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73 Cards in this Set

  • Front
  • Back
temperate phage
phage that can choose to conduct lysis or lysogeny in the host cell
phage genome that is intercalated into th host genome
bacteria that contains the phage DNA, potential host
bacteriophage Replication cycle stages
1. attachment (adsorption) - docks with distal tail fibers
2/3. Penetration/uncoating - occur together
4. Synthesis - gene expression and replication
5. Assembly
6. release
bacteriophage Penetration/uncoating
occur together, sheath inject like needle, linear DNA converted to circular DNA at viral cos sites
bacteriophage synthesis
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)
bacteriophage assembly
genome packaging (heads adssembled first, concatameric DNA threated into head and cut at cos site)
Genetic regulation - lambda genome promotors
Principle: PL (transcribe to left) and PR (transcribe to right)
Secondary: P'R
over half genome encodes for structural genes
PL promotor and its genes
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
PR promotor and its genes (early-late regulation)
Cro: regulator of gene expression
cII: unlocks 'hidden' gene promotrs that are normally not transcribed
O protein
P protein
Q protein: anti-terminator
bacteriphage - intermediate early transciption
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)
delayed-early transcription
where the commitment or lysis or lysogeny occurs
N protein anti-termination
New transcripts: PL - xis, int; PR - cII, O, P, Q
late gene transcription
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
cII protein
unlocks 'hidden' gene promotors (Pre - repressor protein, Pint - integration protein)
Pre promotor
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
cI protein
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
Pint promotor
Int protein (integrase)
if cII present, lots Int made
prophage inserts at specific location @ attlambda locus
lysis/lysogeny of bacteriophage
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
What detemined cII levels?
host proteases degrade cII - host protease increases when cell is healthy --> replicate --> lysis
cIII protein can protect cII from some degradation
How to exist lysogeny
Stress (environment bad so virus should find new host)
Xis and Int proteins used
lysogenic conversion
when virus changed properties of its bacterial host
Properties of concerous cells
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
carcinogenic - something that causes cancer
immortalized cells
cells that are able to replication beyond their 'normal' number of replications - number differs with cell type
transformed cells
subclass of immortalized cells that have become cancerous
Classes most commonly associated with cancer
I (DNA): Adenovirus, Herpesviridaw, Papillomaviridae
VI (RNA): Retroviridae
Hepatitis viruses: Hep B (VII) and Hep C (IV)
Co-factors (contributing factors)
diet, exposure to chemicals, physical activity, tobacoo and alcohol use, heredity, home environment, exposure to UV, infectious disease history
2 main mechanisms to induce Oncogenis
1. Disrupting host genetic integrity - directly alter genes)
2. Interacting with host cell proteins involved in the cell cycle
ways viruses disrupt host genome integrity (3 mechanisms)
1. direct integration (retroviridae)
2. viral replication via its own ori (herpesvirdae, papillomaviridae)
3. non-homologous recombination (Adenoviridae, polymavirdae)
Major know targets for interference/disruption in cell cycle
p53, Rb
viral disruption of p53
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
constructive cell cycle regulator
binds to E2F --> no cell cycle progrssion
Plant viruses common symptoms
moasaicism (blotchiness and deformation), chlorosis (spots), necrosis (dead areas)
retardation of growth, accompanied by mosaicism
excessive cell growth (can --> cancer)
Plant immune system
passive, physical barriers, chemical barriers,
Plant immunity when attacked
Hypersensitive response, methyl salicylate signaling
Hypersensitive repsonse
plant produces arsenal of protesases that recognize proteins from invader (PR proteins)
Methyl Salicylate signaling
pheromone (mint) released into air, used as signal to warn other plants and recruit insects
RNA silencing
suppressing RNA expression with other RNA segments
name varies by organism
require dsRNA
VIGS start (viral induced gene silencing)
RNA virus replicates, producing mRNA molecules that exist in dsRNA form. plant 'senses' this --> silencing of viral mRNA
Sources of viral dsRNA: RNA viruses
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
sources of viral dsRNA: plant DNA viruses (less common)
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
VIGS - plant fights back - Primary signal pathway
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
VIGS - plant fights back - secondary signal pathway
amplify primary signal, --> viral mRNA degradation
VIGS - effect spreads
signal for VIGS transmitted throughout plant (Green flourescent protein experiment) with 21-nt siRNA moving from cell to cell in plasmodesmata
VIGS - systematic immunity process
1. Bind to siRNA (P19 from tombusviruses)
2. inactive dicer (helper component protease [HcPro] from potyviruses)
3. Bind to diRNA (tombusvirus)
group of symtpoms that are suggestive of a particular condition
AIDS definition
26 symptoms and T-cell count (less than 14% lymphocytes)
Problem with Africa/AIDS facts
Bangui definition (Africa 'test' = visual symptoms - diagnosis not universal), science different in multiple places, 'orphan' definition, multiple ways to do estimates
Face of AIDS in the US
female, non-white (hispanic), poor, uneducated, SE region of US
Six hypothesis for the cause of AIDS
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
HIV overview
RNA --> DNA --> RNA --> protein
retroviral RNA integrated into the DNA of host as a provirus - once integrated is in for life
2 stands of HIV
HIV-1: most common, M(main)/N(new)/O(outlier) groups, 11 subtypes
HIV-2: less cytopathic, reproduces slowly
first documented cases
1959 - Africa bantu man
1969 - US 15 yr old prostitute
1976 - Europe Danish surgeon
biological factos of HIV transmission
other STD present - breach in mucosal defenses
low ratews of male circumcision
viral load of infected person
Behavioral/Social factors of HIV transmission
condom use, multiple serial partners, overlapping partners, sex networks, age mixing, povert and women status/dependence
HIV infection
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
prohibits CD4 receptors from being displayed on CD4 surface
binds to receptors and yank them back down so not expressed
HIV symptoms/stages
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
3 classes of treatment
Nukes (mimick nucleotides), non-nukes(intefere with RT enzyme), protease inhibitors (stop cleavage)
Why no HIV vaccine?
don't know how vaccines work in general, dont know enough about retroviruses, HIV mutates, HIV immune responses short lived, money sources reluctant
Why is AIDS still global threat?
vaccine no where in sight, drug therapies expensive and sometime ineffective, lack of global infrastructure, no specific constant symptom, social/emotion dimensions
Protein, self-replicating
disease caused by Prions, Transmissible Spongiform Encephalopathy
Prion replication
bind with and alter the structure of homologous normal proteins
Normal state = more alpha helices, Prion state = more beta sheets
Genetic transmission
autosomal dominant condition
Gene: prnp - codes for a cell surface glycoprotein
PrPc (normal form), PrPsc (prion form)
mutations in the gene cause prion disease
non-genetic transmission
ingestion of contaminated food, Iatrogenic (surgery)
immune system propogate disease regardless of entry (spleen big, B cells, DC)
Why no immun response for prion disease?
PrPc is a normal body protein, immune system can't distinguish from PrPc and PrPsc
Prion disease symptoms - non-human TSE
animals scrap against trees/fences, skiddish/nervous, can't walk straight or balance, complete loss of appetite
Prion disease symptoms - human TSE - classic CJD
68 years death, 4-5 months duration of illness, dementia, early neurologic signs, flourid plaques rare
Prion disease symptoms - human TSE - variant CJD
28 years death, 13-14 months duration of illness, prominent psychiatric/behavioral symptoms, painful dyethesisass, delayed neruologic signs, lots flourid plaques