Chapter 5: Viruses and their multiplication Flashcards

1
Q

Virus description

A

genetic element that can multiply only in a living (host) cell
 Not living, not found on tree of life
 Obligate intracellular parasite: Needs host cell for energy, metabolic intermediates, protein synthesis
 Has its own nucleic acid genome

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2
Q

Virion

A

Virion- extracellular form of a virus
 Exists outside host and facilitates transmission from one host cell to another
 Replication/reproduction occurs only upon infection (entry into host cell)

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3
Q

Viral surface proteins

A

Capsid: the protein shell that surrounds the
genome of a virus
 Naked viruses (e.g., most bacterial and plant
viruses) have no other layers
 Enveloped viruses (e.g., many animal viruses) have
an outer layer consisting of a phospholipid bilayer
(from host cell membrane) and viral proteins
 Nucleocapsid: nucleic acid + protein in enveloped
viruses

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4
Q

V surface proteins significance

A

 Virion surface proteins important for host cell attachment and may include enzymes involved in infection/replication

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5
Q

virulent (lytic) infection

A

replicates and destroys host
 Host cell metabolism redirected to support multiplication and virion assembly

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6
Q

lysogenic infection

A

host cell genetically altered because viral genome becomes part of host genome

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7
Q

Viral genome

A

 either DNA or RNA genomes
 single-stranded or double-stranded
 usually smaller in size and gene content than cells

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8
Q

Group I:

A

double-stranded DNA viruses

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9
Q

Group II

A

single-stranded DNA viruses

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10
Q

Group III

A

double-stranded RNA viruses

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11
Q

Group IV

A

positive sense single-stranded RNA viruses

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12
Q

Group V

A

negative sense single-stranded RNA viruses

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13
Q

Group V

A

single-stranded RNA viruses with a DNA intermediate in their life cycle

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14
Q

Group VII

A

double-stranded DNA viruses with an RNA intermediate in their life cycle

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15
Q

beneficial virus examples

A

 e.g., Arabidopsis infected with plum pox virus
increases drought tolerance
 e.g., insect densovirus infection of rosy apple aphid
results in decreased size and offspring, but wings
form
 e.g., hepatitis G coinfection of HIV patients
decreases HIV replication and infectivity

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16
Q

virus size

A

Most viruses are smaller than prokaryotic cells; ranging from 0.02 to 0.3 μm
 Pandoravirus over 1 μm long
 Poliovirus (~28 nanometers) is size of ribosome

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17
Q

Virion Structure

A

 Some viruses only have one capsid protein
because small size of viral genomes restricts
number of proteins (e.g., tobacco mosaic virus)
 Capsids can be put together through selfassembly (spontaneous) or may require host
cell folding assistance

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18
Q

Capsomere

A

individual protein molecules
arranged in a precise and highly repetitive pattern
around the nucleic acid making up the capsid

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19
Q

 helical symmetry

A

: rod-shaped (e.g., tobacco mosaic virus or T M V)
 length determined by length of nucleic acid
 width determined by size and packaging of capsomeres

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20
Q

icosahedral symmetry

A

spherical
 20 triangular faces, 12 vertices; 5, 3, or 2 identical segments
 most efficient arrangement of subunits in a closed shell
 requires fewest capsomeres

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21
Q

Highly complex structures of virus

A

Virion contains several parts with their own shapes and symmetry
 Most complex are head-plus-tail bacteriophages (e.g., T4)
 Viruses of Acanthamoeba (e.g., Pandoravirus (ovoid with apical pore), Mimivirus (stargate)

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22
Q

 Enveloped Viruses characteristics

A

 have lipoprotein membrane surrounding nucleocapsid
 most (e.g., Ebola) use outer surface proteins to attach and infect
 relatively few enveloped plant or bacterial viruses because of cell walls surrounding cell membrane
 Entire virion enters animal cell during infection
 Enveloped viruses exit more easily

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23
Q

Envelope + fibrils functions

A

 Specificity and penetration controlled in part
by envelope biochemistry
 Fibrils: hairlike polymer structures that attract
amoeba hosts
 Apical pore and stargate function as portals to
release genome

24
Q

Virus enzymes

A

lysozyme
neuraminidases
nucleic acid polymerases

25
lysozyme
makes hole in cell wall to allow nucleic acid entry  also lyses bacterial cell to release new virions
26
neuraminidases (influenza)
 destroy glycoproteins and glycolipids  allows liberation of viruses from cell
27
nucleic acid polymerases
 RNA replicases: RNA-dependent RNA polymerases  Reverse transcriptase: RNA-dependent DNA polymerase in retroviruses
28
Virus culturing
 Bacterial viruses are easiest to grow (hosts in liquid medium or spread as “lawns” on agar and inoculated with virus).  Animal and plant viruses cultivated in tissue cultures (from animal organ in culture medium or hairy root-based system in liquid medium).
29
Titre
number of infectious virions per volume of fluid
30
Plaque assay description
 Plaques are clear zones of cell lysis that develop on lawns of host cells where successful viral infection occurs.  Calculate titre from # of plaques  Analogous to counting colonies  Similar process for animal viruses  Plants much harder: viruses must be purified and counted microscopically or through viral proteinspecific methods
31
Plaque assay mechanism
32
Why is the number of plaque-forming units (pfu) is always lower than direct counts by electron microscopy
 efficiency of infection usually much less than 100%  defective virions or conditions inappropriate for infectivity  Useful for estimating appropriate titre to yield plaques
33
Five steps of viral replication in a permissive (supportive) host
 attachment (adsorption) of the virion  penetration (entry, injection) of the virion nucleic acid  synthesis of virus nucleic acid and protein by host cell as redirected by virus  assembly of capsids and packaging of viral genomes into new virions  release of new virions from host cell
34
The Replication Cycle of a Lytic Bacterial Virus
35
one-step growth curve phases
virion numbers increase when cells burst -Eclipse phase: genome replicated, and proteins translated  Maturation: packaging of nucleic acids in capsids  Latent period: eclipse + maturation  Release: cell lysis, budding, or excretion  burst size: number of virions released
36
Most complex penetration mechanisms found intailed bacteriophages (e.g., T4)
 Virions attach to cells via tail fibers that interact with polysaccharides on E. coli LPS layer  Tail fibers retract, and tail pins contact cell wall  T4 lysozyme forms small pore in peptidoglycan  Tail sheath contracts, and viral DNA enters cytoplasm similar to syringe injection  Capsid stays outside
37
Prokaryotes possess mechanisms to diminish viral infections
Genome injection does not ensure infection  toxin-antitoxin molecules  antiviral CRISPR  restriction endonucleases: enzymes that cleave foreign DNA at specific sites  Some viruses have modified genome that is unaffected by restriction enzymes
38
 Production of T4 Virions and Release
 Virion synthesis takes <30 minutes and ends in release of new virions from lysed cell  Within 1 minute of entry, host-specific protein synthesis ends and phage-specific protein synthesis starts  T4 genome encodes three major sets of proteins: early, middle, and late proteins.  early proteins: enzymes needed for DNA replication and proteins that modify host enzymes to express viral genes  middle and late proteins: head and tail proteins and enzymes required to liberate mature phage particles
39
Time Course of Events in Phage T4 Infection
40
Production of T4 Virions and Release
 Genome is pumped into capsid under pressure using energy-linked packaging motor  Host cell metabolism produces viral proteins and supplies ATP
41
T4 packaging stages
 Empty proheads (bacteriophage head precursors) assembled  Packaging motor assembled at prohead opening and genome pumped into prohead using ATP  Motor discarded and capsid head sealed
42
T4 after packaging mechanism
 After head is filled, T4 tail, tail fibers, and other components are self-assembled  Late enzymes break membrane and peptidoglycan  Lysis occurs, 100+ virions released
43
Virulent
Viruses always lyse and kill host after infection
44
Temperate
Viruses establish long-term, stable relationship but are capable of virulence
45
Lysogeny
Temperate viruses can enter a stage where few viral proteins produced, viral genome is replicated with host chromosome and passed to daughter cells
46
Lysogen
host cell that harbors temperate virus - can result in lysogenic conversion with new genetic properties (e.g., virulence in pathogens)
47
Life cycle of a temperate phage
 examples: lambda and P1  in lysogeny, genome is integrated into bacterial chromosome forming prophage (viral DNA)  lysogeny maintained by phage-encoded repressor protein  Inactivation of repressor induces lytic stage (induction)  Viral DNA excised; phage early, middle, and late proteins produced; virions produced and host lyses  Cell stress (e.g., DNA damage) induces lytic pathway
48
3 key differences between Eu viruses
 Entire virion enters the animal cell  Eukaryotic cells contain a nucleus, the site of replication for many animal viruses  Viroplasms (membrane-bound viral factories) form in some eukaryotic cells to increase virion assembly rate and protect from host defense
49
Viral Infection of Animal Cells features (specificity)
 Studied in cell culture  Bind specific host cell receptors, typically used for cell-cell contact or immune function (e.g., poliovirus and HIV receptors)  Viruses often infect only certain tissues because different surface proteins expressed by different tissues/organs
50
Viral infection of animal cell mechanisms (entry)
Host cell entry occurs by fusion with cytoplasmic membrane or endocytosis  Uncoating occurs at the cytoplasmic membrane or in the cytoplasm  Viral DNA genomes enter nucleus, most viral RNA genomes are replicated or converted to DNA within nucleocapsid
51
animal Virion envelope assembly
 After genome packaging, many animal viruses must be enveloped  Occurs during exit through lysis or budding when virus picks up part of cell’s cytoplasmic membrane and uses it as part of envelope
52
Animal virion infection outcomes
 Virulent infection: lysis of host cell, most common  Latent infection: Viral DNA exists in host genome as provirus (similar to lysogeny) and virions are not produced; host cell is unharmed unless/until virulent pathway is triggered.  Persistent infections: slow release of virions from host cell by budding does not result in cell lysis.  Infected cell remains alive and continues to produce virus  Transformation: conversion of normal cell into tumor cell
53
Possible Effects of Animal Virus Infection of Host Cells diagram
54
Viral Infection of Plant Cells similarity to animal cells
Plant viruses share many animal viral traits (e.g., mostly RNA genomes, complete virion enters cell, viral factories form)
55
Major differences for plant viruses
Three major differences:  Wider host range  Mostly not enveloped  Transmission different
56
Plant viruse overview
Plant cell wall prevents entry by endocytosis and fusion  Viruses enter through wounds or penetration by insects, nematodes, fungi  Vectors: pests that transfer viruses to other host cell types  After entry, capsid removed, genome replicated, (in nucleus) new virions assembled  Movement proteins help viruses travel through plasmodesmata (channels) connecting cells; can infect entire plant V
57
Viral infection of plants mechanism