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Unit 2 > Unit 2 - Week 3 - Hanes 2, Wilkens 1 and 2, and Moffat 7 > Flashcards

Unit 2 - Week 3 - Hanes 2, Wilkens 1 and 2, and Moffat 7 Flashcards

1
Q

What cells does polio enter the bloodstream through?

A

M cells in gut, reovirus also does this

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2
Q

In rotavirus, diarrhea is almost pure:

A

virions

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3
Q

First degree viremia leads to:

A

Replication of virus in internal organs
May occur w/o symptoms
(incubation period)

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4
Q

Second degree viremia leads to:

A

Dissemination of the virus to organs where it is shed

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5
Q

The pustules of VZV are presentation of first or second degree viremia?

A

Second

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6
Q

How does first degree viremia come about?

A

Localized infection attracts lymphocytes, which carry the virus to lymph nodes, then the virus replicates and travels through bloodstream to target organs

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7
Q

An example of a virus causing an acute infection:

A

Common cold, rhinovirus

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8
Q

An example of a virus causing a rare, late complication, but whose period of latency renders the virus undetectable:

A

Measles returns as SSPE, Subacute Sclerosing Panencephalitis. The virus is NOT shedding, this is a disease episode only.

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9
Q

An example of a virus causing a latent infection:

A

VZV…virus undetectable in drg…Zoster. Virus is shed before and after both disease episodes

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10
Q

An example of a slow infection:

A

Prion disease

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11
Q

An example of a chronic disease where the virus is shed for life:

A

Hepatitis B

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12
Q

An example of a chronic disease where the virus is shed for life, followed by late disease:

A

HIV

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13
Q

Name the types of viral infections:

A
  1. Acute
  2. Persistent (Chronic)
  3. Latent (Chronic)
  4. Slow (Chronic)
  5. Transforming
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14
Q

Host response to viral infection involves:

A

interleukin, interferon, T cells, antibody complexes

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15
Q

Symptoms of viral disease such as fever, tissue damage, rash, aches, pains, nausea, are mainly caused by:

A

host response to infection

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16
Q

Identifiers of Norwalk Virus:

A

Norovirus
+ssRNA
a gastroenteritis

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17
Q

Why is RSV particularly dangerous for children?

A

If forms a syncitium in the lungs, fusing lung cells together and rendering them unable to exchange oxygen. Infected cells are prone to apopotosis.

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18
Q

Herpes Stromal Keratitis is an example of:

A

How the immune response can cause lasting damage (corneal scarring from HSV reactivation)

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19
Q

Smallpox is acquired through the:

A

respiratory tract, disseminates through blood, sheds through skin pustules

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20
Q

Viruses that enter through the respiratory tract include:

A 
Rhinovirus
Smallpox
Epstein Barr
Adenovirus
RSV
Infleunza
Herpes simplex virus
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21
Q

Viral replication sites in the body include:

A 
Liver
Kidney
Lung
Mucous membranes
Skin
(Virions shed from all these places)
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22
Q

In an HIV sample, what kind of tissue is most virus found in?

A

Blood plasma
Lymphocytes
CSF

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23
Q

In bacteria, cis-acting sites are:

A

Operons

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24
Q

The main step of eukaryotic gene expression is:

A

Transcription initiation

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25
Q

What does CAP stand for? What is it? What does it do?

A

CAP - catabolite activator protein, a bacterial gene regulatory protein - binds DNA to stimulate transcription, for example activating the lac operon

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26
Q

Name the common eukaryotic DNA binding domains of transcription regulatory proteins

A
  1. Leucine zipper
  2. Recognition alpha helix
  3. Zinc finger
  4. Homeodomain
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27
Q

Fun fact!

A

Helicase is not needed for transcription because amino acid functional groups can contact specific DNA bp’s without the need to unwind the DNA. Sequence specificity

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28
Q

p53 normal function is to act as a:

A

transcription repressor

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29
Q

What is polycistronic mRNA?

A

The mRNA transcript for an entire bacterial operon.

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30
Q

The presence of glucose in a bacterial cell normally:

A

represses the lac operon

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31
Q

cAMP in a bacterial cell is abundant when:

A

glucose is unavailable, and is responsible for allowing CAP to turn on the lac operon.

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32
Q

Most transcription factors are ____, meaning that their domains function interchangeably.

A

modular

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33
Q

Modularity of transcription factors (often dimers or heterodimers) have what consequences for disease?

A

Fusion of different parts of different factors, is as the result of a chromosomal translocation, can have negative consequences.

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34
Q

Give an example of a modular TF gone wrong:

A

25% of pre-B-ALL t(1;19) translocations, the protein fusion converts Pbx1 into a potent activator.

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35
Q

Activators stimulate transcription by helping assemble __1__ at the promoter. Typical activators work via a large __2__ made up of about 25 proteins. Other activators work by recruiting __3__-modifying enzymes.

A
  1. RNA Pol II
  2. mediator complex
  3. chromatin
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36
Q

Enhancers are __1__-acting sequences that bind activators, and can be upstream or downstream from the promoter.

A
  1. cis
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37
Q

What is T-cell ALL and what does it have to do with enhancers?

A

T-cell acute lymphoblastic leukemia, 5-10% of which is caused by a translocation that results in an enhancer for a T-cell being put next to a HOX11 homeodomain protein gene, which gets overexpressed.

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38
Q

What are the two main chromatin modifications for transcription?

A
  1. Covalent histone modifications
  2. ATP-dependent nucleosome remodeling (move, slide, exchange) by chromatin remodeling enzymes, a special class of ATPases
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39
Q

What are the main types of histone modifications for transcription control?

A
  1. Acetylation of Lys (H3) - to activate
  2. Deacetylation of Lys (H3) - to repress
  3. Methylation of Lys, Arg (H3) - can activate or repress
  4. Phosphorylation of Ser/Thr (H2A, H3) - coupled to acetylation.
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40
Q

Histone modifications occur mostly on the __1__ tails of histones __2__ and __3__ which protrude from the core nucleosome. Generally, HATs, histone acetyltransferases, __4__ while HDACs, histone deacetylases, __5__ transcription.

A
  1. N-terminal
  2. H3
  3. H4
  4. activate
  5. repress
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41
Q

Acetyl group has what charge?

A

Negative (binds to Lys)

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42
Q

Regulatory proteins work together as a ____ to control the expression of a eukaryotic gene

A

committee

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43
Q

A single transcription factor may control multiple genes, for example:

A

Steroid receptor. Their effect depends on the other regulators bound to a gene in a particular cell.

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44
Q

Name 3 ways in which TF’s themselves are regulated:

A
  1. Phosphorylation
  2. Intracellular trafficking
  3. Selective degradation
    * *These mechanisms are usually controlled by extracellular signaling which is communicated across the plasma membrane to gene regulatory proteins inside the cell
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45
Q

What is RNA-seq and why is it so important?

A

RNA-seq can measure whole genome presence of RNAs and their relative abundance, which gives a global picture of gene expression levels. Custer analysis of RNS seq can show “signatures” of certain disease processes.

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46
Q

DNA microarray can measure relative:

A

mRNA levels

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47
Q

Beta globin gene is only expressed in:

A

Adult:

erythroid cells in bone marrow

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48
Q

Deletion of the __1__ silences the entire cluster preventing beta globin production, which results in a severe anemia called __2__.

A
  1. LCR

2. Beta thalassemia

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49
Q

Cell “memory” is often transmitted through transcriptional mechanisms:

A
  1. Autoregulation

2. Epigenetic inheritance via modification of chromatin and DNA

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50
Q

What is transcriptional autoregulation?

A

Gene A is made by accident, whose function once translated is to enhance or activate itself.

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51
Q

Modification of DNA in epigenetics is referred to as:

A

imprinting, associated in general with repression

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52
Q

Rett syndrome has what MOI?

A

X-linked

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53
Q

Bacteria have __1__ RNA polymerase, which humans have __2__.

A
  1. One

2. Three

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54
Q

Do bacterial have transcription factors?

A

No, RNA Pol can do it alone

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55
Q

An example of an immunomodulatory antiviral treatment is:

A

alpha-interferon

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56
Q

What are the 4 main types of antiviral treatments?

A
  1. Nucleoside analogs
  2. Non-nucleoside analogs
  3. Protease inhibitors
  4. Entry inhibitors
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57
Q

What is an example of an antiviral entry inhibitor

A

Enfuvirtide, for HIV

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58
Q

Nucs and non-nucs target:

A

viral genoma replication

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59
Q

A neuraminidase inhibitor functions at what stage of the viral cycle?

A

Prevents assemby and release of virions

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60
Q

How does Acyclovir work?

A

Acyclovir, for herpesvirus, is a substrate of viral thymidine kinase, and takes the place of thymidine. Thus, acyclovir-P-P-P is incorporated into the viral DNA and becomes a chain terminator.

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61
Q

What is rebound in viral therapy?

A

Virus replication resumes when the drug is removed.

62
Q

What is virilogic breakthrough?

A

Because viruses are all “clouds,” in that they are groups of mutations all together, chances are a therapy for a virus will wipe out all but one or a few types of viruses that have naturally become resistant. This results in the breakthrough of that type of virus, during therapy. After the therapy stops, any remaining original virus can compete with the resistant virus.

63
Q

Acyclovir is a nucleoside analog of:

A

guanosine

64
Q

Acyclovir is most effective against:

A

HSV 1 and 2, but can also be used to VZV and Zoster

65
Q

Gancyclovir is similar to acyclovir in that, but is different how?

A

Same MOA, also a guanosine analog. Different bc highly toxic and mutagenic/tumorogenic!

66
Q

Ganciclovir is intended for tx of:

A

CMV, in people that really really need it

67
Q

What are the two broad-spectrum DNA antivirals?

A

Foscarnet and Cidofovir, both IV only, both nephrotoxic

68
Q

Why are HBV treatments the same as for HCV and HIV?

A

Because the HBV life cycle includes some reverse transcriptase activity

69
Q

Foscarnet is for:

A

All herpesviruses

70
Q

Cidofovir is for:

A 
Adenovirus
Papillomavirus
Poxvirus
CMV
Herpesvirus
71
Q

Pegylated interferon alpha is for:

A

HBV

72
Q

Who should receive HBV treatment?

A

People with HIV/HCV coinfection
People who have active, chronic HBV disease
People at risk for progression to hepatocellular carcinoma or cirrhosis

73
Q

The generic name for Tamiflu is:

A

Oseltamivir

74
Q

The generic name for Relenza is:

A

Zanamivir

75
Q

Zanamivir and Oseltamivir function to:

A

Prevent budding from host cell in influenza

76
Q

What is one major structural advantage to Zanamivir and Oseltamivir?

A

They function without having to enter the host cell bc they inhibit viral neuraminidase (sialidase)

77
Q

Ribavirin is ___1__ and functions against __2__ viruses.

A
  1. Nucleoside analog of guanosine
  2. RNA, approved for HCV and RSV
    does NOT work against Ebola
78
Q

What is the current therapy for HCV?

A

Ribavirin plus pegylated interferon alpha

79
Q

What is the major hurdle in HCV tx?

A

Not all HCV genotypes respond to the drugs we have, not to mention the side effects and long-term therapy regimen involved.

80
Q

What is the function of Sofosbuvir for HCV?

A

Inhibits RDRP, thereby acting as a chain terminator, combine with standard therapies.

81
Q

Ledipasvir is used for:

A

HCV

82
Q

Daclatasvir is used for:

A

HCV

83
Q

What does NRTI stand for?

A

Nucleoside Reverse Transcriptase Inhibitor, it is a class of HIV drugs, chain terminator for cDNA creation

84
Q

Maraviroc is for__1__ and acts to __2__.

A
  1. HIV

2. Inhibit entry

85
Q

Darunivir is for __1__ and acts to __2__.

A
  1. HIV

2. Protease inhibitor

86
Q

Efavirenz is for __1__ and acts to __2__.

A
  1. HIV

2. NNRTI

87
Q

Tenofivir is for __1__ and acts to __2__.

A
  1. HIV

2. NRTI

88
Q

Raltegravir is for __1__ and acts to __2__.

A
  1. HIV

2. Integrase inhibitor

89
Q

Stribild is made of:

A

4 drug combination of elvitegravir (integrase inhibitor), cobicistat (liver enzyme to help break down drugs in liver), emtricitabine (RT inhibitor), tenofovir (NRTI)

90
Q

The genetic code is almost universal except for:

A

mitochondria

91
Q

What is codon degeneracy?

A

Multiple codons encode for a single amino acid

92
Q

What are the three stop codons?

A

UAA, UAG, UGA, aka nonsense codons

93
Q

What does an aminoacyl tRNA synthetase do?

A

It is an enzyme that attaches the amino acid to the tRNA

94
Q

What is an aminoacyl tRNA?

A

tRNA with amino acid attached

95
Q

What is the anticodon base I?

A

Inosinic acid, similar to G

96
Q

Where is the amino acid attached to the tRNA?

A

3-OH end, via a high energy bond

97
Q

What are the steps in attaching an amino acid to a tRNA?

A
  1. Amino acid hydrolyzes ATP –> Amino acid-P = Aminoacyl adenylate
  2. Reaction of activated amino acid with 3-OH part of tRNA to form aminoacyl tRNA
    ATP + aa + tRNA –> aminoacyl tRNA* + AMP + PPi
98
Q

How many high energy phosphoanhydide bonds are hyrdolyzed for each amino acid transferred to tRNA?

A

2

99
Q

What is the difference between tRNA^ser and Ser-tRNA^ser?

A

The latter has the amino acid attached, and is thus “charged” or aminoacylated.

100
Q

True or False: tRNA synthetases are specific to their tRNA AND its amino acid, and are structurally unrelated to one another, ranging from 34 to more than 1000 amino acids.

A

True

101
Q

The A site stands for, and functions to:

A

Aminoacyl site of the ribosome, located on the large ribosome. This is the docking area for the new tRNA.

102
Q

The P site stands for, and functions to:

A

Peptidyl site of the ribosome, located on the large ribosome, the site where the amino acid is transferred from the tRNA to the peptide chain.

103
Q

Proper alignment of the tRNA requires, in addition to codon:anticodon interaction, pairing between the tRNA and specific segments of:

A

16S and 23S rRNA

104
Q

What is the major difference between prokaryotic and eukaryotic transcription?

A

Transcription and translation are spatially separated in eukaryotes (the former in the nucleus, and the latter in the cytoplasm). In prokaryotes, translation is often started before transcription is complete.

105
Q

What is the step of translation initiation?

A

mRNA binds to ribosome and is aligned in the correct reading frame, initiator amino-acyl tRNA binds, and the ribosome assembles.

106
Q

What is the process of termination in translation?

A

Release factor(s) bound to GTP bind to stop codon in A-site, peptidyl tRNA in P-site is hydrolyzed to release the peptide chain and leave the tRNA in the P site. tRNA, release factors and mRNA are released from the ribosome after GTP hydrolysis and ribosome dissociates into large and small subunits.

107
Q

How does the ribosome know how to align the mRNA so that the initiation codon is distinguished from the other AUG?

A

Prokaryotes - Shine-Delgarno sequence upstream from the relevant AUG
Eukaryote - at the end of every 5’ cap there is attached a 7-methyl guanine residue (known as the 5’ cap), which is found by the Met-tRNAi^met.

108
Q

What is the Kozak sequence?

A

A small consensus sequence upstream of the first AUG may also aid in positioning the ribosome for initiation of translation.

109
Q

What is formyl methionine-tRNA [fMet-tRNA^fMet]?

A

Prokaryotes use this to initiate translation

110
Q

Prokaryotes have how many initiation factors? What do they do?

A

3
IF-3 and IF-1 bind to the small ribosomal subunit and promote the dissociation of small and large ribosomal subunits so that a new round of protein synthesis can be initiated. Also helps the 30S bind to the Shine-Delgarno sequence.
IF-2 binds to initiator fMet-tRNA^fMet and GTP, allowing it to bind to the small ribosomal subunit.

111
Q

What is an eIF?

A

eukaryotic initiation factor

112
Q

In a step that expends energy in the form of a high-energy phosphoanhydride bond in GTP, the large ribosomal subunit binds as:

A

the initiation factors are expelled from the ribosome

113
Q

As with the IF’s, the ___ are not part of the ribosome, they only attach for their specific job.

A

EFs

114
Q

How many elongation factors do prokaryotes have?

A

Three: EF-Tu, EF-Ts, EF-G

115
Q

This prokaryotic EF binds GTP to the aminoacyl tRNA and brings them to the A site on the ribosome, which requires hydrolysis of GTP and leaves the inactive EF-GDP complex:

A

EF-Tu

116
Q

This prokaryotic EF regenerates EF-Tu after it has done its job:

A

EF-Ts

117
Q

This prokaryotic EF moves mRNA by 3 bp (from A to P) in a reaction that involves the hydrolysis of GTP:

A

EF-G

118
Q

Prokaryotic EF-G does that same job as eukaryotic:

A

eEF-2

119
Q

What is the function os eEF-1?

A

It has 2 subunits that together perform the same functions as EF-Tu and EF-Ts.

120
Q

How is the peptide bond formed in the ribosome?

A

The new aminoacyl tRNA at the A site attacks the aminoacyl tRNA linkage at the P site, resulting in the transfer of the peptide chain to the tRNA on the A site, all catalysed by peptidyl transferase on the ribosome.

121
Q

Translocation from the P to the E site requires:

A

GTP hydrolysis, catalysed by EF-G/eEF-2

122
Q

Prokaryotes have how many release factors?

A

Three: RF-1, RF-2 and RF-3

123
Q

Eukaryotes have how many release factors?

A

One, eRF

124
Q

Binding of the RF alters the activity of the __1__ causing it to add __2__ instead of an amino acid to the peptidyl -tRNA. This removes the peptide from the tRNA. The uncharged tRNA is moved to the __3__.

A
  1. Peptidyl transferase
  2. H2O
  3. E site
125
Q

What is the error rate for translational proofreading?

A

1 in 10^4, or 1 in every 25 protein molecules

126
Q

Proofreading is accomplished by:

A

Aminoacyl synthetase has a site for recognizing and removing an incorrectly bound tRNA

127
Q

How many GTPs are expended when the polypeptide is released?

A

One

128
Q

How many GTPs are expended for initiation of translation?

A

One

129
Q

How many GTPs are expended for elongation of the polypeptide?

A

Two

130
Q

Since protein synthesis is so expensive, it’s usually controlled at the __1__ by regulating the availability of __2__.

A
  1. initiation step

2. eIF-2

131
Q

eIF-2 can be phosphorylated by specific protein kinases to decrease:

A

rate of translation

132
Q

eIF-2 brings the __1__ to the __2__ ribosome and is inactivated as GTP is hydrolyzed and the initiation complex is formed.

A
  1. initiator tRNA

2. 40S

133
Q

Normally, eIF-2-GDP is recycled to eIF-2 GTP via interaction with:

A

eIF-2B

134
Q

Phosphrylation of eIF-2-GDP by a protein kinase locks the eIF-2/eIF-2B complex in the:

A

inactive, GDP-bound form.

135
Q

Synthesis of globin in reticulocytes only occur when:

A

Its iron-containing prosthetic group, heme, is available for assembly into hemoglobin.

136
Q

In the absence of heme, cells activate ____, which phosphorylates eIF-2.

A

HCI, heme-controlled inhibitor

137
Q

This structure protects 5’ end of mRNA from ribonucleases and allows eukaryotic cells to distinguish between mRNA and other RNA.

A

5’ cap

138
Q

This structure is recognized by one of the eIFs in the small ribosomal subunit and is required for translation of most mRNAs

A

5’ cap

139
Q

This often contains sequences important for translational efficiency:

A

5’ UTR

140
Q

This often contains signal sequences that target the mRNA to be translated at specific places in the cell (ie the ER):

A

3’ UTR

141
Q

This can contain sequences important for mRNA stability:

A

3’ UTR

142
Q

This stabilizes the 3’ end of the mRNA

A

Poly-A tail

143
Q

What is aconitase?

A

Aconitase is also known as the iron response factor, IRF. In the absence of iron, it binds to a specific stem-loop structure, the IRE (iron response element) present in the mRNA of both the ferritin mRNA and the transferrin receptor mRNA.

144
Q

The presence of excess iron releases:

A

aconitase from the IRE, causing an increase in ferritin translation, and a decrease in transferrin receptor translation.

145
Q

siRNA and miRNA are usually:

A

18-25 nucleotides long

146
Q

What is the function of endogenous short-interfering or micro RNA?

A

Can down-regulate translation by inducing mRNA degradation.

147
Q

What is the function of exogenous dsRNA?

A

It is processed to siRNA by Dicer.

148
Q

How does poliovirus control the host translation of mRNA?

A

Its viral protease cleaves the 5’ caps, so that host mRNA is not efficiently recognized by ribosomes, thus viral translation takes off in its place.

149
Q

Name three ribosomal inhibitors:

A
  1. Tetracycline
  2. Ricin/Abrin
  3. Streptomycin
  4. Erythromycin
  5. Chloramphenicol
150
Q

The discovery of dsRNA in a cell causes the release of:

A

Interferons (IFNs)

151
Q

How do interferons function against viral presence?

A

They bind to the cell surface and activate 2 proteins:

  1. Ribosome-associated protein kinase, which phosphorylates eIF-2 (like HCI)
  2. 2,5A synthetase which produces polymers of ATP that activate an endoribonuclease that cuts both cellular and viral mRNAs

Unit 2 (11 decks)

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