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73 Cards in this Set
- Front
- Back
temperate phage
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phage that can choose to conduct lysis or lysogeny in the host cell
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prophage
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phage genome that is intercalated into th host genome
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lysogens
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bacteria that contains the phage DNA, potential host
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bacteriophage Replication cycle stages
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1. attachment (adsorption) - docks with distal tail fibers
2/3. Penetration/uncoating - occur together 4. Synthesis - gene expression and replication 5. Assembly 6. release |
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bacteriophage Penetration/uncoating
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occur together, sheath inject like needle, linear DNA converted to circular DNA at viral cos sites
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bacteriophage synthesis
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gene expression - 3 classes of mRNA (intmd-early, delayed-early, late), host cell DNA-dependent RNA polymerase required for all activities
Replication - early replication (theta forms, two replication forks), Late replication (rolling circle) |
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bacteriophage assembly
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genome packaging (heads adssembled first, concatameric DNA threated into head and cut at cos site)
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Genetic regulation - lambda genome promotors
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Principle: PL (transcribe to left) and PR (transcribe to right)
Secondary: P'R over half genome encodes for structural genes |
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PL promotor and its genes
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N protein: anti-terminator - continue trasncription past normal point
Xis: required for prophage exist from DNA host Int: required for prophage integration into host DNA and exit DNA |
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PR promotor and its genes (early-late regulation)
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Cro: regulator of gene expression
cII: unlocks 'hidden' gene promotrs that are normally not transcribed O protein P protein Q protein: anti-terminator |
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bacteriphage - intermediate early transciption
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Cro protein from PR promotoe
N Protein - transcription from PL stop at en dof N protein gene, transcription from PR stop at end of cro gene - N causes to continue past (anti-terminator) |
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delayed-early transcription
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where the commitment or lysis or lysogeny occurs
N protein anti-termination New transcripts: PL - xis, int; PR - cII, O, P, Q |
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late gene transcription
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happens after DNA replication
Q protein - anti-terminator Cro protein kicks into actio - binds to operator elements on PL and PR --> blocks further transcription, phage construction |
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cII protein
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unlocks 'hidden' gene promotors (Pre - repressor protein, Pint - integration protein)
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Pre promotor
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1. directs transcription of cI gene --> expression of cI protein
2. promotes transcription that are antisense to PR transcripts for cro protein --> cro mRNA cna't be processed into protein |
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cI protein
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binds to OL and OR, stopping early protein that would lead to late proteins but would also lead to own synthesis so...also unlocks another hidden promotor (PRM) so only transcription of cI transcribed
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Pint promotor
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Int protein (integrase)
if cII present, lots Int made prophage inserts at specific location @ attlambda locus |
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lysis/lysogeny of bacteriophage
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cII makes judgement of level
lots cII - cI produced that inibits other proteins from being expressed to lysogeny little cII - cro protein take charge b/c little cI --> inhibit others --> lysis, lytic |
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What detemined cII levels?
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host proteases degrade cII - host protease increases when cell is healthy --> replicate --> lysis
cIII protein can protect cII from some degradation |
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How to exist lysogeny
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Stress (environment bad so virus should find new host)
Xis and Int proteins used |
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lysogenic conversion
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when virus changed properties of its bacterial host
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Properties of concerous cells
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can divide into 3/4 daughter cells, don't attach as tightly to extracellular matrix, lose specific function, higher insult survival, higher nutrient demand, unorganized, abnormal nuclei
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oncogenic
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carcinogenic - something that causes cancer
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immortalized cells
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cells that are able to replication beyond their 'normal' number of replications - number differs with cell type
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transformed cells
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subclass of immortalized cells that have become cancerous
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Classes most commonly associated with cancer
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I (DNA): Adenovirus, Herpesviridaw, Papillomaviridae
VI (RNA): Retroviridae Hepatitis viruses: Hep B (VII) and Hep C (IV) |
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Co-factors (contributing factors)
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diet, exposure to chemicals, physical activity, tobacoo and alcohol use, heredity, home environment, exposure to UV, infectious disease history
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2 main mechanisms to induce Oncogenis
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1. Disrupting host genetic integrity - directly alter genes)
2. Interacting with host cell proteins involved in the cell cycle |
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ways viruses disrupt host genome integrity (3 mechanisms)
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1. direct integration (retroviridae)
2. viral replication via its own ori (herpesvirdae, papillomaviridae) 3. non-homologous recombination (Adenoviridae, polymavirdae) |
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Major know targets for interference/disruption in cell cycle
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p53, Rb
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viral disruption of p53
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p53 produced when cells sustain damage, oncogenic virus disrupts p53 with E6 protein
E6 bind to p53 and prohibit it from interacting --> signal for destruction |
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rb
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constructive cell cycle regulator
binds to E2F --> no cell cycle progrssion |
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Plant viruses common symptoms
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moasaicism (blotchiness and deformation), chlorosis (spots), necrosis (dead areas)
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Hypoplasia
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retardation of growth, accompanied by mosaicism
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hyperplasia
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excessive cell growth (can --> cancer)
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Plant immune system
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passive, physical barriers, chemical barriers,
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Plant immunity when attacked
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Hypersensitive response, methyl salicylate signaling
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Hypersensitive repsonse
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plant produces arsenal of protesases that recognize proteins from invader (PR proteins)
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Methyl Salicylate signaling
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pheromone (mint) released into air, used as signal to warn other plants and recruit insects
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RNA silencing
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suppressing RNA expression with other RNA segments
name varies by organism require dsRNA |
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VIGS start (viral induced gene silencing)
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RNA virus replicates, producing mRNA molecules that exist in dsRNA form. plant 'senses' this --> silencing of viral mRNA
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Sources of viral dsRNA: RNA viruses
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most common: replicative form (RF) of RNA virus bends back onot itself, forming dsRNA
less common: retrotransposons (retrovirus-like) integrate into DNA and generate temporary dsRNA from terminal repeat binding |
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sources of viral dsRNA: plant DNA viruses (less common)
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Pararetroviruses: only dsDNA virus on plants, mRNA has TR which pari forming dsRNA
Geminivirus: ssDNA forms rolling circle and transcription is bidirectional, forming dsRNA viroid NA tends to form hairpins |
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VIGS - plant fights back - Primary signal pathway
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DCL1 and DCL2 (dicer enzymes in the nucleus) bind --> to cytoplasm --> find dsRNA and cleave to produce small-interfering RNA (siRNA) --> siRNA unwind by helicase and combine with protein into RNA-inducing slencing complex (RISC)--> binds to viral mRNA, degraded
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VIGS - plant fights back - secondary signal pathway
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amplify primary signal, --> viral mRNA degradation
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VIGS - effect spreads
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signal for VIGS transmitted throughout plant (Green flourescent protein experiment) with 21-nt siRNA moving from cell to cell in plasmodesmata
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VIGS - systematic immunity process
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1. Bind to siRNA (P19 from tombusviruses)
2. inactive dicer (helper component protease [HcPro] from potyviruses) 3. Bind to diRNA (tombusvirus) |
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syndrome
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group of symtpoms that are suggestive of a particular condition
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AIDS definition
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26 symptoms and T-cell count (less than 14% lymphocytes)
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Problem with Africa/AIDS facts
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Bangui definition (Africa 'test' = visual symptoms - diagnosis not universal), science different in multiple places, 'orphan' definition, multiple ways to do estimates
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Face of AIDS in the US
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female, non-white (hispanic), poor, uneducated, SE region of US
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Six hypothesis for the cause of AIDS
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1. 2 stage model
2. HIV 3. Drug-AIDS (chemical) 4. Co-factor (HIV subviral + DNA helper) 5. Multifacotrial - malnutrition, HIV, etc. 6. viral overload - too many latent viruses --> HIV |
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HIV overview
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RNA --> DNA --> RNA --> protein
retroviral RNA integrated into the DNA of host as a provirus - once integrated is in for life |
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2 stands of HIV
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HIV-1: most common, M(main)/N(new)/O(outlier) groups, 11 subtypes
HIV-2: less cytopathic, reproduces slowly |
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first documented cases
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1959 - Africa bantu man
1969 - US 15 yr old prostitute 1976 - Europe Danish surgeon |
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biological factos of HIV transmission
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other STD present - breach in mucosal defenses
low ratews of male circumcision viral load of infected person |
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Behavioral/Social factors of HIV transmission
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condom use, multiple serial partners, overlapping partners, sex networks, age mixing, povert and women status/dependence
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HIV infection
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1.Dendritic cells - APC's pick up and migrate to lymphoid tissues - jump to CD4+ T cells
2. Macrphages - APCs 3. reduce CD4+ T cells |
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Nef
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prohibits CD4 receptors from being displayed on CD4 surface
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Vpu
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binds to receptors and yank them back down so not expressed
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HIV symptoms/stages
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1. Acute infection: 2-8 weeks, DC infected and transfered to CD4+Tcells, most highly infectious, CD8+ Tcells (killer T) destroy HIV, B cells produce antibodies (serocovnersion) --> rebound CD4 slightly
2. Asymptomatic Stage: 3-??yrs, antibodies temporary lock on HIV replication, CD4 slowly drop, HIV mutating 3. Symptomativ stage: immune system crashes 4. AIDS: CD4 less than 200cell/mL --> death |
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3 classes of treatment
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Nukes (mimick nucleotides), non-nukes(intefere with RT enzyme), protease inhibitors (stop cleavage)
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Why no HIV vaccine?
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don't know how vaccines work in general, dont know enough about retroviruses, HIV mutates, HIV immune responses short lived, money sources reluctant
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Why is AIDS still global threat?
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vaccine no where in sight, drug therapies expensive and sometime ineffective, lack of global infrastructure, no specific constant symptom, social/emotion dimensions
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Prion
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Protein, self-replicating
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TSE
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disease caused by Prions, Transmissible Spongiform Encephalopathy
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Prion replication
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bind with and alter the structure of homologous normal proteins
Normal state = more alpha helices, Prion state = more beta sheets |
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Genetic transmission
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autosomal dominant condition
Gene: prnp - codes for a cell surface glycoprotein PrPc (normal form), PrPsc (prion form) mutations in the gene cause prion disease |
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non-genetic transmission
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ingestion of contaminated food, Iatrogenic (surgery)
immune system propogate disease regardless of entry (spleen big, B cells, DC) |
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Why no immun response for prion disease?
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PrPc is a normal body protein, immune system can't distinguish from PrPc and PrPsc
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Prion disease symptoms - non-human TSE
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animals scrap against trees/fences, skiddish/nervous, can't walk straight or balance, complete loss of appetite
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Prion disease symptoms - human TSE - classic CJD
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68 years death, 4-5 months duration of illness, dementia, early neurologic signs, flourid plaques rare
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Prion disease symptoms - human TSE - variant CJD
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28 years death, 13-14 months duration of illness, prominent psychiatric/behavioral symptoms, painful dyethesisass, delayed neruologic signs, lots flourid plaques
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