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139 Cards in this Set
- Front
- Back
What is a gene? Where is it found in? |
A linear sequence of DNA nucleotides; found in chromatin/ strands of DNA |
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What happens when a cell expresses a gene? |
It makes proteins |
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A gene sequence changed, what is expected to happen to the protein product |
Will not function properly |
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Overall flow of information during gene expression/ protein synthesis? |
DNA➡️RNA➡️Amino Acids |
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3 forms of RNA; roles; which are involved with transcription/ translation? |
1. mRNA: messenger, uses DNA as a template to polymerize RNA; transcription 2. rRNA: ribosome, acts as enzyme complex to polymerize amino acids into polypeptides; translation 3. tRNA: transfer, transfers amino acids from cytoplasm to ribosomes for polymerization; translation |
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What is a codon? What RNA is codon found in? |
3-lettered word sequence used to make amino acids; found in mRNA |
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What is an anticodon? Which RNA is it found in? |
3 lettered word sequence complementary to codon, found in tRNA |
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Transcription & where does it occur in? |
Makes mRNA in nucleus |
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3 sequential processes of transcription & what happens in each step? |
1. Initiation: RNA polymerase & transcription factors attach to promoter (@TATA) to unzip DNA helix 2. Elongation: RNA polymerase reads DNA template 3'➡️5' and polymerizes RNA 5'➡️3'. Forms 1° transcript 3. Termination: RNA polymerase detaches, releasing 1° RNA transcript |
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Promoter |
Site on DNA that RNA polymerase can bind to, to initiate transcription |
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What must happen to mRNA after it is transcribed |
Must be processed further |
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Transcribe this sequence into mRNA TAC-ATA-AAA-GGC-CCG-ATC |
AUG-UAU-UUU-CCG-GGC-UAG |
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What happens during RNA processing? ⭐️STEPS⭐️ |
⭐️SPLICESOMES HAPPEN⭐️ 1. Introns are excised out 2. Exons are spliced together 3. Cap & tail is added to ends |
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Where does RNA processing occur? |
Nucleus |
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What cellular components carry out RNA processing? |
Splicesomes |
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What are Exons? Are the excised or spliced? |
DNA nucleotide sequences used to make proteins; spliced together |
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What are introns? Are the excised or spliced? |
DNA nucleotide sequences not used to make proteins; Excised out |
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What might happen if a secretion protein activates prematurely? |
Can harm the cell |
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Besides intron excised and exons spliced, how else is mRNA modified in RNA processing? |
Adds cap & tail for guidance & prevention of pre-degradation |
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Where does the mature mRNA that has been fully transcribed & processed go to? |
Cytoplasm to be translated |
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Translation & occurs in? |
Reads mRNA to make amino acids sequence of a polypeptide; occurs in cytoplasm |
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3 sequential processes of translation & happenings |
1. Initiation: a) mRNA bonds to small ribosome rRNA subunit b) tRNA w/ methionine & UAC anti-codon joins @start codon (AUG) near ribosome P site c) Large ribosome subunit joins to complete ribosome 2. Elongation: a) 2nd tRNA amino acid joins at A site b) 1st amino acid bonds with 2nd amino acid c) mRNA moves through ribosome moving 1st tRNA (w/o A.A) to E site to exit & open up for new tRNA d) APE cycle repeats; empty tRNA's reloaded w/ a.a 3: Termination: a) release factor attaches to a stop codon( UAA, UAG, UGA) b) Last tRNA releases polypeptide & exits ribosome c) Ribosome subunits disassemble |
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Which tRNA (anti-codon) initiates translation ? |
UAC |
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What amino acid does UAC (1st tRNA anti-codon) deliver? |
MET |
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What does APE stand for? Recall what happens |
Arrival➡️Polymerize➡️Exit |
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The 3 stop codons |
UAA, UAG, UGA |
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Beyond folding, what 3 ways are proteins routinely modified? |
1. Proteolysis: cut 2. Glycosylation: + sugars 3. Phosphorylation: + phosphate |
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What is the overall role that modification serves? |
To activate a protein |
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Mutation is? |
A change in the DNA polynucleotide sequence |
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What kind of mutations can be transmitted to offsprings |
Mutations that occur in the germ cells |
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How do adaptive and maladaptive mutations differ? |
Adaptive: evolve Maladaptive: diseases |
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Do mutations occur spontaneously? |
Yes |
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During which cellular process do mutations occur? |
Replicating genetic material (Allele- crossover) |
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During which cellular process are mutations manifested into physical traits? |
DNA synthesis |
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What is a mutagen? And their impacts on mutation? + Examples |
Agents that cause DNA mutation; Increases rate & severity of mutation as cells are exposed to mutagens; EX: Ionizing radiation: UV, radioactive decay Various chem agents: Arsenic, Benzene Biological agents: Viruses like HPV |
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What is a point mutation |
Changes in DNA base pairs |
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What is substitution mutation |
When a single base pair is replaced by another base pair in the DNA sequence |
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What is a deletion or insertion mutation |
Delete: 1 or more BP taken away Insert: ! or more BP added |
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What is a frame shift mutation |
The deletion or insertion of BP's in a DNA sequence |
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What is a silent mutation? Why is it considered silent? |
Changes in BP's usually in the introns or 3rd position of a 3-lettered DNA sequence; Considered silent because they do not alter 1° |
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Silent mutation can be exploited for what practical purpose? |
Used to identify people via finger prints ect. |
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What is a nonsense mutation?How much do they alter? What types of alleles are most-likely nonsensical? |
One that causes a pre-mature stop codon; always alters 1° & 3°; Recessive alleles (r, i) |
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What is a missense mutation? How much do they alter? What types of alleles could be missensical? |
One that changes the 1st or 2nd position; Always alters 1° and sometimes 3°; Co-dominant & Incomplete dominance (IA, IB- HbB, HbS) |
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Similarities and differences of nonsensical and missensical mutations? |
Nonsense: Always 3°, stops reading, can't/ short protein Missense: Sometimes 3°, change 1st or 2nd position, new protein Similar: Always changes 1°, Both are Substitute mutations |
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What kind of mutation is Hemophilia A? (Xcl) What gene is altered? Which chromosome is it found in? |
Nonsense; Factor 8; X sex chromosome |
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What is FVIII? What role does it play in our body? |
1/13 factors; allows us to clot blood |
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Which cells normally express FVIII? |
Liver cells & Blood vessels |
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Basic treatment for hemo A? Is there a cure? |
Acute: Immediate Prophylactic: Daily, prevention; No Cure |
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What kind of mutation causes sickle cell anemia? (HbS) Which gene on which chromosome is mutated? |
Missense; HbB- globin gene on homolouge 11 |
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What is B-globin and what larger molecule does it help make? What role does the larger molecule then play in the body? |
A subunit protein that makes hemoglobin protein; helps transport O2 throught the body |
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What cells normally express B-globin? |
RBC's |
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What (or where) is the difference between B-globin & S-globin? |
In the 6th amino acid |
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What happens to a RBC that makes S-globin? How does this impact a person? |
Sickle- cell shaped; Person will have sickle cells, low oxygen transportation and immune system will attack RBC's |
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What is the basic treatment for SCA? Cure? |
Limit exertion, manage pain & inflammation; Cure: Bone marrow transplant |
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What is deletion mutation? What happens to the length of that gene? |
When one or more BP's are taken away; Length shortens |
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What is insertion mutation? What happens to the length of that gene? |
When one or more BP's are added; Length grows |
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What is frame shift mutation? |
+ or - of 1 or more BP's in a DNA nucleotide sequence |
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What factor determines the severity of frame shift mutation? |
Where the frame shift takes place on the sequence |
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Disease example of deletion/ frame shift mutation?
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Cystic fibroses |
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What factor has prevented cure from genetic diseases? |
The mutation occurs in all the cells |
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What is gene therapy? How might it overcome the barrier between genetic diseases and finding a cure? |
Kills all cells inside a persons body and replaces them with cells that have the "healthy" allele. They will reproduce the healthy allele and person will not have disease anymore |
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What kind of cells can be cured by gene therapy? Why are such cells good candidates for gene therapy? What hurdles remain for gene therapy? |
Cells that are still participating in the cell cycle (that reproduce still); Cells need to be able to replicate the good allele through out the body; Need to make sure gene is expressed at right time & perfect amount or else side effects |
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Are all mutations harmful? |
No |
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What role does the environment have in determining if an allele is bad or good? What is the HbS example? |
Depends on where the person lives if the allele will benefit them or not; Mild SCA is the best out of No or Full SCA in Malaria prone regions while No SCA is best in developed countries |
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What role does viruses play in gene therapy? |
We need a virus with the "good" allele to introduce in the patient |
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Which geographic region does HbS increase in frequency and why? |
Africa, people there are victims of Malaria & having Mild SCA that attacks the Malaria inside the sickle RBC's gives them a better survive rate than No or Full SCA. |
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What role does mutation serve in the process of adaption and evolution? |
It is the ultimate source of variation that can give beneficial phenotypes that allow a person to adapt and evolve better in their enviornment |
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What does Pathogenic mean? |
They may cause diseases |
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Are viruses alive? Can they metabolize or proliferate on their own? |
No |
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What are viruses and molecules that make them up? |
Aggreate (combinations): 4-1,000 genes worth of nucleic acid encapsulated in a capsid |
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Capsid |
A protein coat |
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Viral envelope? Do all viruses have it? |
Stolen from host cell phospholipid and host glycoproteins that surround the virus giving it even more protection; only some have |
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3 factors that determine whether or not a virus can enter a host cell? |
1. capsid 2. viral envelope 3. host cell receptors |
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Where do the enzymes necessary for a virus to replicate & build new capsids come from? |
Comes from host cell and sometimes + viral cell enzymes if they have any |
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Viral lytic cycle compared to viral lysogenic cycle? |
Lytic: Kills a host cell; Lyses Lysogenic: Doesn't kill a host cell; replicates with host cell |
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What criteria are used to classify animal viruses? |
1. Type of nucleic acid (DNA or RNA?) 2. 1 or 2 strands 3. Capsid shape 4. Has viral envelope or no? |
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Difference between a DNA & RNA virus? |
dsDNA, ssDNA, dsRNA, & ssRNA (with more classification on ssRNA)
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Group 'papovavirus, herpesvirus, & parvovirus' in dsDNA or ssDNA |
I.dsDNA: Papovavirus, Herpesvirus II.ssDNA: Parvovirus |
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DNA ONLY: Classify by viral envelope & not |
I. Papovavirus: No, Herpesvirus: Yes II.Parvovirus: No |
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Which general diseases/ conditions do we develop when infected by DNA viruses? |
I. Papovavirus: Paoillomavirus (warts, cervical cancer), Herpesvirus: H.Simplex 1 (cold sores), 2 (genital warts), Shingles, chicken poxs II.Parvovirus: mild rash |
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Group the following viral families/viruses of dsRNA or types of ssRNA: rotavirus, rhinovirus influenza,flavivirus, paramyxovirus, HIV |
III. dsRNA: Rotavirus IV:ssRNA for mRNA(+sense):Rhinovirus, flavivirus V: ssRNA template for RNA(-sense): influenza, paramyxovirus VI: ssRNA template for DNA synth: HIV |
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Additional ssRNA criteria + difference/ definitions of each? |
IV: +sense, used as mRNA V: -sense, used as template to make mRNA by host VI: Retro, used as template to make DNA by reverse transcriptase |
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RNA viruses only: Which have a viral envelope or not? |
III: Rotavirus: No IV: Rhinovirus:No, Flavivirus: Yes V:Influenza &Paramyxovirus: Yes VI: HIV/AIDS: Yes |
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General diseases caused by RNA viruses in hoomans? |
III: Reovirus- Rotavirus (diarrhea) IV: Picornavirus- Rhinovirus (common cold), Flavivirus- West Nile, Yellow fever, Hep C V:Orthomyxovirus- Influenza (Flu), Paramyxovirus (Measles & mumps) VI: Retrovirus- HIV/AIDS |
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What kind of virus is HIV? |
Retrovirus |
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What is the role of reverse transcriptase? |
Reads viral RNA to make viral DNA. That viral DNA is incorporated into host genome |
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What is a provirus? |
DNA of both virus & host combined
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What cells can be infected with HIV? |
WBC's (CD4 +T cells)
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How is HIV transmitted from one individual to another? |
Blood/ bodily fluids via sex, gestation/ breast feeding, sharing needles
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What is AIDS? |
When HIV infects WBC's causing serious immune system problems
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Why do patients with AIDS take "cocktail" treatments? |
Patiens cannot defend themselves against any other pathogens so must rely on medicine to defend for them
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How do most antiviral drugs work? |
Disrupt replication cycle of virus with competitive inhibitors |
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What is a competitive inhibitor? |
Blocks enzyme active site directly |
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Which type of enzyme(s) would be competitively inhibited via an anti viral drug? |
DNA polymerase |
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How can an antiviral drug apply selective pressure on a viral population? |
Only kills some of the virus causing the survivors to all become adaptive to the chemical environment |
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If all of the viral partials are exactly the same can antiviral drugs apply selective pressure? |
No |
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If all of the viral partials are exactly the same can antiviral drugs apply selective pressure? |
No |
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What does antiviral drug resistance mean? |
The virus has grown a resistance/ immunity toward the drug |
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If all of the viral partials are exactly the same can antiviral drugs apply selective pressure? |
No |
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What does antiviral drug resistance mean? |
The virus has grown a resistance/ immunity toward the drug |
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Which enzyme was originally competitively inhibited by 3TC |
HIV reverse transcriptase (cytosine analog) |
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How would you expect the frequency of viral particles that were & were not compatible inhibited by 3TC to change in patient who is administered 3TC |
Were= virus already immune Were not= Will die but will build immune system |
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Which class of viruses are herpesvirus classified? Envelope? |
dsDNA (I.) , Yes |
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Which kind of human tissues do herpesvirus effect? |
Epithelia (skin) |
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What results when herpes are expressed? |
Ulcers: open wounds |
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How are herpesvirus transmitted from person to person? |
Skin-to-skin contact |
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What part of the body does HSV-1 infect & cause ulcers to form? |
On/ near lip |
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What does it mean that HSV-1 retrogrades? What nerve does it infect & become latent? |
Goes backwards up the nerve; Ganglia of trigeminal nerve |
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Known triggers for HSV-1 to "anterograde" back into epithelium to cause users? |
UV, illness, stress. |
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Is there a cure for herpes? Treatment? |
No cure; Treatments: Docosanol (Abreva): Cell-binder inhibitor Valacyclovior (Valtrex):DNA pol inhibitor |
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Which class of virus are HPV viruses classified? Envelope? |
dsDNA, No envelope |
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What kind of human tissue do HPVs infect? Results of expression? |
Keratinocytes, cells found in basal layer of stratified squamous epithelium (skin); warts/ cancer |
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How are HPV transmitted to people? |
Skin-to-skin |
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HPV is "nessecary but not sufficient" to form cancer meaning? |
Can't do it alone? |
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Cure for HPV? Treatment? Vaccine? |
No cure; no treatment; Yes vaccines |
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What is a vaccination? Goals of vaccinating a person against pathogens? |
Introducing pathogen antigens to invoke immunization against future infections |
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Which pathogens have we developed vaccines for, viruses or bacteria? |
Both |
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Characteristics used to discern among prokaryotes & eukaryotes? |
Pro's lack nucleus, internal membranes and membrane bound organelles |
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3 general morphologies (shapes) expressed by bacteria |
Coccus, bacillus, spirilform |
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How are HPV transmitted to people? |
Skin-to-skin |
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3 factors influence bacterial pathogenicity? |
1. Cell wall 2. Outer membrane 3. Virulence factors |
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4 virulence factors |
1. Flagella( +/- taxis) 2. Capsule 3. Fimbeane (bio films) 4. Sex pillus |
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Can virulence factors cause host inflammation? |
Yes |
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How is a genome of a bacterium organized? |
Single, circular |
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HPV is "nessecary but not sufficient" to form cancer meaning? |
Can't do it alone? |
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Cure for HPV? Treatment? Vaccine? |
No cure; no treatment; Yes vaccines |
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What is a vaccination? Goals of vaccinating a person against pathogens? |
Introducing pathogen antigens to invoke immunization against future infections |
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Which pathogens have we developed vaccines for, viruses or bacteria? |
Both |
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Characteristics used to discern among prokaryotes & eukaryotes? |
Pro's lack nucleus, internal membranes and membrane bound organelles |
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3 general morphologies (shapes) expressed by bacteria |
Coccus, bacillus, spirilform |
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What role does a bacterium a cell wall play? |
1. Maintain cell wall 2. Protect 3. Prevents rupture in hypotonic environments |
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Which compound is used extensively to make bacterial cell walls? |
Peptideglycan |
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Compare Gram + & - |
+: thick peptideglycan -: thin peptideglycan w/ an putee membrane |
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Plasmids |
Smaller rings of self-replicated SNA that have few-10s of genes |
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Endoscope |
Resistant packaging of cell genome when times are tough |
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How do bacteria reproduce? |
Binary fission |
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Do bacteria transcribe/ translate genetic material? Do they undergo RNA processing? |
Yes, No |
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Bacteria are haploid, meaning they lack...? |
The ability to recombo genes |
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3 mechanisms (+ how they work) for horizontal gene transfer? |
1. Transformation: DNA uptake from decomposing cohorts 2. Transduction: Transfer via viral bacteriophages (phages) 3. Conjunction: sex pillus exchange plasmids |