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Immunology and Infection > Bacteria and Viruses > Flashcards

Bacteria and Viruses Flashcards

1
Q

what are the different process of an infectious agent in the environment and a host?

A

transmission. infection. clearance or establish and persist.

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2
Q

what is the concept of kochs postulates?

A

proved a specific microorganism causes a disease. one microbe one disease concept.

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3
Q

what are the 4 steps of kochs postulates?

A
  1. Microorganisms found in abundance in organisms suffering but not in healthy ones
  2. MO isolated from diseased and grown in pre-culture
  3. cultured MO should cause disease when introduced into an organism
  4. then isolated and identified
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4
Q

what are the critical comments of kochs postulates?

A
  • ethics
  • is there a disease model? the pathogen may be host specific.
  • does the tissue/organ have isolatable pathogens
  • is the pathogen culturable, if you can’t culture then you don’t know if its there
  • assumes that disease is caused by one microbe
  • disease is not due to microbes
  • no role for host response
  • doesn’t apply to viruses
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5
Q

what is the microbiome?

A

mixture of bacteria you have. genetic material of all microbes that are found in the body.
- microbial protectors

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6
Q

how can the microbiome protect?

A
  1. 1 pathogen and 1 colonisation resistor

2. 1 pathogen and 1 resistant consortia (combination that can resist infection)

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7
Q

by what mechanisms can the microbiome protect?

A
  • indirect or direct mechanisms

- intestinal commensal microbiota provides colonization resistance against a wider range of pathogens

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8
Q

what are the direct mechanisms of the microbiome?

A
  • nutrient competitor
  • direct toxicity
  • metabolic products
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9
Q

what are the indirect mechanisms?

A
  • metabolic products

- immune induction

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10
Q

what is a nutrient competitor?

A

eg if there’s a limit of carbon depends who gets there first

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11
Q

what is direct toxicity?

A
  • systems where bacteria will directly inject a toxin to kill
  • use selectively
  • could be diffusible
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12
Q

what are metabloc products?

A

-products that talk to the body or work with and against microbes

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13
Q

what are the features of e.coli?

A
  • some strains are pathogens others are commensal

- bacterial genome variation

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14
Q

what are the features of vibrio cholera?

A
  • always cuases disease
  • variation in severity
  • bacterial genome differences
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15
Q

what are the features of staphyloccocus epidermis?

A
  • commensal
  • sometimes causes disease
  • breach of host defenses and state of immune system
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16
Q

what are e.coli pathotypes the result of?

A
  • DNA accquisition

- DNA deletion plasmids

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17
Q

what has whole genome sequencing found in e,coli genome?

A

pathogenicity (associated) islands (PAIs)

  • regions in the genome derived by horizontal gene transfer
  • absent in non-pathogenic strains/serotypes
  • encode for virulence factors
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18
Q

what are PAMPs?

A
  • pathogen associated molecular patterns
  • lipid A of LPS (gram -ve), peptidoglycans,flagella, DNA by host receptors TLRs
  • present in pathogens and commensals
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19
Q

what are some examples of virulence factprs?

A
  • toxins
  • adhesions
  • sidephores
  • immunology modulatory factors
  • type 3 secretion system
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20
Q

what is the structure of LPS?

A
  • O antigen repeat ofunits
  • core oligosaccharide
  • Lipid A is the PAMP of LPS (TLR4 stimulator)
  • can look different through the O antigen
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21
Q

what are the features of the O antigen of LPS?

A
  • antigenic
  • immunodominant
  • antibodies use for specific parts of the composition and linkage in the O-antigen units
  • basis for serotyping/O factor classification and some vaccines
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22
Q

what is the T3SS?

A
  • complex molecular ‘syringe’, gram -ve
  • inserts bacterial effector proteins into the host cell
  • manipulates the host
  • alters in diverse ways depending on the activity of the effector proteins
  • can sense this through mechanical contact and chemical variations
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23
Q

what are 2 bacterial causes of diarrhoeal disease?

A
  1. vibrio cholera

2. EHEC (enterohemorraghic e.coli)

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24
Q

what is vibrio cholera?

A
  • colonises the small intestine
  • causes the loss of fluid and electrolytes
  • cholera toxin
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25
Q

what is the role of the cholera toxin?

A
  • causes increased adenylate cyclase activity in the host cell
  • cAMP levels up
  • changes sodium/chloride flux in-out of the cell
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26
Q

what are the virulence factors of vibrio cholera?

A
  • TCP adhesion, to adhere to tissues

- muccinase, enzyme, muccin degraded and helps bacteria get through

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27
Q

what is the reservoir for vibrio cholera?

A

lies in the ocean, on chitin surfaces specifically with pili

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28
Q

how is vibrio cholera transmitted?

A
  • found in contaminated water
  • poor sanitation
  • chitin surfaces (attachment substrate) eg phytoplankton and zooplankton
  • lack of clean water
  • social upheaval
  • natural disease
  • need to filter water
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29
Q

what is meant by vibrio cholera biofilm?

A
  • vibrio cholera attached to chitin can form biofilm

- community of bacteria attached to a solid surface and encased in a self-made protein matrix

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30
Q

what has been tested to target vibrio cholera?

A

phage therapy: phage cocktail and 3 phages in reducing colonisation of an infant mouse

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31
Q

how is there host susceptibility to vibrio cholera?

A
  • host genetic and nutriotional factors affect susceptibility of the infant mouse
  • blood group dependent
  • some are better receptors for the toxin
  • better receptor = stronger binding and more severe infection
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32
Q

describe the blood-group dependent disease found in vibrio cholera

A
  • role Vc flagella and muccinase for colonisation, penetrance
  • role host: presentation of blood group antigen on intestinal cells
  • nature of the blood group antigen determines cholera toxin binding affinity
  • strong binding of toxin = increased risk of cellular uptake of toxin
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33
Q

what is EHEC?

A
  • cattle are the reservoir
  • in anterior of cow intestine
  • targets human small intestine
  • bloody diarrhoea
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34
Q

what is important in the virulence of EHEC?

A
  • shiga toxin
  • T3SS
  • PAI
  • s7cE metalloprotease
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35
Q

what is the shiga toxin in EHEC?

A
  • extracellular cytotxin
  • enters through endocytosis
  • targets ribosomes and inhibits translation
  • cell apoptosis
  • kidney damage
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36
Q

what is the s7cE metalloprotease in EHEC?

A

cleaves glycoproteins and reduces muccin levels

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37
Q

what are sp5 and sp15 in EHEC?

A

stx producing prophage

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38
Q

what does LEE stand for?

A

locus of enterocyte effacement

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39
Q

what is LEE in EHEC?

A
  • enterocyte polarised epithelial cells living in the small intestine
  • 2 step adhesion (attacking and effacing)
  • encodes for the EHEC T3SS apparatus
  • extracellular, basla body
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40
Q

what is the process of LEE encoding EHEC T3SS?

A
  • enables the A/E lesion
  • Tir produce by EHEC
  • enters host cell and inserted into the membrane
  • now a receptor for bacterial cells surface adhesion or intimin
  • Tir and other effectors orchestrate actin polymerisation at attachment site an extensively target host cell trafficking processes
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41
Q

how is expression of T3SS tightly regulated?

A

regulated through local and global regulators, quorum sensing, environmental signals

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42
Q

what genes do microbes prioritise?

A
  • express genes needed to grow,adapt and survive
  • cost of expression drains energy
  • if they spend energy on one thing they may not grow as much
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43
Q

what do microbes rely on to survive and grow?

A
  • temperature, nutrients, pH and iron

- these could be harmful if not right

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44
Q

why are nutrients needed?

A

essential for growth and signals the bacterial environment

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45
Q

why is the carbon source important?

A
  • generally bacteria want glucose
  • glucose is produces the most ATP (highest energy yield)
  • need to sense and integrate into regulatory network
  • can use as a cue for the environment eg glucose poor turn on virulence factors
46
Q

what is catabolite repression?

A

preferential utilization of the best carbon and energy source

47
Q

what happens if you give bacteria both glucose and lactose?

A
  • grow and then stop then grow
  • glucose disapears first
  • then lactose is used
  • has a mechanism for only selecting glucose
48
Q

when does vibrio cholera turn its virulence factors on?

A

expression of virulence genes is low when cAMP-CRP is high

49
Q

what is CRP?

A

cAMP binding protein, binds DNA

  • is a transcriptional activator
  • only does this when cAMP is present (facilitates binding)
  • global regulator
50
Q

what is the mechanism of cAMP-CRP?

A
  1. glucose imported through proteins
  2. activates adenylate cyclase
  3. makes cAMP from ATP
  4. inactive cAMP is inactive and becomes active
  5. binds DNA - transcriptional activator
51
Q

how is lactose stopped from being used when glucose is present?

A
  • glucose transported into the cell
  • LacZYA is repressed
  • phosphate is passed through a range of proteins and to glucose get glucose 6 phosphate
  • protein that donates the phosphate binds to LacY
  • blocks lactose entering
52
Q

what is the phosphorylation state of IIAGLC?

A

transmits information about glucose transport, adenylate cyclase inactive, cAMP low

53
Q

what is the inducer exclusion?

A

IIACGLC blocks lactose permease,LacI represses

54
Q

what happens when there is no more glucose?

A
  • bacterial cell adpats
  • IIAGLC stays phosphorylated and activates AC, cAMP increase, lac permease not blocked
  • inducer present - lactose binds to LacI
  • CRP-CAMP active and lac operon transcription increases
55
Q

what is an operon?

A

one regulatory region controls expression of more than one gene . facilitates a coordinated response

56
Q

what is the lac operon?

A
  • 3 genes
  • trancriptional unit
  • multiple proteins made from one regulatory event
  • local has one target (LacI)
  • global has many targets (CAMP-CRP)
57
Q

what is a local operon?

A
  • one target
  • encoded right in that area
  • only controls transcription of its own operon
58
Q

what is a global operon?

A
  • many target
  • at lac and around 360 genes
  • might be a lot of other genes turning on when theres no glucose for example
  • used as a signalling process
59
Q

what is a regulon?

A

all the genes that fall under the control of a specific regulatory protein

  • facilitates coordinated expression
  • everything turned on when there’s low glucose (regulon)
  • show with a mutant that all these are controlled by cAMP-CRP (direct or indirect)
60
Q

what environments does vibrio cholera have to transition between?

A

aquatic and the small intestine

61
Q

how does vibrio cholera exist in an aquatic environment?

A
  • exists as planktonic bacteria or bacteria bound to biotic and abiotic surfaces
  • TCP adhesion used to bind to surfaces
  • CRP plays a role in expression of TCP
62
Q

when does vibrio cholera express virulence factors?

A
  • if conditions are right
  • bacterial attachment is followed by virulence factor production
  • under direct control of CRP
  • leading to sites of colonzation from which cholera toxin is secreted
63
Q

how does quorum sensing work in vibrio cholera?

A
  • due to high localised cell density quorum sensing is activated
  • leads to the repression of virulence factors
64
Q

how can you measure gene expression?

A

reporter genes eg GFP

- know how much of the gene is being transcribed

65
Q

how do reporter genes work?

A
  • put a reporter gene behind the RBS (ribosome binding sites)
  • essentially putting things on the genome to get translation
  • transcriptional fusion: operon fusions,reports on transcrption
  • transcription- would include the reporter gene canmeasure expression
66
Q

what does quorum sensing sense?

A
  • extracellular signals
  • who is out there
  • is there enough of us
  • sense which bacteria its next
  • conversational between bacteria and eukaryotic cells
  • little chemicals secreted then sensed and integrated
67
Q

what does quorum sensing allow?

A

allows individuals to gain group behaviour
- attachment
- biofilm
- sporulation
- light (aquatics)
distinguish between self or closely related bacterial species

68
Q

what is used in quorum sensing in gram +ve bacteria?

A

short peptiders (auto-inducer)

69
Q

what is used in quorum sensing in gram-ve bacteria?

A

AHL or HSL

  • variable structures
  • different recognition systems
70
Q

how do EHEC use quorum sensing?

A
  • expression highly regulated
  • Qsec
  • specific AHL sensed by QsecB
71
Q

what are the two components of the quorum sensing signalling system?

A
  • signals

- output

72
Q

what is an example of the process of quorum sensing?

A
  • have a sensor domain, response regulator
  • sensor protein autophosphorylates
  • passed to response regulator
  • becomes phosphorylated
  • binds to DNA
73
Q

what is an sRNA?

A
  • small non-coding RNAs
74
Q

what is the role of sRNA?

A
  • mainly control expression
  • affect translation initiation
  • destabilize target mRNA
  • work in trans
  • inhibit translation initiation and block access to RBS
75
Q

what can microbes sense to determine its location?

A
  • temperature

- can indicate if its in or out of host and controls expression of virulence factors

76
Q

what is an option of sensing temperature?

A

RNA thermosensor

77
Q

how is temperature sensed in listeria?

A
  • master regulator of virulence is transcription activator PrfA which is thermoregulated
  • RNA structure is altered
  • exposure of ribosmal binding site
  • a stem loop structure blocks translation initiation at 30 degrees but melts away at 37 degrees
78
Q

what defines a virus?

A
  • obligate intracellular parasites
  • depend on biochemical machinery of host cells to replicate; not considered living
  • can’t make energy or proteins independent of host
  • replication is by self-assembly of individual components
79
Q

what does a virus have to be?

A
  • must be infectious to survive in nature
  • must use host processes to produce their components
  • viral components must self-assemble
80
Q

what are the different viral structures?

A

naked or enveloped

81
Q

what is a enveloped virus?

A
  • envelope
  • capsid
  • nucleic acid
  • must stay wet
  • spreads through large droplets
  • does not need to kill cells to spread (buds)
82
Q

what is a naked virus?

A
  • capsomers
  • nucleic acid
  • capsid
  • more stable in the face of environmental stress
  • spreads more easily
  • survives in the gut, poor water treatment
83
Q

what is a nucleic capsid?

A
  • genome with a protein capsule

- can be RNA or DNA

84
Q

what is a virion?

A
  • infective viral particle

- nucleocapsid = the virus particle = virion

85
Q

what are spikes?

A
  • protein/glycoprotein (viral proteins)
  • protrude from the surface
  • contact the host cell and can attach
  • obvious to the immune system
86
Q

where is the envelope of a virus obtained?

A

from host cell

87
Q

what are the different classifications of viral DNA?

A 
DNA
-dsDNA
-ssDNA
RNA
- dsRNA
-ssRNA (retroviruses)
88
Q

why does the virus need to make copies of its genome?

A

to make viral proteins

89
Q

what are different classes of proteins that the viral genome codes for?

A
  1. proteins of progeny viral particles
  2. enzymes for genome replication
  3. proteins to interfere with host immune defenses
90
Q

what is transcription?

A
  • making +strand RNA (mRNA)

- either from DNA or for some viruses from - RNA

91
Q

what is translation?

A

proteins from mRNA

92
Q

how do you make a new viral particle?

A
  1. make mRNA - viral proteins

2. make nucleic acids, copies of own genome

93
Q

how is -RNA made into viral proteins?

A
  • enters the cell
  • copied into +ve mRNA
  • translated to proteins (get viral polymerase)
  • help copy the -RNA to +RNA to -RNA
  • assembly: have structural proteins, -ve sense RNA, makes a new particle
94
Q

what is the infectious cycle of a virus?

A
  • attachment to host cell (tissue specificity)
  • penetrate the cell
  • uncoating of the virus particle
  • replication
  • assembly
  • release
95
Q

what are the 2 penetration strategies?

A
  1. membrane fusion (for enveloped especially)

2. endocytosis; initial entry through endocytosis followed by escape involving fusion with the endosomal membrane

96
Q

where is the virus particle assembled?

A

intracellularly

97
Q

what defines where a virus will thrive/survive?

A
  • host cell surface and host cell metabolics

- host cell and viral properties define how fast viral particles are released

98
Q

what is an example of a retrovirus?

A
  • HIV
99
Q

how is a retrovirus infect?

A
  • requires virion enzyme reverse trancriptase
  • stages in the nucleus and the cytoplasm
  • viral genome integrates into the host cell chromosomal DNA: persistent infection
  • viruses are packaged in cytoplasm and released by budding
100
Q

what is an example of +strand ssRNA?

A

hepatitis C

101
Q

what is the process of a +strand ssRNA (hepititas C)?

A
  • lifecycle is extra nuclear
  • progency viruses released by budding
  • has very specific glycoproteins which bind to receptors on host cell
  • enters and uncoats
  • +strand is translated directly
  • produces a polyprotein which is then cleaved
  • produces a polymerase
102
Q

what is an example of -strand ssRNA?

A

influenza

103
Q

what are the key features of the influenza virus?

A
  • carry unique enzymes in capsids that facilitate replication
  • entire lifecycle is extra nuclear but influenza transcription takes place in the nucleus
  • progeny viruses released by budding
  • has spike glycoproteins
104
Q

what are the 2 key glycoproteins of influenza?

A

hemagglutinin

neuramindase

105
Q

what is the role of hemagglutinin?

A

receptor recognition on host cell, sialic acid binding

106
Q

what is the role of neuraminidase?

A
  1. helps virus approach target cells by cleavage
  2. assists in fusion
  3. facilitates release of new virions by preventing reattachment to dying host cells through HA
107
Q

what are hemagglutinin and neuraminidase susceptible to?

A

antigenic drift and shift which produces new strains

- can cause epidemics and pandemics

108
Q

what is antigenic shift?

A
  • have a broad host range
  • in asia people live in close contact with animals so it can spread
  • need to predict the H and N types and make vaccines
109
Q

why role does polymerase in influenza?

A
  • makes so many
  • there will be errors with RNA
  • helps evade the immune system
110
Q

what is significant about HIV reverse transcriptase?

A
  • highly error prone
  • means many genomic variants are made every time the RNA gets reverse transcribed to DNA
  • when combined with selection get rapid evolution
111
Q

why are there very few antiviral drugs?

A
  • there are a limited choice of targets for antiviral drugs
  • can cause drug resistance
  • high mutation rates
112
Q

what are the various transmission routes microbes?

A
  • food and water
  • human to human (air and oral/faecal)
  • vector eg mosquito

Immunology and Infection (13 decks)

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