Immunology and Infection > Bacteria and Viruses > Flashcards

Bacteria and Viruses Flashcards

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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
what is the role of the cholera toxin?
- causes increased adenylate cyclase activity in the host cell - cAMP levels up - changes sodium/chloride flux in-out of the cell
26
what are the virulence factors of vibrio cholera?
- TCP adhesion, to adhere to tissues | - muccinase, enzyme, muccin degraded and helps bacteria get through
27
what is the reservoir for vibrio cholera?
lies in the ocean, on chitin surfaces specifically with pili
28
how is vibrio cholera transmitted?
- 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
29
what is meant by vibrio cholera biofilm?
- vibrio cholera attached to chitin can form biofilm | - community of bacteria attached to a solid surface and encased in a self-made protein matrix
30
what has been tested to target vibrio cholera?
phage therapy: phage cocktail and 3 phages in reducing colonisation of an infant mouse
31
how is there host susceptibility to vibrio cholera?
- 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
32
describe the blood-group dependent disease found in vibrio cholera
- 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
33
what is EHEC?
- cattle are the reservoir - in anterior of cow intestine - targets human small intestine - bloody diarrhoea
34
what is important in the virulence of EHEC?
- shiga toxin - T3SS - PAI - s7cE metalloprotease
35
what is the shiga toxin in EHEC?
- extracellular cytotxin - enters through endocytosis - targets ribosomes and inhibits translation - cell apoptosis - kidney damage
36
what is the s7cE metalloprotease in EHEC?
cleaves glycoproteins and reduces muccin levels
37
what are sp5 and sp15 in EHEC?
stx producing prophage
38
what does LEE stand for?
locus of enterocyte effacement
39
what is LEE in EHEC?
- enterocyte polarised epithelial cells living in the small intestine - 2 step adhesion (attacking and effacing) - encodes for the EHEC T3SS apparatus - extracellular, basla body
40
what is the process of LEE encoding EHEC T3SS?
- 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
41
how is expression of T3SS tightly regulated?
regulated through local and global regulators, quorum sensing, environmental signals
42
what genes do microbes prioritise?
- 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
43
what do microbes rely on to survive and grow?
- temperature, nutrients, pH and iron | - these could be harmful if not right
44
why are nutrients needed?
essential for growth and signals the bacterial environment
45
why is the carbon source important?
- 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
what is catabolite repression?
preferential utilization of the best carbon and energy source
47
what happens if you give bacteria both glucose and lactose?
- grow and then stop then grow - glucose disapears first - then lactose is used - has a mechanism for only selecting glucose
48
when does vibrio cholera turn its virulence factors on?
expression of virulence genes is low when cAMP-CRP is high
49
what is CRP?
cAMP binding protein, binds DNA - is a transcriptional activator - only does this when cAMP is present (facilitates binding) - global regulator
50
what is the mechanism of cAMP-CRP?
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
how is lactose stopped from being used when glucose is present?
- 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
what is the phosphorylation state of IIAGLC?
transmits information about glucose transport, adenylate cyclase inactive, cAMP low
53
what is the inducer exclusion?
IIACGLC blocks lactose permease,LacI represses
54
what happens when there is no more glucose?
- 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
what is an operon?
one regulatory region controls expression of more than one gene . facilitates a coordinated response
56
what is the lac operon?
- 3 genes - trancriptional unit - multiple proteins made from one regulatory event - local has one target (LacI) - global has many targets (CAMP-CRP)
57
what is a local operon?
- one target - encoded right in that area - only controls transcription of its own operon
58
what is a global operon?
- 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
what is a regulon?
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
what environments does vibrio cholera have to transition between?
aquatic and the small intestine
61
how does vibrio cholera exist in an aquatic environment?
- 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
when does vibrio cholera express virulence factors?
- 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
how does quorum sensing work in vibrio cholera?
- due to high localised cell density quorum sensing is activated - leads to the repression of virulence factors
64
how can you measure gene expression?
reporter genes eg GFP | - know how much of the gene is being transcribed
65
how do reporter genes work?
- 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
what does quorum sensing sense?
- 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
what does quorum sensing allow?
allows individuals to gain group behaviour - attachment - biofilm - sporulation - light (aquatics) distinguish between self or closely related bacterial species
68
what is used in quorum sensing in gram +ve bacteria?
short peptiders (auto-inducer)
69
what is used in quorum sensing in gram-ve bacteria?
AHL or HSL - variable structures - different recognition systems
70
how do EHEC use quorum sensing?
- expression highly regulated - Qsec - specific AHL sensed by QsecB
71
what are the two components of the quorum sensing signalling system?
- signals | - output
72
what is an example of the process of quorum sensing?
- have a sensor domain, response regulator - sensor protein autophosphorylates - passed to response regulator - becomes phosphorylated - binds to DNA
73
what is an sRNA?
- small non-coding RNAs
74
what is the role of sRNA?
- mainly control expression - affect translation initiation - destabilize target mRNA - work in trans - inhibit translation initiation and block access to RBS
75
what can microbes sense to determine its location?
- temperature | - can indicate if its in or out of host and controls expression of virulence factors
76
what is an option of sensing temperature?
RNA thermosensor
77
how is temperature sensed in listeria?
- 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
what defines a virus?
- 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
what does a virus have to be?
- must be infectious to survive in nature - must use host processes to produce their components - viral components must self-assemble
80
what are the different viral structures?
naked or enveloped
81
what is a enveloped virus?
- envelope - capsid - nucleic acid - must stay wet - spreads through large droplets - does not need to kill cells to spread (buds)
82
what is a naked virus?
- capsomers - nucleic acid - capsid - more stable in the face of environmental stress - spreads more easily - survives in the gut, poor water treatment
83
what is a nucleic capsid?
- genome with a protein capsule | - can be RNA or DNA
84
what is a virion?
- infective viral particle | - nucleocapsid = the virus particle = virion
85
what are spikes?
- protein/glycoprotein (viral proteins) - protrude from the surface - contact the host cell and can attach - obvious to the immune system
86
where is the envelope of a virus obtained?
from host cell
87
what are the different classifications of viral DNA?
``` DNA -dsDNA -ssDNA RNA - dsRNA -ssRNA (retroviruses) ```
88
why does the virus need to make copies of its genome?
to make viral proteins
89
what are different classes of proteins that the viral genome codes for?
1. proteins of progeny viral particles 2. enzymes for genome replication 3. proteins to interfere with host immune defenses
90
what is transcription?
- making +strand RNA (mRNA) | - either from DNA or for some viruses from - RNA
91
what is translation?
proteins from mRNA
92
how do you make a new viral particle?
1. make mRNA - viral proteins | 2. make nucleic acids, copies of own genome
93
how is -RNA made into viral proteins?
- 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
what is the infectious cycle of a virus?
- attachment to host cell (tissue specificity) - penetrate the cell - uncoating of the virus particle - replication - assembly - release
95
what are the 2 penetration strategies?
1. membrane fusion (for enveloped especially) | 2. endocytosis; initial entry through endocytosis followed by escape involving fusion with the endosomal membrane
96
where is the virus particle assembled?
intracellularly
97
what defines where a virus will thrive/survive?
- host cell surface and host cell metabolics | - host cell and viral properties define how fast viral particles are released
98
what is an example of a retrovirus?
- HIV
99
how is a retrovirus infect?
- 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
what is an example of +strand ssRNA?
hepatitis C
101
what is the process of a +strand ssRNA (hepititas C)?
- 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
what is an example of -strand ssRNA?
influenza
103
what are the key features of the influenza virus?
- 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
what are the 2 key glycoproteins of influenza?
hemagglutinin | neuramindase
105
what is the role of hemagglutinin?
receptor recognition on host cell, sialic acid binding
106
what is the role of neuraminidase?
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
what are hemagglutinin and neuraminidase susceptible to?
antigenic drift and shift which produces new strains | - can cause epidemics and pandemics
108
what is antigenic shift?
- 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
why role does polymerase in influenza?
- makes so many - there will be errors with RNA - helps evade the immune system
110
what is significant about HIV reverse transcriptase?
- 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
why are there very few antiviral drugs?
- there are a limited choice of targets for antiviral drugs - can cause drug resistance - high mutation rates
112
what are the various transmission routes microbes?
- food and water - human to human (air and oral/faecal) - vector eg mosquito
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