Exam #3 Flashcards

1
Q

who is fred griffith

A

he did an experiment that helped in the identification of DNA as genetic material

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2
Q

how did fred Griffith do his experiments

A

1) he was studying strepocaccus phrumonine
2) he took dead S & living R and put into mouse, you then get living R & S. this is because DNA from dead S suriviced heat treatment & transformed same R into S

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3
Q

what is the summary of fred Griffiths expierments

A

1) living R & proteins (S)= R bacteria
2) living R & RNA (S)= R bacteria
3) living R & DNA(S)= S bacteria

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4
Q

what is the general structure of DNA

A
  • 2 strands that bse-pair

- run antiparallel

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5
Q

what is DNA made out of

A
  • sugar phosphate backbone

- bases; adeneine, thymine : guanine, cytsoine

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6
Q

viruses can infect any cell type on planet

A

know this

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7
Q

in viruses, protein/DNA machines that trick cells into copying them

A

know this

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8
Q

viruses are usually very specific

A

know this

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9
Q

viruses are the most abundant life form on the planet

A

know this

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10
Q

what are the pros about viruses

A
  • made of biological macromolecules (protein/DNA)
  • reproduce
  • evolve
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11
Q

what are the cons about viruses

A
  • not cells
  • no metabolism
  • parasites that must commandeer host cell machinery -> make more viruses
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12
Q

viruses are smaller than bacteria

A

know this

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13
Q

the spike of a virus does what

A

attach to host cell

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14
Q

what does the capsid of a virus does what

A

protein shell that protects the genome

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15
Q

what is the envelope of a virus made up of

A

lipid bilayer that is stolen from host cell (plasma membrane)

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16
Q

what is the 3 types of structures of viruses

A
  • helical capsid (HIV/influenza)
  • icosahedral capsid (polio)
  • complex (smallpox virus)
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17
Q

what is the helical capsid in the structure of the virus

A
  • hollow tube of protein

- contains groove that binds nucleic acid

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18
Q

what is the icosahedral capsid structure of the virus

A

20 equilateral triangles of capsid proteins

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19
Q

RNA virus must have a specific enzyme called what

A

RdRP = RNA dependent, RNA polymerase

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20
Q

what are the types of viral genomes

A

DNA, RNA

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21
Q

what is the DNA genome

A
  • dsDNA

- ssDNA

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22
Q

what is the RNA genome

A
  • dsRNA
  • ssRNA
    • +ssRNA (equivilant to mRNA –> viral genome can be translated
    • -ssRNA (complementary + copy must be made before translation)
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23
Q

the virus makes RNA from RNA template

A

know this

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24
Q

what are the size of the viral genome

A

1) small
- use our enzymes & pathways
2) genes are densily packed->overlapping reading frames , this produces more genome copies during replication

takes surprisnly few proteins to make a vital particle

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25
Q

what is the acronym of the viral life cycle

A
APUTTGAR
A- attachment to viral receptor(on host cell)
P- penetration of plasma membrane
U- Uncoat the genone from capsid
T- transcription of RNA
T- translation of protein
G- genome replication
A- assembly of virus
R- release of Virus

TTG= makes viral(vital?) parts

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26
Q

viral assembly is directed by

A

late genes= gene that is expressed later in the early gene=RdRP

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27
Q

what is the process of capturing nucleic acid/proteins

A
  • concerted-genome associates with capsid during synthesis
  • sequential-genome inserted into completed capsid
  • not a perfect process, many particles released during an infection are just empty capsids, with no nucleic acid
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28
Q

how do naked viruses release

A

cell lysis is the most common

- virus accumulates inside the host cell until cell bursts

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29
Q

how do enveloped viruses released

A

membrane is derived from host cell as virus leaves

viral spike proteins are inserted into membrane by host cell and captured by virus upon release

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30
Q

what are the possibilities of the viral release in an evelopled virus

A
  • bud off plasma membrane
  • bud off nuclear membrane
  • processing through ER/Golgi system
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31
Q

cytopathic effects definition

A

degenerative changes in host cell after viral infection

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32
Q

what are the mechanisms of the cytopathic effects

A
  • membrane disruptions
    - lyisis, budding, accumulation of spike proteins
  • virus uses host cell resources
    - DNA/RNA nucleotides, Amino Acids
  • Direct toxic effects of viral proteins
  • virus causes infected cells to clump together(syncytia)
  • virus transforms infected cell into malignant cell
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33
Q

syncytia is what

A

fused together cells

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34
Q

how does the body/cell fights back against the virus

A

interferon induced antiviral state

  • interferon (IFN) is produced in many infected cells
  • IFN makes human cell an inhospitable place for virus
    - cell stops making DNA/RNA nucleotides
    - cells stop dividing
    - cell initates apoptosis(programmed cell death)
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35
Q

attachment/infection of host cell, what is rapid replication

A

acute

  • rapid resolution
    ex. influenza, ebola, rhino
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36
Q

attachment/infection of host cell, what is virus is dominant(they hide out)

A

latent

  • varicella zoster
    ex. herpes, simplex 1&2
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37
Q

attachment/infection of host cell, what is slow and steady release

A

chronic

- hepatisis B

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38
Q

attachment/infection of host cell, what is malignancy and what causes it

A
cancerous
causes by 
    - virusus 1/3
    - environment 1/3
    - genetics 1/3++
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39
Q

what is cancer

A

tumor-lump of tissue due to abnormal cell growth

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40
Q

metastasis cells from tumor spread through body

A

know this

41
Q

cancer development-complex process involves what

A

involves multiple mutations or dysregulation events

42
Q

what are oncogenes

A

cancer causing genes

43
Q

what are proto-oncogenes

A

send “go” signal, required for normal growth, but if mutated or overexpressed,will cause cancer

44
Q

what are tumor suppressors

A

send “step” signal, regulate cell cycle progression, monitor DNA damage

45
Q

tumor suppressors can induce what

A

can induce apoptosis-programmed cell death if damage is detected to protect from development of cancer

46
Q
cause cancer
1* proto on cogene
2* tumor supp. 
match them
1+ loss of function mutation
2+ gain of functional mutation
A

1*proto on cogene with 2+ n of functional mutation

2* tumor supp. with 1+ loss of function mutation

47
Q

Epstein-Barr virus causes what

A

Burkitt’s lymphoma and nasopharyngeal cancer

0- there is evidence that in order to develop this cancer, the person must also be infected with malaria-weakens the immune system

48
Q

hepatisis B virus causes what

A

causes liver cancer (hepatomas)

49
Q

what are the mechanisms of hepatisis B

A

a) integration of virus geneome into host genome disrupts genes (instertional mutagenesis)
b) cirrhosis(scarring of the liver)

50
Q

what % of infants, young children, and adukts will be affected with hepatiss B

A

infants= 90% will develop chronic infection
young child = 25-50% will become chronic
adult= 5-10% will become chronic

51
Q

hepatisis C causes what

A

infects liver, causes liver cancer

can cause cancer through cirrhosis-scarring results from liver cells that divide over and over in an attempt to repair damage caused by viral infection

52
Q

in hepatisis C, what will happen in the 100 cases

A

per 100

  • 85= develop chronic infection
  • 70= will develop liver disease
  • 5-20= will develop cirrhosis
  • 1-5= will die from cancer
53
Q

what is human herpes virus 8 and HIV assoiciated with

A

associatd with Kaposi’s sarcoma, cancer of the skin and mucus membranes

54
Q

Kaposi’s sarcoma is much more likely if a patient is also infected with HIV

A

know this

55
Q

what aer the different types of human papillomaviruses and what are the #

A

out of 100

  • 60 causes skin warts
  • 40 infect mucus membranes(can cause gential warts)
    - out of these 40, 9 are associated with anogenitfal cancer
56
Q

what are the cancogence types of HIV

A
  • immortalize infected cells
  • activate polymerase
  • produce proteins that ca destroy tumor surprssors
    - p53=moniotors DNA damage
    - Rb= cells excel check point
  • secrete progrowth stimulatord
57
Q

what is associated with human t-cell lymphotrophic virus 1 & 2

A

retrovirus, associated with leukemia(blood cancer)

  • rare in us, common in Africa
  • 5% chance of developing leukemia if infected with virus
58
Q

dsDNA oncoviruses what do they produce

A
produce proteins that bind & inactivate tumor surpressors
produce vital(viral?) oncogenes
59
Q

retroviruses and cancer cause what are carry what

A
cause insterional mutageneis
carry oncogenes
   - stimulate growth
   - decrease adhesion tp tissue
   - molecular piracy
60
Q

why is it benefitical for virus to cause cancer

A
  • alternations to immune system
  • growing tumor provides more host cells
  • metostsisis=viral speed
  • cnacer has higher metabolic rate=more resoruces for virus
61
Q

what is mycolgy

A

the study of fungi

62
Q

what is fungi

A

eukaryptic organisms

63
Q

what ia yeast

A

unicellular fungus

64
Q

what is hyphae

A

filaments of fungal cells

65
Q

what is mycelium

A

cluster of hyphae

66
Q

what is reproduction

A

either asexual or sexual

67
Q

most fungi are what

A

saprobes(lives off dead/decaying organic matter) but some are human pathogens

68
Q

fungi require

A

require dark, moist environemts to prevent drying out

69
Q

fungi release

A

hydrolytic enzymes tp digest external subsrates

70
Q

what is the largest organism in the world

A

humungous fungus of eastern Oregon
2400-8600 years old
covers 2,384 acres

71
Q

fungal infections are called

A

mycoses

72
Q

fungal infections don’t dominate the field of infectiuous human health
they are usually opportunisituc pathogens

A

know this

73
Q

what is aflatoxin

A

caricinogenic produced by aspergillus fungi that infect cereals, peanuts, and peppers.

can also cause serious liver damage

74
Q

fungi toxins are a serious problem in parts of asia and Africa less of a problem in the US
farmers must be careful with silage to avoid producuing aflatoxin

A

know this

75
Q

fungi-toxins

what is st. Anthony’s fire

A

caused by consumption of erogotamine toxin produced by claviceps fungus that infects rye

  • makes mooth muscles contract (abortions and gangrene) creates hallunications
  • purified erotamine Is used today t control post-partum bleeding
76
Q

what are the protists

A

eukar[yotic microorganisms

77
Q

protists

- what is protozoa

A

chemooorgantrophs

78
Q

protists

- what is algae

A

photosynthetic protists

79
Q

protists

- reprouction

A

asexual or sexuak

80
Q

what is encysrment

A

differentiates into simple, resting stage form called a cysr

81
Q

what are the 3 main functions of encystment

A
  • survive harsh conditions
  • reproductive forms
  • serve as the mechaniams of transfer between hosts in infectious species, followed by excystment
82
Q

excystment needs to form a cysts to survive outside body and infect new host

A

know this

83
Q

what are the 3 mechanisms of genetic exchange in bacteria

A
  • transformation-naked DNA is taken up from the environment
  • conjugation-exchange
  • transduction-transfer of genes via viral infection
84
Q

what are the mechanisms of antibiotic resistance

A
  • destruction of anitobiotic
  • pump out antibiotic
  • protein target changes, cant allow antibiotic binding
85
Q

antibiotic don’t cause what

A

don’t cause mutations that lead to anitbioti resistance

86
Q

the presence of antibiotic selects what

A

selects for the survivial of bacteria naturally resistant to the antibiotic

87
Q

what are mutations

A
  • alternations in DNA sequence
    • wrong base incorporated
    • insertions or deletions of DNA sequence
88
Q

what are spontaneous mutations(accidents)

A
  • purine-purine substitutions

- pyrimidone-pyrimidine substituions

89
Q

what is induced mutations (external cause)

A
  • UV light exposure
  • X-ray radiation(fragments DNA)
  • chemical exposure
    - base analogs
    - interacating agents
90
Q

what is quorum sensing

A

the exchange and detection of signaling molecules in population of bacteria that coordinates gene expression

91
Q

quorum sensing is present in essentially all bacteria

A

know this

92
Q

vibrio fisheri are bioluminescent bacteria that are often found in symbiotic realtiionships with marine organisms

A

know this

93
Q

only display bioluminescence when assembled in large populations

A

know this

94
Q

what are bioflims

A

complex aggregates of bacteria helf together by extracullular polymers(polysaccarhides, proteims, DNA)

95
Q

where are biofilms formed

A

in aqueous environments when free swimming bacteria attach to surface. recruit other bacteria to join and form colony.

96
Q

where are biofilms found

A

found on living material and non-living material medical devices l

97
Q

biolfims are very hard to remove, very hard to kill with disinfectants, very hard to kill with antibiotics

A

know this

98
Q

E. Coli makes 2 porins, what are they

A

OmpC- has small opening-is expressed when there are high concentrations of nutrients

OmpF-has large opening - is expressed when there are low concentrations of nutrients

99
Q

what is the benefit for bacteria of the lac operon organization

A
  • bacterium wont waste its supplies/resources on making something it doesn’t need
  • matches gene expression