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Micro Exam 3 > Exam 3-Ch 20-25,27,32-36 > Flashcards

Exam 3-Ch 20-25,27,32-36 Flashcards

1
Q

Virus

A

Genetic element that CANNOT replicate independently of a living/host cell

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2
Q

DEFINITION OF: Virion/Virus Particle

A

Extracellular form of a virus that exists outside the host and facilitates transmission from 1 host cell to another

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3
Q

STRUCTURE of Virion/Virus Particle

A

Nucleic acid genome surrounded by a protein coat and sometimes, other layers of material
-also contains enzymes necessary for infection

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4
Q

Enzymes Found In Virion

A
  1. Lysozyme
  2. Polymerases
  3. Neuraminidases
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5
Q

Function of Lysozyme

A
  1. Makes hole in cell wall

2. Lyses bacterial cell

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6
Q

Function of nucleic acid Polymerases

A
  1. Replication fo viral genome

2. Transcription of virus-specific RNA

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7
Q

Function of Neuraminidases

A
  1. Aids in release from the host
  2. Cleaves glycosidic bonds
  3. Allows liberation of viruses from cell
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8
Q

What must all viral genomes make in order to be translated?

A

mRNA

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9
Q

How are viruses classified?

A

Based on the hosts they infect

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10
Q

What are the classes of viruses?

A
  1. Bacterial viruses (bacteriophages)
  2. Archael Viruses
  3. Animal Viruses
  4. Plant Viruses
  5. Other Viruses
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11
Q

Nucleocapsid

A

Complete complex of nucleic acid and protein packaged in the virion

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12
Q

What are the 2 kinds of symmetry a nucleocapsid can have?

A
  1. Helical/Rod-shaped

2. Icosahedral/Spherical

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13
Q

Describe the helical structure of a nucleocapsid.

A
  1. Units of hollow tubes w/ protein walls assemble to form a cylindrical tube
  2. Within capsid, RNA genome is wound up and lies in a groove formed by the protein subunits
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14
Q

Describe the icosahedral structure of a nucleocapsid.

A
  1. 20 equilateral triangular faces + 12 vertices

2. most efficient arrangement of subunits in a closed shell

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15
Q

Naked Nucleocapsid

A

Consists of nucleic acid, capsid, and some enzymes needed for replication & infection

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16
Q

Enveloped Virus

A

Virus that contains additional layers around the nucleocapsid

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17
Q

What type of cells do enveloped viruses infect and why?

A

Eukaryotic cells

Why: virus envelope contains phospholipids which aren’t normally found in bacterial or prokaryotic cells

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18
Q

What happens when the enveloped virus exits the host cell?

A

It takes a bit of the host cell membrane (in the form of an envelope)
-in envelope, some/all reg cell membrane proteins are replaced w/viral proteins & some proteins form a binding layer b/w the envelope & capsid

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19
Q

Spikes/Peplomers

A

Glycoproteins found on the outside of the envelope

  • essential for attachment
  • can be used to identify virus b/c shape is cell specific
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20
Q

Complex Viruses

A

Virions composed of several parts, each w/ separate shapes and symmetries

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21
Q

Bacteriophage

A

Viruses that infect bacteria

-Structure=icosahedral heads + helical tails

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22
Q

Name 2 characteristics that differentiates the Mimivirus from small obligate intracellular bacteria.

A
  1. Mimivirus particles don’t undergo division but are formed by assembling preformed components
  2. Mimivirus has no protein translation apparatus (ribosomes) and no systems to produce biological energy (ATP)
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23
Q

Capsid

A

protein shell that surrounds the genome of a virus particle

-made of a # of protein molecules arranged in a precise & highly repetitive pattern around the nucleic acid

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24
Q

Capsomere

A

subunit of the capsid

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25
Q

Self-Assembly

A

Capsomeres generally self-assemble themselves around the nucleic acid

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26
Q

Protomers

A

Protein subunits that make up capsomers

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27
Q

Why is a host so important to a virus?

A

In order for the virus to replicate, it must use the host cell’s machinery to make more virions

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28
Q

What are the 5 phases of Viral replication?

A
  1. Attachment/Adsorption
  2. Pentration/Entry
  3. Synthesis
  4. Assembly
  5. Release
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29
Q

Attachment/Adsorption

A

Virus attaches to a susceptible host cell

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30
Q

Penetration/Entry

A

Virion or its nucleic acid enters the cell

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31
Q

Synthesis

A

Virus redirects host cell machinery to synthesize virus’s nucleic acid and protein by cell metabolism

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32
Q

Assembly

A

self assembly apsids and viral genomes are packaged into new virions (maturation)

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33
Q

Release

A

Mature virions are released from the host cell

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34
Q

What are the 2 ways virions can be released from the host cell?

A
  1. Budding (if enveloped virion)

2. Lysing (if naked virion)

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35
Q

What are the 2 phases of the latent period (virus replication)?

A
  1. Eclipse

2. Maturation

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36
Q

Eclipse Period

A

Early enzymes and nucleic acids are made

-no infectious particles present

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37
Q

Maturation Period

A

Protein coats for virions are made

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38
Q

Burst Size

A

Characteristic number of virions released after each replication cycle (specific to each virus)
-can range from a few to thousands

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39
Q

Length of replication cycle in bacteria viruses vs animal viruses?

A

Bacteria=20-60 mins

Animal=8-40 hrs

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40
Q

Burst TIme

A

Time from phage (virus) adsorption to release

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41
Q

What does a virion require in order to attach to a specific host cell?

A

Complementary Receptors

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42
Q

Complementary Receptors

A
  • Found on the surface of susceptible host and its infecting virus
  • Can be a protein, carbohydrate, glycoprotein, lipids, lipoproteins or complexes
  • in host cells, they carry out normal cell functions (Ex. uptake of proteins)
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43
Q

What happens when a virus attaches to a host cell?

A

Surface of cell and virus changes to facilitate penetration

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44
Q

Permissive Cell

A

Host cell that allows the complete replication cycle of a virus to occur

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45
Q

3 ways virion/genetic matter goes into host cell

A
  1. Fusion (mainly by enveloped virions)
    =of viral envelope w/ host membrane->nucleocapsid enters
  2. Endocytosis (by both naked & enveloped virions)
    =in vesicle; endosome aids in viral uncoating
  3. Injection (mainly by complex virions)
    =of nucleic acid
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46
Q

Bacteriophage T4

A

Virus of E.coli

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47
Q

Steps of Bacteriophage T4 Penetration Mechanism

A
  1. Attach to cells via tail fibers that interact w/ polysaccharides on E.coli cell envelope
  2. Tail fibers retract & tail core makes contact w/ E.coli cell wall
  3. Lysozyme-like enzyme forms small pore in peptidoglycan
  4. Tail sheath contracts & viral DNA passes into cytoplasm
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48
Q

Eukaryotic Host Defense Mechanisms

A
  1. Immune Defense Mechanism

2. RNA interference (RNAi)

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49
Q

RNA interference (RNAi)

A

Detects foreign RNA and cuts it up

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50
Q

Prokaryotic & Archaic Host Defense Mechanisms

A
  1. CRISPR

2. Restriction Modification System

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51
Q

Restriction Modification System

A

DNA destruction system that only works against double stranded DNA viruses (i.e. ssDNA and ALL RNA viruses are unaffected)
-uses restriction enzymes/endonuceases to cleave DNA at specific sequences

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52
Q

Why does the restriction modification system not destroy DNA of host cell?

A

Modification of host’s own DNA at restriction enzyme recognition sites prevents cleavage of own DNA

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53
Q

Viral/Bacteriophage Defense Mechanisms

A
  1. Chemical modification of viral DNA
  2. Production of proteins that inhibit host cell restriction system
  3. Contain restriction systems to destroy host DNA
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54
Q

2 examples of Chemical modification of viral DNA

A
  1. T-Even bacteriophages GLUCOSYLATE their DNA to prevent endonuclease attack
  2. METHYLATE their DNA
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55
Q

When does chemical modification of viral DNA occur?

A

After genomic replication by modification proteins encoded by the virus

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56
Q

CRISPR Defense

A

Adaptive immune system that transforms elements of invading phages into RNA that matches the phage’s nucleic acids
-This signals the bacteria to the presence of foreign genetic material, thus inducing the destruction of the phage

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57
Q

Bacteriophages Method To Evade CRISPR Defense

A

Developed its own CRISPR/Cas system that destroys the bacteria’s version

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58
Q

Types of Viral Genomes

A 
DNA: double & single stranded
Double stranded can be linear or circular
RNA: double & single stranded
3 types of single stranded RNA:
1. +   2. -   3. segmented
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59
Q

Positive Sense (+) RNA

A

Genomes that are ready for immediate translation into proteins

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60
Q

Negative Sense (-) RNA

A

Genomes have to be converted into the proper form to be made into proteins

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61
Q

Segmented RNA

A

Individual genes exist on sep pieces of RNA

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62
Q

Once a host has been infection, what must the virus do first?

A

Generate messenger RNA (mRNA)

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63
Q

RNA replicase

A

Specific RNA-dependent RNA polymerase needed by all RNA viruses to create DNA template needed to make RNA

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64
Q

What’s the method?: dsRNA (+/-) virus–>mRNA(+)

A

Transcription of minus strand

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65
Q

What’s the method?: ssRNA(+) virus–>mRNA(+)

A

Used directly as mRNA

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66
Q

What’s the method?: ssRNA(-) virus–>mRNA(+)

A

Transcription of minus strand

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67
Q

What’s the method?: ssRNA(+) retrovirus–>mRNA(+)

A
  1. Reverse transcription
  2. Forms dsDNA intermediate
  3. Transcription of minus strand
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68
Q

What’s the method?: dsDNA(+/-) virus–>mRNA(+)

A

Transcription of minus strand

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69
Q

What’s the method?:ssDNA(+) virus–?mRNA(+)

A
  1. Synthesis of other strand
  2. dsDNA intermediate
  3. Transcription of minus strand
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70
Q

Positive-strand RNA virus

A

Single-stranded RNA genome w/ same orientation as its mRNA

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71
Q

Negative-strand RNA virus

A

Single-stranded RNA genome with orientation complementary to its mRNA

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72
Q

Retrovirus

A

Animal virus responsible for causing certain types of cancers and AIDS (acquired immunodeficiency syndrome)

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73
Q

Where are DNA viruses replicated and assembled in a eukaryotic host cell?

A

Host cell’s nucleus`

=b/c it must be converted into a messenger RNA (which occurs in nucleus) to start protein synthesis

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74
Q

Where are RNA viruses replicated and assembled in a eukaryotic host cell?

A

Host cell’s cytoplasm

-doesn’t need to go into nucleus b/c it’s already in RNA form

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75
Q

Differences between early proteins and late proteins

A

Early: act catalytically, made in small amounts, made soon after infection

Late: structural components (ex. head & tail), made in large amounts, made later

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76
Q

Importance of Early Proteins

A

Necessary for replication of virus nucleic acid

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77
Q

Importance of Late Proteins

A

Components of virus coat

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78
Q

Generally, what sizes do viruses range between?

A

0.01-0.4 micrometers

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79
Q

How many steps are in the budding process, and what type of virus does this?

A

Steps: 4

Done By: Enveloped Viruses

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80
Q

1st Step of Budding

A
  1. Viral envelope proteins are inserted into host cell’s plasma membrane and line the cytoplasmic side of plasma membrane
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81
Q

2nd Step of Budding

A
  1. Nucleocapsids are directed to plasma membrane by host cell’s microtubules
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82
Q

3rd Step of Budding

A
  1. Host cell’s plasma membrane protrudes outward & nucleocapsids become surrounded by matrix-lined plasma membrane
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83
Q

4th Step of Budding

A
  1. Neck of protruding membrane is pinched off and the mature virus is released
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84
Q

What are common characteristics of Bacteriophages/Bacterial Viruses?

A
  1. Genome= dsDNA
  2. Naked (although some have lipid envelopes)
  3. Structurally complex (ie have heads, tails, etc)
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85
Q

What are the 2 types of viral life cycles?

A
  1. Virulent Mode

2. Temperate Mode

86
Q

Virulent Mode

A

Viruses lyse host cells after infection

-generally an active virus and released via lytic mode

87
Q

Temperate Mode

A

Viruses replicate their genomes IN TANDEM w/ host genome WITHOUT killing host

  • virus can be lysogenic OR passive
  • in animal viruses, this is a ‘latent’ infection
88
Q

What type of genome did the first viruses have and who did they infect?

A

Genome: linear, dsDNA

Infected: Enteric Bacteria

89
Q

What is significant of the DNA of T4 that makes it resistant to all known restriction enzymes?

A
  • contains the modified base, 5-hydroxymethylcytosine
  • modification is on cytosine where a H is replaced by CH2OH which is the site of glucosylation
  • how? b/c T4 encodes its own nucleotide so it can modify cytosine rather than using host cell’s cytosine
90
Q

How long does it take the T4 bacteriophage to complete its life cycle (ie attachment->lysis)?

A

Less than 20 minutes

91
Q

What type of bacteriophage is T4?

A

Virulent (i.e. release from host cell is via lysis)

92
Q

What does the control of T4 mRNA synthesis in the host cell require?

A

Production of proteins that sequentially modify the specificity of the host RNA polymerase so that it recognizes phage T4 middle promoters and guides RNA polymerase to these sites

93
Q

How do T4 early promoters make proteins?

A
  1. Must be ready by HOST RNA polymerase

2. Requires HOST sigma factor

94
Q

What happens after T4 early promoters make early proteins?

A

Phage makes phage-encoded anti-sigma factor which binds to host sigma factor and shuts it down

95
Q

What is the function of phage-specific proteins (T4)?

A

Modify RNA polymerase

96
Q

What does the transcription of T4 late promoters require?

A

New T4-encoded sigma factor.

97
Q

How does T4 increase the efficiency of phage production?

A

Digests the host DNA

98
Q

What is the function of T4 late genes?

A

Express enzymes that lyses the cell wall to release progeny phages

99
Q

Which parts of host translation does the virus takeover?

A
  1. mRNA availability to cytoplasmic ribosomes
  2. cell signaling pathways that regulate translation factor abundance, localization & activity
  3. ribosome recruitment
100
Q

What are the factors that determine the strategy the virus uses to take control of host cell’s translation process?

A
  1. Virus life cycle
  2. Type of host cell it infects
  3. Method of host cell’s translation control
101
Q

What does it mean when we say the T4 DNA is TERMINALLY REDUNDANT?

A

Base sequence is repeated at both ends

102
Q

What is the benefit of having terminally redundant ds DNA?

A

Allows for formation of concatamers

103
Q

Concatamers

A

Long strands of DNA consisting of several units linked together
-allows for more accurate cleaving of genome for viral progeny packaging

104
Q

How is bacteriophage dsDNA packaged into the viral head?

A
  1. Terminase attaches to end of concatamer
  2. Terminase docks DNA onto the procapsid portal of the viral feed
  3. DNA gets injected into the head
  4. Terminase cuts the DNA and ends packaging
  5. A cap is used to block the procapsid portal and stabilize capsid
105
Q

Terminase

A

Phage-encoded enzyme used in dsDNA packaging

106
Q

Procapsid portal

A

Region on viral head where viral DNA is inserted

107
Q

Temperate Phage

A

Special DNA phages that undergo adsorption & penetration but are NOT replicated or released immediately

108
Q

Prophage Stage

A

Inactive stage where temperate phages insert their DNA into the host’s chromosome

109
Q

Lysogeny

A

Stage where the host chromosome carries the bacteriophage DNA

  • temperate phage DNA gets copied along w/ host’s so host cell’s progeny will contain temperate phage DNA
  • > can lead to lysogenic conversion
110
Q

Lysogen

A

A bacterium containing a prophage

111
Q

Lysogenic conversion

A

When a bacterium acquires a new trait from its temperate phage

112
Q

Prophage

A

A phage that has inserted its DNA into the host’s chromosome and enters an inactive stage

113
Q

What type of phage is the lambda phage?

A

A temperate phage

-i.e. it can either go into the lytic cycle or lysogenic cycle

114
Q

In what ways can the temperate phage change the phenotype of its host?

A
  1. Bacteria can become immune to superinfection

2. Phage may express pathogenic toxins or enzymes useful to bacteria

115
Q

Name 2 advantages of lysogeny for viruses.

A
  1. Phage remains viable and protected in genome but may not replicate
  2. Multiplicity of infection ensures survival of host cell and therefore survival of virus
116
Q

Induction

A

Synthesis of new phage particles (initiated by a change in cell conditions) to mediate release of phage particles via lysis

117
Q

Characteristics of Lambda Phage

A
  1. Linear, dsDNA genome

2. Has complementary single stranded cohesive end regions

118
Q

Cohesive End Regions

A

Regions of DNA 12 nucleotides long found at the 5’ terminus of each strand of dsDNA

119
Q

What happens to the lambda phage’s dsDNA upon penetration?

A
  1. Cyclizes and forms a double stranded circle

2. cos site is formed via connection of cohesive ends

120
Q

Where in E.coli’s chromosome does the lambda DNA insert itself when the lambda phage is lysogenic?

A

At the lambda attachment site (attlambda)

121
Q

What’s needed in order for lambda DNA to attach to E.coli’s chromsome at the attlambda?

A

Lambda integrase.

  • cuts both E.coli chromosome and lambda cyclic DNA to make staggered ends
  • DNA ligase used to seal the pieces together

*cos site is not where integrase cuts cyclic DNA

122
Q

What controls whether the lytic cycle or lysogeny occurs?

A

Genetic Switch

123
Q

How are linear concatemers of DNA synthesized by the lambda phage?

A

Via rolling circle replication

124
Q

Describe the 2 stages of rolling circle replication.

A
  1. One strand is nicked by endonuclease, a long ss concatamer is made from 5’ end of the intact strand
  2. 2nd strand is made using the ss concatemer as a template
125
Q

Key Promotor Proteins In Genetic Switch

A
  1. cl protein/lambda repressor
  2. Cro repressor
    - they lie on opposite sides of the operator region
    - each controls direction of transcription which determines which cycle phage enters
126
Q

cl protein/lambda repressor

A

Protein that causes repression of lambda lytic events by preventing all transcriptions except from PRM via repression of other lambda-encoded proteins

-commits lambda phage to LYSOGENY

127
Q

Cro repressor

A
  1. controls activation of lytic events by repressing PL and PRM which indirectly represses expression of the lambda cII and cIII proteins
    - when made in large amounts, commits lambda phage to LYTIC CYCLE
  2. increases transcription of itself (Cro)
  3. increases transcription of Q
128
Q

cII and cIII proteins.

A

Lamba proteins needed to induce synthesis of cI and to maintain lysogeny

129
Q

what is the relationship and its importance between cII and cIII?

A

cIII protects cII against attacks from host cell’s protease (FtsH-HflB)

importance: keeps cI stable

130
Q

List the proteins key in maintaining that transcription of a temperate phage favors lysogeny?

A
  1. Activated PL & PRM
  2. N (anti-terminator)
  3. Q (anti-terminator)
  4. cII & cIII
131
Q

Function of the anti-terminators N

A

Prevents the production of late proteins and lysis

132
Q

What 2 things are accomplished with high levels of cII to promote lysogeny?

A
  1. ↑ in int(integrase) gene transcription which catalyzes integration of lambda into host genome
  2. ↑ transcription of cl gene (ie lambda repressor) by binding to PRM promoter which activates transcription of cI
133
Q

Function of Q

A

Activates genes needed for the lytic cycle

134
Q

In order for lysis to occur, what must the prophage do?

A

Site Specific Recombination

135
Q

Site Specific Recombination

A
  1. 2 ends of phage genome exchange their phosphodiester backbone linkages in order to separate from the host molecule
  2. phage DNA circularizes and initiates a lytic cycle

*when exiting, can pick up some of host cell’s genes

136
Q

Factors That Can Cause Exit From Lysogeny

A
  1. Random
  2. Triggered by environmental stress (ex. uv light)
  3. Events that threaten host survival
137
Q

What type of genome do most archaeal viruses have?

A

dsDNA

-can be linear or circular

138
Q

What defines a new archaeal virus family?

A

Unusual morphologies

139
Q

What is significant of the archael virus, Sulfolobus turreted icosahedral virus (STIV), method of release from the host cell?

A

Rather than lysing or budding, it starts structural formation on the external cell surface of host–>creates these pyramid-like surfaces, builds until it releases (so kind of like slow budding)

140
Q

What are the 4 possible consequences of viral infections in animal cells?

A
  1. Persistent Infections
  2. Latent Infections
  3. Transformation
  4. Cell Fusion
141
Q

Persistent Infections

A

Virions are released from host cell w/out resulting in cell lysis
-infected, intact cell remains alive and continues to produce and release virus

142
Q

Latent Infection

A

Delay between infection by the virus and lytic events

143
Q

Transformation

A

Conversion of normal cell into tumor cell

144
Q

Cell Fusion

A

2 or more cells become 1 cell with many nuclei

145
Q

What type of genome does the poliovirus have?

A

Positive-Strand RNA

146
Q

What happens first to the poliovirus genome when it enters a eukaryotic cell?

A

Its ENTIRE genome gets translated DIRECTLY and produces a polyprotein that undergoes self-cleavage to make 20 smaller proteins needed for nucleic acid replication and virus assembly

147
Q

Polyprotein

A

Single long, giant protein

148
Q

Does the polyprotein of the poliovirus contain replicase?

A

Yes

149
Q

Herd Immunity

A

State where a large enough fraction of the population is immune to a disease that it decreases the risk of someone getting the disease to ~0%

150
Q

How many cases of mumps have been confirmed in an outbreak at Ohio State University?

A

37

151
Q

Describe the structure and type of genome the Mumps Virus (MuV) has.

A

Genome: single stranded neg-sense RNA

Structure:

  • spherical
  • enveloped
  • F glycoprotein spikes
152
Q

What species does the MuV infect?

A

Only humans

153
Q

Describe the structure and type of genome of the Coronavirus (CoV)

A

Genome: positive strand RNA virus

Structure:

  • club-shaped glycoprotein spikes on surface
  • produces monocistronic mRNA
154
Q

Monocistronic mRNA

A

mRNA that only codes for 1 specific protein

155
Q

What do coronaviruses cause?

A

Respiratory infections such as SARS

156
Q

Where does replication and assembly of the coronavirus occur within the cell?

A

Replication=In cytoplasm

Assembly=In golgi

157
Q

How is the mRNA of the coronavirus transcribed?

A
  1. translation of (+) strand mRNA to make complementary (-) mRNA
  2. (-) mRNA strand is transcribed by RNA replicase to make both monocistronic mRNAs and copies of (+) mRNA
158
Q

In humans, where is the major site of coronavirus replication?

A

Epithelial cells of the respiratory tract

159
Q

What is MERS (middle east respiratory syndrome)

A

Type of coronavirus that can be spread person to person, also leads to respiratory infections
-originated from an individual’s exposure to bats or camels

160
Q

How are negative-strand RNA viruses able to be translated in the host cell?

A

Virus brings its own enzyme to use for transcription.

161
Q

Describe the genome and type of virion the influenza virus is.

A

Genome: negative strand RNA
-segmented genome

Virion: enveloped polymorphic virus

162
Q

What are the 2 types of surface proteins found on the influenza virus that interact with the host cell surface.

A
  1. Hemagglutinin

2. Neuraminidase

163
Q

Function of Hemagglutinin

A

Causes clumping of red blood cells

164
Q

Function of Neuraminidase

A

Breaks down sialic acid component (found on surface of epithelial cell) of host cytoplasmic membrane
-aids in attachment

165
Q

What are the differences between the 3 subtypes (A,B,C) of the influenza virus?

A

A: can cause flu-like symptoms and those within this type are named according to types of H and N spikes displayed on their surface. infects a wide variety of mammals and main cause of human epidemics & pandemics

B: cause flu-like symptoms but not as severe as A and not subdivided

C:also infects mammals but rarely cause disease. genetically and morphologically dif from A and B

166
Q

Describe the adsorption of the influenza virus into the host cell.

A
  1. HA spikes bind to mucoproteins containing terminal N-acetyl neuramini acid (NANA=sialic acid) groups
  2. virus is engulfed into endocytotic vesicles and then into endosomes via endocytosis
167
Q

What happens after the influenza virus is adsorbed into host cell?

A
  1. Ribonuclear proteins are translocated to the nucleus

2. Genome segments are transcribed by 3 polymerase polypeptides associated w/ each genome segment

168
Q

Antigenic Drift

A

Structure of neuraminidase and hemagglutinin proteins (on influenza proteins) are subtly altered
-leads to minor changes & epidemics; occurs every 2-3 yrs

169
Q

Antigenic Shift

A

Portions of the RNA genome from 2 genetically distinct strains of virus infecting the same cell are reassorted–>generates virions that express a unique set of surface proteins
-leads to major changes & pandemics; occurs every 10 yrs

170
Q

What is the cause behind the species barrier for the influenza virus?

A

Type of species a specific type of influenza virus is able to infect is determined by dif forms of sialic acid present on the virus glycoproteins (in particular, on the haemagglutinin protein)

171
Q

What type of genome does the phiX174 bacteriophage have?

A

Circular (+) single-stranded DNA contained within an icosahedral virion

172
Q

What do phiX174 virus particles use to bind to target cells?

A

Lippolysaccharides (LPS)

173
Q

What happens to the phiX174 DNA once its been injected by the capsid proteins into the host cell’s cytoplasm.

A
  1. ssDNA gets coated with host SSBs and is immediately rendered super coiled
  2. Host polymerase converts the supercoiled (+) ssDNA into replicative form DNA I (RFI)
174
Q

Replicative Form DNA/ ds RFI DNA

A

Made via replication of supercoiled SSDNA by host polymerase

-Used to produce more phiX174 (+) ssDNA forms which in turn will generate more RF forms

175
Q

Describe the state of the early viral genes within 20-30 mins of infection by phiX174.

A

Early viral genes are transcribed by host RNA polymerase and produce viral replication proteins
-Within this time frame, they will produce a sufficient amount of viral A protein

176
Q

Viral A Protein

A
  • Cleaves RFI DNA (+) strand at origin of replication
  • Initiates replication by covalently attaching itself to the DNA
  • RFII molecule is generated
  • Cleaves and ligates new strand after 1 new progeny strand has been created (ie 1 revolution)
177
Q

How does (+) strand replication of phiX174 occur?

A

via rolling circle replication

178
Q

Where does procapsid assembly and maturation for phiX174 occur within the host cell?

A

Cytoplasm

179
Q

Are the late viral genes of phiX174 transcribed by the host’s or the virus’s RNA polymerase?

A

Host’s

180
Q

Function Viral Protein C

A

Binds to replication complex and induces packaging of newly synthesized (+) DNA into procapsids

181
Q

How are progeny phiX174 phages released from the host cell?

A
  1. Viral lysozymes attack the host cell’s peptidoglycan walls
  2. Lysis occurs
182
Q

Describe the genome and structure of T7.

A

Genome: linear dsDNA
-genome always enters host cell in SAME orientation

Structure: icosahedral head and very short tail

183
Q

Why must the T7 genome always enter the host cell in the same orientation?

A

B/c the order of genes on the T7 chromosome influences regulation of virus replication

184
Q

What does the T7 bacteriophage infect?

A

E.coli

185
Q

Describe T7 DNA replication.

A
  • Uses T7 DNA polymerase
  • Involves terminal repeats and formation of concatamers
  • Characteristic bubble & Y forms
186
Q

What are concatamers made from in T7 DNA replication?

A

Unreplicated portions are paired via T7 phage polymerase and then ligased

187
Q

Where can pathogens come from?

A

Animate: humans, animals
Inanimate: water, soil, food

188
Q

What do we call an infection when it’s passed from animal to human?

A

Zoonoses

189
Q

What do we call the natural environmental location in which a pathogen normally resides?

A

Reservoir

190
Q

What do we call a situation in which a microorganism is established and growing in a host, whether or not the host is harmed.

A

Infection

191
Q

Define: immunity

A

the active ability to resist disease

192
Q

What is the difference between infection and disease.

A

Disease is the pathologic state that results when the infection damages/disrupts tissues and organs

193
Q

Define: Disease

A

Damage/injury to the host that impairs host function

194
Q

Name 2 things a pathogen must overcome in order to infect the host.

A
  1. Overcome surface barriers in order to reach underlying tissue
  2. Overcome resistance by host
195
Q

Name 2 kinds of resistance the host cell puts up against a pathogen.

A
  1. Nonspecific resistance (innate)

2. Specific immune response (adaptive)

196
Q

What is the function of the immune system?

A

To recognize foreign substances/microbes and act to neutralize/destroy them

197
Q

Ability of host to resist a particular disease/infection

A

Immunity

198
Q

Describe the nonspecific immune response

A
  • acts as the 1st line of defense
  • offers resistance against ANY microbe/foreign material
  • lacks immunological memory
199
Q

Describe the specific immune response

A
  • offers resistance against a SPECIFIC foreign agent

- has immunological memory which increases effectiveness on repeated exposure to agent

200
Q

What does a pathogen need in order to survive?

A
  1. A host (i.e. suitable environment)
  2. A source of nutrients
  3. Protection from harmful elements
201
Q

What tool does the pathogen have to help protect it from harmful elements?

A

Virulence factors

202
Q

What are the 6 general steps of pathogen infection?

A
  1. Exposure to pathogens
  2. Adherence to skin/mucosa
  3. Invasion through epithelium
  4. Colonization & growth (production of virulence factors)
  5. Toxicity-can be local or systemic
  6. Invasiveness: further growth at original & distant sites
    - all lead to tissue damage/disease
203
Q

Where does the pathogen enter the host?

A

Portals of entry

ex. skin, gastrointestinal, respiratory, blood transfusion, etc

204
Q

What are the structures a pathogen uses to adhere to the host cell?

A

Pili/fimbriae and adhesins that bind to complementary receptor sites on host cell

205
Q

What is Virulence?

A

The degree/intensity of pathogenicity.

206
Q

What determines the degree to which the pathogen causes damage, invasion, and infectivity?

A
  • Virulence factors

- pathogen’s ability to survive outside the host

207
Q

Define: Toxigenicity

A

Ability to produce toxins

208
Q

Define: Toxin

A

Specific substance that damages host

209
Q

Define: Intoxications

A

Diseases that result from entry of a specific preformed toxin into host

210
Q

Define: Toxemia

A

Condition caused by toxins in the blood of the host

Micro Exam 3 (2 decks)

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