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Micr 221 > Exam > Flashcards

Exam Flashcards

1
Q

Examples of how viruses drive evolution of hosts

A

Beneficial relationships
- selective advantage - the moths
- HERVS
- molecular negotiations

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2
Q

how has the study of virus replication enhanced our understanding of molecular cell biology

A
  • retroviruses
  • hervs
  • exploitation (gene therapy etc)
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3
Q

Fundamental differences between viruses and other infectious agents

A

Virus:
- submicroscopic
- assembly via pre-formed components
- dont grow/divide
- dont encode for metabolis, ribosomes, etc
- rewuire 5 part strategy to infect

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4
Q

principles behind plaque assay

A

plaque = succesful infection
only shows infectious viruses #
see progression over time

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5
Q

structural features of viral particles

A
  • capsid
  • core
  • envelope
  • spike proteins
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6
Q

Types of capsids

A

icosahedral
helical

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7
Q

Traits of a capsomere

A
  • icosahedral symmetry
  • 20 triangular faces
  • 12 vertices
  • 11 identical
  • 1 special (pore)
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8
Q

Functions of virus envelope

A

hold spike proteins
- host-range determination
- entry
- assembly // egress
- evasion from immune system

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9
Q

advantages of envelope

A

have spike proteins
does not lyse cell

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10
Q

types of viral genomes

A

mRNA
DNA
RNA

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11
Q

expression of + mRNA genome

A

immediately translatable

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12
Q

expression of dsDNA

A

—> mRNA

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13
Q

expression of + ssDNA

A

—> dsDNA —> mRNA

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14
Q

expression of dsRNA

A

—> mRNA

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15
Q

expression of + RNA

A

—> -RNA —> mRNA

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16
Q

Expression of -RNA

A

—> mRNA

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17
Q

expression of +RNA via DNA intermediate

A

—> -DNA —> dsDNA —> mRNA

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18
Q

how is a single step growth experiment performed

A
  1. every cell infected with MOI 10
  2. absorbed at 4
  3. Penetrated at 37
  4. Plaque assay
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19
Q

what step of a plaque assay in energy dependent

A

penetration

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20
Q

key features of growth curve

A

eclipse period: absorption —> appearance of infection
latent period: absorption —> release of infection

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21
Q

Steps of infection

A
  1. attachment
  2. penetration
  3. uncoating
  4. expression
  5. replication
  6. assemble / egress
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22
Q

examples of penetration

A
  • endocytosis
  • fusion with cellular membrane
  • pH independent ( at cell surface)
  • pH dependent (in acidic endosome)
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23
Q

steps of pH dependent penetration

A
  1. spike proteins attach viral cell to host
  2. proteins want to unfold - coil coil interraction
  3. pH drops
  4. receptors interract
  5. protein rearrangement
  6. membranes attach and seperate
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24
Q

dna vs rna gene expression

A

DNA
- in nucleus
- need RNA pol 2
RNA
- in cytoplasm
- needs enzymes made

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25
Q

egress: naked vs envelope

A

naked: lysis + cell death
envelope: budding

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26
Q

how can histological detection of virus assemble be used to diagnose viral diseases

A

inclusions

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27
Q

what are inclusions

A

very high [] of capsid proteins in infected cells
detectable via light microscopy

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28
Q

Shared properties of all herpesviruses

A
  • icosaheral
  • spikes
  • dsDNA
  • ABY proteins
  • cell death
  • inclusions
  • latent infections
  • close contact transmission
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29
Q

alpha proteins

A

dna binding proteins
regulation gene expression

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30
Q

beta proteins

A

enzymes for metabolism + replication

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31
Q

gamma proteins

A

structural

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32
Q

3 groups of herpesviruses

A

Gamma
Alpha
Beta

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33
Q

Gamma herpes causes what

A

EBV - mono

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34
Q

where is latency of gamma herpes

A

B lymphocytes

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35
Q

what does alpha herpes cause

A

HSV 1,2, VZV

36
Q

where is latency of hsv 1 and vzv

A

peripheral neurons

37
Q

what does beta herpes cause

A

HCMV

38
Q

where is latency of beta herpes

A

monocytes and lymphotyes

39
Q

where is beta herpes replicated

A

kidney and secretory glands

40
Q

Herpes absorbtion

A

4 glycoprotein receptors
envelope fuses w plasma membrane
tegument proteins enter cell
- VP16 = transcription factor for alpha genes
- Ribonuclease cuts host RNA to stop host replication
Capsid + microtubles = transport to nucleus

41
Q

herpes uncoating and expression

A
  • capsid portal aligns with pore of nucleus
  • cannot retain pressure
  • genome flys into nucleoplasm
  • genome circularizes
  • VP16 —> alpha genes —> beta proteins —> concatameric dna —> Y proteins
42
Q

herpes capsid assemble

A
  1. portal forms
  2. dna pumped into capsid
  3. protease activate — removes scaffolding
43
Q

what is a b capsid

A

scafolding not removed, no genome

44
Q

what is an a capsid

A

scafolding removed
support not added in time
can’t withstand preasure
empty

45
Q

herpes envelopment and egress

A
  1. nuclear regress
  2. capsid buds into nuclear membrane = perinuclear membrane capsid = PRIMARY ENVELOPMENT
  3. deenvelopment = in cytoplasm
  4. incorporated into particles
    a) tegamund binds to proteins
    b) secondary envelopment
    - buds into trans-golgi network
    - fuses with plasma membrane
    - deenvelops into extracellular space
46
Q

poxvirus replication cycle

A
  1. infection
  2. early mRNA
  3. translation —> A proteins
    - some leave as immunity factors
  4. A proteins = transcription factors —> intermediate mRNA
  5. intermediate proteins = late transcription factors
  6. late proteins —> packaged in factory
  7. envelopes
  8. exit
    a) lysis
    b) secondary membrane via budding
47
Q

how does poxvirus differ from other DNA viruses

A
  • closed ends
48
Q

poxvirus dna replication

A
  1. closed ends dsDNA
  2. nuclease nicks one end
  3. hairpins form
  4. replicated from 3’ to 5’
  5. repeated to form concatameres
  6. cleaved into individual genomes
49
Q

viral pathogenesis

A

The process of disease by virus in host

50
Q

determinants

A
  • interaction w target
  • lethality (of cells)
  • host response
  • immunopathology

shoot the target. did you kill it. how did it respond. what symptoms did they have.

51
Q

viral factors of pathogensis

A
  • dose
  • route
  • tissue
  • genotype

DSTG
dude, swear to god it wasnt me, it was the virus

52
Q

host factors of pathogensis

A
  • age
  • immune status
  • genotype
  • nutritional status
  • otehr infections

**Think questions that a dr would ask

53
Q

how can viruses infect GI tract

A

Peyer’s patches

M cells bring virus to patches
Then spreads

54
Q

modes of dissemination

A

viremia
- blood to tissue
[ epitheleal cells —> shed into tissue —> can cause hemmoraging]
[transcytosis: across epithelial —> basal membrane]
[diapedesis: through cells]

CNS
- peripheral nerves
- olfactory nerve bodies in nose
- diapedesis

55
Q

stages of viremia

A
  1. passive: initial infection in blood
  2. primary: infection —> lymphnodes
  3. secondary: infection —> new tissue + blood
56
Q

acute infections

A

**When entire replication cycle completes
rapid onset, rapid resolution
sign of good immune system

57
Q

Chronic/latent infection

A

**When complete replpication cycle fails

  • long term symptoms
58
Q

Latent infection

A

** Replication halts in latent phase within nucleus of certain cells
reactivates from triggers

59
Q

examples of cytopathic effects from virus

A
  • inhibition of protein synthesis
  • damage to cell lysosomes
  • change to plasma membranes
  • inclusions
  • apotsis
60
Q

apotosis vs necrosis

A

necrosis
- results from damage to cell
- loss of membrane integrity = death
- inflammation

Apotosis
- programmed cell death from signalling
- no inflammation

61
Q

Intrinsic immunity

A
  • pre existsing
  • first line of defense
62
Q

examples of intrinsic immunity

A
  • apoptosis
  • autophagy/zenophagy
  • host reduction factors (SAMHD1)
  • Epigenetic transcriptional silencing of vitaal genomes
63
Q

SAMHD1

A
  • limits availability of dNTPs
  • needed in retroviruses for dna intermediate
64
Q

How can viruses protect against SAMHD1

A

VPX
- taggs SAMHD1 w ubiquadone
- polymerized
- signalled to proteosome to be degraded

65
Q

Epigenetic transcriptional silencing of vital genomes (DNA viruses)

A
  • viral genome loaded with histones
  • histones make genome compact
  • compact = can’t transcribe
66
Q

How do viruses protect against Epigenetic transcriptional silencing of vital genomes (DNA viruses)

A
  • ICP0 and Us3
  • degrade and prevent PML nuclear bodies from folding histones
67
Q

Innate immune system examples

A
  • cytokines
  • sentinel cells
  • natural killer cells
  • complement
68
Q

Adaptive immune system examples

A
  • B and T cells
  • memory
69
Q

Explain how type I interferon system works

A
  • Ligand binds receptor on one chain
  • both chains come together
  • Jax activated
  • Phosphorylation of JAX
  • Phosphorylate STATs
  • STATS form dimer with IRF9
  • complex enters nucleus
  • Binds to ISRE
  • Transcription of ISGs
70
Q

How does PKR prevent infection

A
  • Binds to dsRNA of virus
  • Protein unfolds and phsophorylates self to activate
  • dimerizes
  • Phosphorylates EIF2alpha to prevent binding of GTP

***stop protein synthesis = apoptosis

71
Q

How does OAS/RNaseL work to prevent infection

A
  • activated by dsDNA
  • activates RNaseL
  • degrades cellular mRNAs
  • inhibts protein synthesis
  • apoptosis
72
Q

virus mediated inhibition of OAS/RNaseL

A

RNaseL inhibitor binds to dsRNA so RNaseL can’t

73
Q

differences between MHCI and MCHII

A

1:
- expressed on all nucleated cells
- binds endogenous peptides
- Recognized by CD8+ cells

2:
- expressed only on antigen presenting cells
- binds exogenous peptides
- recognized by CD4+

74
Q

Maturation of MHCii

A
  • antigen enters cell
  • proteosome degrades it within endosome
  • MHCII leaves ER via invarient chain
  • vesicle fuses with endosome
  • new vesicle moves to surface
  • CD4 helps bind MCHII to CD4 cell
75
Q

Maturation for MHCI

A
  • MCHI complex formed in ER
  • Proteosome cuts up protein into peptides
  • Peptide binds to MCHI
  • MCHI leave ER to Golgi
  • Exits to surface of cell
  • CD8 binds MCHI to CD8 cell
76
Q

how are antibodies produced

A
  • b cell receptors match
  • b cell activates
  • endocytosis virus
  • degrades
  • gives peptides to helper cell
  • produces cytokines
  • cytokines bind receptors on B cell
  • JAX SATS initiated
  • B cell differentiates
  • one b memory and one b lasma
    plasma cell created antibodies
77
Q

how can antibodies work

A
  • neutralization
  • opsonization
  • antibody dependent cell dependent cytotoxicity
78
Q

how do viruses inibit surface expression of MHCII

A

prevent trafficking out of ER
prevent delivery to surface

79
Q

How can viruses inbhibit NK cell function

A

Produce false activation receptor

80
Q

how is poliovirus spread

A

injected
GI tract
lymphnodes
blood
blood brain barrier
spinal cord
horns

81
Q

inactivated vs oral polio virus

A

inactive
- safe for immunicpompromised
- no associated disease
- more exapensive
- dont prevent transmission

oral
- cheaper
- live virus
- can cause paralysis

82
Q

Acyclovir MOA

A
  • bound to guanine
  • no 3’ end
  • can’t add any other nucleotides because no 3’ end
83
Q

pleconaril

A

stabilizes virus particle + prevents uncoating
physically blocks receptor

84
Q

hervs

A

retrovirus remnants in the human genome
8%

85
Q

How do polydnaviruses aid in the replicative cycle of parasitic
wasps such as Cotesia congregata?

A

Inject eggs and a virus into worm
virus protects eggs against host immune
Worms dies as eggs hatch
Use nutrients of worm to grow

Micr 221 (3 decks)

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