is associated with the recent chikungunya virus infections?

A

A. albopictus

283
Q

Recent chikungunya virus infection structural change?

A

One amino acid change in viral E1 glycoprotein

284
Q

Rubella and Influenza seasonality

A

Nov - July

285
Q

Poliomyelitis seasonality

A

North pole- Towards the end of the year
South pole- Towards the beginning of the year

286
Q

Seasonality of influenza according to humidity

A

Low % humidity, higher transmission as droplet nuclei form

287
Q

What is incidence

A

New cases/ Defined time period

288
Q

What is prevalence

A

Number of cases at a given time

289
Q

Mortality rate

A

Deaths / Total infections

290
Q

Morbidity rate

A

Illness/ Total infections

291
Q

Case fatality ratio

A

Deaths/ Total with disease

Virology (4 decks)

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