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62 Cards in this Set

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Infection of Animals - docking
Multistage process that may bind 103 receptors - low affinity adhesion ("rolling")(1st contact with carbs), primary receptor binding (usually protein), secondary/co-receptor binding proofreading
Influenza docking (animal)
docks with only 1 receptor, variations in H binding abilities dictate host range in influenza virus
Interactions: Virus = hemaglutin; Cell = N-acetylneuraminic acid (sailic acid sugar)
HIV docking (animal)
envelop virus, makes 3 docking contacts
1. Low affinity (rolling): Virus = cyclophilin A, Cell = heparan
2. Primary receptor: Virus = gp120 (bind with CD4), cell = CD4 (on helper T cells)
3. Co-receptor: Virus = gp120, cell = CCR5 or CXCR4
Once gp120 contact both, gp41 (different glycoprotein) acts as syringe to inject genetic material into target cell
Dengue fever docking (animal)
uses host antibody responses against it, antibodies bind in attempt to neutralize virus, cell with antibody receptors (Fc receptors) bind to virus thinking it is neutralized
After docking...nucleic acid into cell via 2 ways? (animal viruses)
Membrane fusion (fuse with bilayer) and endocytosis (plasma membrane buds in and pinches off, vesicle fuse with endosome)
Once inside...(animal viruses)
enters nucleocapsid - if naked then rapid association with polymerase/ribosomes
Infection highly inefficient
How can virus infect plant cells?
Only if disruption in cell wall and cytoplasm exposed - via mechanical means (wind) or animal vector (herbivore eats) --> specificity of virus b/c of vector
Once inside plant cell...
cytoplasmic proteins and ions cause virus to uncoat, plasmodesmata serves as highway between cells, virus moves along plasmodemata
Three strategies for injecting nucleic acid into plant cell after docking
1. Sheath injection (head-tail DNA bacteriophage) - sheath as needle with tail pins anchor
2. Page-pilius retraction (DNA phages) - dock with pili, then pili pulled into cell where virus uncoats
3. 'A-protein' facilitations (RNA phages) - attached to pili, but doesn't uncoat inside, rather 'A-protein' penetrates pilus membrane and escorts nucleic acid into cell pulling it like trailer
Replication Cycle Stages
Attachment, Penetration, Uncoating, Synthesis, Assembly, Release (APUSAR)
DNA replication
DNA strand antiparallel, semiconservative replication
Use DNA polymerase - move 5'--> 3' (add base to 3' end of original)
DNA replication problem of how solve so copy off both strands...
1. Leading (continuous)/Lagging Strand (discontinuous, Okazaki fragment with DNA ligase)
2. Temporally Discontinuous (one strand up one side and then back down other side) - can be unstable for large genomes
DNA replication problem of how start (DNA polymerse can't start from scratch)
RNA primers - use host cell RNA polymerse to generate primer, DNA latch on to primers which are later digested off
"End-Replication" problem
DNA replication - once RNA primer digested off, DNA polymerase can't work back to fill in gap, thus genome shrinks every cycle
Eukaryotes solution - repetitive ends (telomeres regenerate them)
Prokaryotes solution - circular genomes
Viruses solution - multiple
Class I viruses: dsDNA circular
Model: Papovavirus
single ori, RNA primers used, 2 replication forks (2 leading, 2 lagging strands), theta-form intermediate, forks converge to fill in RNA primer spots, --> 2 circles linked, Topoisomerases seperate 2 circles
Infection of Animals - docking
Multistage process that may bind 103 receptors - low affinity adhesion ("rolling")(1st contact with carbs), primary receptor binding (usually protein), secondary/co-receptor binding proofreading
Influenza docking (animal)
docks with only 1 receptor, variations in H binding abilities dictate host range in influenza virus
Interactions: Virus = hemaglutin; Cell = N-acetylneuraminic acid (sailic acid sugar)
HIV docking (animal)
envelop virus, makes 3 docking contacts
1. Low affinity (rolling): Virus = cyclophilin A, Cell = heparan
2. Primary receptor: Virus = gp120 (bind with CD4), cell = CD4 (on helper T cells)
3. Co-receptor: Virus = gp120, cell = CCR5 or CXCR4
Once gp120 contact both, gp41 (different glycoprotein) acts as syringe to inject genetic material into target cell
Dengue fever docking (animal)
uses host antibody responses against it, antibodies bind in attempt to neutralize virus, cell with antibody receptors (Fc receptors) bind to virus thinking it is neutralized
After docking...nucleic acid into cell via 2 ways? (animal viruses)
Membrane fusion (fuse with bilayer) and endocytosis (plasma membrane buds in and pinches off, vesicle fuse with endosome)
Once inside...(animal viruses)
enters nucleocapsid - if naked then rapid association with polymerase/ribosomes
Infection highly inefficient
How can virus infect plant cells?
Only if disruption in cell wall and cytoplasm exposed - via mechanical means (wind) or animal vector (herbivore eats) --> specificity of virus b/c of vector
Once inside plant cell...
cytoplasmic proteins and ions cause virus to uncoat, plasmodesmata serves as highway between cells, virus moves along plasmodemata
Three strategies for injecting nucleic acid into plant cell after docking
1. Sheath injection (head-tail DNA bacteriophage) - sheath as needle with tail pins anchor
2. Page-pilius retraction (DNA phages) - dock with pili, then pili pulled into cell where virus uncoats
3. 'A-protein' facilitations (RNA phages) - attached to pili, but doesn't uncoat inside, rather 'A-protein' penetrates pilus membrane and escorts nucleic acid into cell pulling it like trailer
Replication Cycle Stages
Attachment, Penetration, Uncoating, Synthesis, Assembly, Release (APUSAR)
DNA replication
DNA strand antiparallel, semiconservative replication
Use DNA polymerase - move 5'--> 3' (add base to 3' end of original)
DNA replication problem of how solve so copy off both strands...
1. Leading (continuous)/Lagging Strand (discontinuous, Okazaki fragment with DNA ligase)
2. Temporally Discontinuous (one strand up one side and then back down other side) - can be unstable for large genomes
DNA replication problem of how start (DNA polymerse can't start from scratch)
RNA primers - use host cell RNA polymerse to generate primer, DNA latch on to primers which are later digested off
"End-Replication" problem
DNA replication - once RNA primer digested off, DNA polymerase can't work back to fill in gap, thus genome shrinks every cycle
Eukaryotes solution - repetitive ends (telomeres regenerate them)
Prokaryotes solution - circular genomes
Viruses solution - multiple
Class I viruses: dsDNA circular
Model: Papovavirus
single ori, RNA primers used, 2 replication forks (2 leading, 2 lagging strands), theta-form intermediate, forks converge to fill in RNA primer spots, --> 2 circles linked, Topoisomerases seperate 2 circles
Class I Viruses: dsDNA circular/linear
Model: Herpesviridae (herpes simplex, EBV) and Siphoviridae (bacteriophage lambda)
linear while in virion, circular upon infection, use concatemer strategy (solve end-replication problem)
Early Phase: ori, 2 replication forks generated going in opposite directions, theta-form intermediates - 'circle amplification' phase
Late phase: 'rolling circle' replication, concatemers result and cleaved into segments, functional genomes packaged and exported in virions
Class I Viruses: dsDNA linear
Model: Adenoviridae and Poxviridae
Temorally discontinuous replication
Adenoviridae replication
Ori at end (tails), may use double or single ori
Use protein (pTp) instead of RNA primer to initiate replication
sometimes form 'pan-handle' intermediates
Poxviridae
complementary sequences fold back on one another
Use site-specific nicking of DNA at one or two sites
Nicking site = ori
DNA polymerase latches on and goes
Special folding may result ot make replication more efficient
concatemers result if only 1 nicking site is used
Class II viruses: ssDNA circular
Model: Microviridae (thetaX174)
dsDNA intermediate before replicate (Replicative form [RF])
mechanism of replication unknown
Class II Viruses: ssDAn linear
Model: Parvoviridae (autonomous viruses and satellite)
either + or - strand
convert to dsDNA for replication
genome doubles back on self (sequence is self-complementary)
nicking at final steps
Dependecy vs. Autonomy
Autonomy contigent on genome size - large genome is more autonomous
Class I Viruses: dsDNA circular/linear
Model: Herpesviridae (herpes simplex, EBV) and Siphoviridae (bacteriophage lambda)
linear while in virion, circular upon infection, use concatemer strategy (solve end-replication problem)
Early Phase: ori, 2 replication forks generated going in opposite directions, theta-form intermediates - 'circle amplification' phase
Late phase: 'rolling circle' replication, concatemers result and cleaved into segments, functional genomes packaged and exported in virions
Class I Viruses: dsDNA linear
Model: Adenoviridae and Poxviridae
Temorally discontinuous replication
Adenoviridae replication
Ori at end (tails), may use double or single ori
Use protein (pTp) instead of RNA primer to initiate replication
sometimes form 'pan-handle' intermediates
Poxviridae
complementary sequences fold back on one another
Use site-specific nicking of DNA at one or two sites
Nicking site = ori
DNA polymerase latches on and goes
Special folding may result ot make replication more efficient
concatemers result if only 1 nicking site is used
Class II Viruses: ssDNA circular
Model: Microviridae (thetaX174)
before replicate must go through dsDNA intermediate (replicative form [RF])
mechanism of replication unknown
Class II Viruses: ssDNA linear
Model: Parvoviridae (true viruses and satellites)
+ or - strand
convert to dsDNA for replication
genome doubles back on itself (sequence is self-comlementary)
nicking in final steps
Dependency vs. Autonomy
Antonomy contingent on genome size - larger genome is more autonomous
RNA replication
RNA strands antiparallel, polymerase 5'-->3' (start at 3' end of strand), virus bring replicases along
ssRNA temporaily use dsRNA as intermediate
ssRNA genomes produce 'antigenome' strands that are complimentary to fulfill dsRNA intermediate requirement
No RNA primer or pTp - sequences at end of strands initiate replication
Defective-Interfereing (DI) Nucleic acid
Both DNA and RNA viruses (RNA studied)
'Replication Error' from in complete replication (crossing over) or aborted replications (polymerase 'falls off')
DI genesis: Panhandle Intermediates and crossing over mishap (8 loop cut off)
Multiple types of DI
Class III Viruses: dsRNA
Model: Reoviridae (capsid within capsid)
Unique: nucleic acid never completely uncoats after entering cell, stays in special viral package, only mRNA exists (why replicate through mRNA intermediate)
RDRP generates mRNA
mRNA serves as both mRNA and + for dsRNA
RNA replication
RNA strands antiparallel, polymerase 5'-->3' (start at 3' end of strand), virus bring replicases along
ssRNA temporaily use dsRNA as intermediate
ssRNA genomes produce 'antigenome' strands that are complimentary to fulfill dsRNA intermediate requirement
No RNA primer or pTp - sequences at end of strands initiate replication
Defective-Interfereing (DI) Nucleic acid
Both DNA and RNA viruses (RNA studied)
'Replication Error' from in complete replication (crossing over) or aborted replications (polymerase 'falls off')
DI genesis: Panhandle Intermediates and crossing over mishap (8 loop cut off)
Multiple types of DI
Class III Viruses: dsRNA
Model: Reoviridae (capsid within capsid)
Unique: nucleic acid never completely uncoats after entering cell, stays in special viral package, only mRNA exists (why replicate through mRNA intermediate)
RDRP generates mRNA
mRNA serves as both mRNA and + for dsRNA
What is dsRNA made from? (Class III viruses)
mRNA codes for its own polymerase
1971 Shonberg experiment with [3H]uridine
+ sense mRNA used as template
Class IV Viruses
Model: Picornaviridae
+ sense ssRNA serves as its own mRNA
uses dsRNA intermediate
Special features: 5' end - VPg protein (interacts with host elongation factors); 3' end - poly-A tail (polymerase attachment)
Picornavirdae Replication
Genome (+ sense) enters cytoplasm, associates with cytoplsmic membranes, proteins transcribed, - sense strand generated forming replication intermediate (RI), mostly + sense RNA is made but some - sense RNA for more RI, VPg proteins attach (mechanism unknown), + sense strands exported in virions
Class V Viruses: - sense ssRNA
Mononegavirals - non-segmented genomes, 4 families --> bornaviridae, filoviridae, paramyxoviridae, rhabdaviridae
Segmentes genome families (3) --> arenviridae, bunyviridae, orthomyxoviridae
Model: Rhabdoviridae (rabies) and Orthomyxoviridae (influenza)
some segmented, some not
b/c - sense, must utilize RDRP in virion
Rhabdovirus Nucleocapsid 3 components
Nucleoprotein (NP) - associated with RNA
P protein (phosphoprotein)
L protein (large p.) - catalytic component
Rhabdovirus replication
genome (- sense) enters cytoplasm, replications take place in cytoplasm or nucleus, proteins transcribed, + sense strand generated forming replication intermediate (RI), mostly - sense RNA made but some + sense RNA fro more RI
Orthomyxovirus 4 components
NP (structural protein), PA,PB1,PB2 (transcription/replication complex proper - combine to form complex)
Orthomyxovirus replication
each segment replicate independently, similar to rhabdovirus, virus must contain 1 of each segment to be infection (multiple copies usually present)
Sub viral entities 3 types of cell entry
Viroids (ener as naked nucleic acid), satellite viruses (through help of master virus), and nucleic acid
How sub viral entities replciate without own enzymes?
Viroid - co-op plant cell enzyme
Satellites - host enzyme, master virus proteins
Host-cell DNA-dependent RNA-polymerase = likely enzyme of replication
Sub viral entities replication process
1 - nucleic acid circularizes
2 - RNA polymerase II initiate replication from uncharacterized origin
3 - rolling circle replication, concatemres produced
4 - self-cutting with ribozyme
5 - antigenome circularizes and polymerase replicates the antigenome
6 - tolling circle replication, concatemers produced
7 - selff-cutting ribozyme
8 - nucleic acids exported
Ribozyme
genetic sequences that adopt 3D structure, can automatically cleave nucleic acids around them at specific sites, cleave subviral genome concatemer into specific lengths, harbor ligase activites in sunvirals