Download Characteristics of Viruses

MICROBIOLOGY
WITH DISEASES BY TAXONOMY, THIRD EDITION
Chapter 13
Characterizing and Classifying Viruses, Viroids, and Prions
Lecture prepared by Mindy Miller-Kittrell, University of Tennessee, Knoxville
Copyright © 2011 Pearson Education Inc.
Characteristics of Viruses
• Virus
– Miniscule, acellular, infectious agent having either DNA or RNA
– Causes many infections of humans, animals, plants, and
bacteria
– Causes most of the diseases that plague the industrialized world
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Characteristics of Viruses
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Cannot carry out any metabolic pathway
Neither grow nor respond to the environment
Cannot reproduce independently
Recruit the cell’s metabolic pathways to increase their numbers
No cytoplasmic membrane, cytosol, organelles (with one exception)
Have extracellular and intracellular state
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Characteristics of Viruses
• Extracellular State
– Called virion
– Protein coat (capsid) surrounding nucleic acid
– Nucleic acid and capsid also called nucleocapsid
– Some have phospholipid envelope
– Outermost layer provides protection and recognition sites for
host cells
• Intracellular State
– Capsid removed
– Virus exists as nucleic acid
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Virions, complete virus particles
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Figure 13.1
Characteristics of Viruses
• Genetic Material of Viruses
– Show more variety in nature of their genomes than do cells
– Primary way scientists categorize and classify viruses
– May be DNA or RNA, but never both
– Can be dsDNA, ssDNA, dsRNA, ssRNA
– May be linear and segmented or single and circular
– Much smaller than genomes of cells
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The relative sizes of genomes
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Figure 13.2
Characteristics of Viruses
• Hosts of Viruses
– Most viruses infect only particular host’s cells
– Due to affinity of viral surface proteins for complementary
proteins on host cell surface
– May be so specific they only infect particular kind of cell in a
particular host
– Generalists – infect many kinds of cells in many different hosts
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Some examples of hosts of viral infections
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Figure 13.3
Sizes of selected virions
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Figure 13.4
Characteristics of Viruses
• Capsid Morphology
– Capsids
– Protein coats that provide protection for viral nucleic acid and
means of attachment to host’s cells
– Composed of proteinaceous subunits called capsomeres
– Capsomere may be made of single or multiple types of
proteins
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The shapes of virions
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Figure 13.5
The complex shape of bacteriophage T4
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Figure 13.6
Enveloped viruses
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Figure 13.7
Characteristics of Viruses
• The Viral Envelope
– Acquired from host cell during viral replication or release
– Envelope is portion of membrane system of host
– Composed of phospholipid bilayer and proteins
– Some proteins are virally coded glycoproteins (spikes)
– Envelope’s proteins and glycoproteins often play role in host
recognition
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Classification of Viruses
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Table 13.2-1
Classification of Viruses
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Table 13.2-2
Viral Replication
• Dependent on hosts’ organelles and enzymes to produce new virions
• Lytic replication
– Replication cycle usually results in death and lysis of host cell
• Stages of lytic replication cycle
– Attachment
– Entry
– Synthesis
– Assembly
– Release
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Viral Replication
Animation: Viral Replication: Overview
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The lytic replication cycle in bacteriophage
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Figure 13.8
Pattern of virion abundance in lytic cycle
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Figure 13.9
Viral Replication
Animation: Viral Replication: Virulent Bacteriophages
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Viral Replication
• Lysogeny
– Modified replication cycle
– Infected host cells grow and reproduce normally for generations
before they lyse
– Temperate phages
– Prophages – inactive phages
– Lysogenic conversion results when phages carry genes that alter
phenotype of a bacterium
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Bacteriophage lambda
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Figure 13.10
The lysogenic replication cycle in bacteriophages
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Figure 13.11
Viral Replication
Animation: Viral Replication: Temperate Bacteriophages
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Viral Replication
• Replication of Animal Viruses
– Same basic replication pathway as bacteriophages
– Differences result from
– Presence of envelope around some viruses
– Eukaryotic nature of animal cells
– Lack of cell wall in animal cells
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Viral Replication
• Replication of Animal Viruses
– Attachment of animal viruses
– Chemical attraction
– Animal viruses do not have tails or tail fibers
– Have glycoprotein spikes or other attachment molecules that
mediate attachment
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Three mechanisms of entry of animal viruses
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Figure 13.12
Viral Replication
• Replication of Animal Viruses
– Synthesis of animal viruses
– Each type of animal virus requires different strategy
depending on its nucleic acid
– DNA viruses often enter the nucleus
– RNA viruses often replicate in the cytoplasm
– Must consider
– How mRNA is synthesized
– What serves as template for nucleic acid replication
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Synthesis of proteins and genomes in animal RNA viruses
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Figure 13.13
Viral Replication
• Replication of Animal Viruses
– Assembly and release of animal viruses
– Most DNA viruses assemble in nucleus
– Most RNA viruses develop solely in cytoplasm
– Number of viruses produced depends on type of virus and
size and initial health of host cell
– Enveloped viruses cause persistent infections
– Naked viruses are released by exocytosis or lysis
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The process of budding in enveloped viruses
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Figure 13.14
Pattern of virion abundance in persistent infections
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Figure 13.15
Viral Replication
Animation: Viral Replication: Animal Viruses
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Viral Replication
• Replication of Animal Viruses
– Latency of animal viruses
– When animal viruses remain dormant in host cells
– May be prolonged for years with no viral activity
– Some latent viruses do not become incorporated into host
chromosome
– Incorporation of provirus into host DNA is permanent
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The Role of Viruses in Cancer
• Animal’s genes dictate that some cells can no longer divide and
those that can divide are prevented from unlimited division
• Genes for cell division “turned off” or genes inhibiting division
“turned on”
• Neoplasia
– Uncontrolled cell division in multicellular animal; mass of
neoplastic cells is tumor
• Benign vs. malignant tumors
– Metastasis
– Cancers
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The oncogene theory of the induction of cancer in humans
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Figure 13.16
The Role of Viruses in Cancer
• Environmental factors that contribute to the activation of oncogenes
– Ultraviolet light
– Radiation
– Carcinogens
– Viruses
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The Role of Viruses in Cancer
• Viruses cause 20–25% of human cancers
– Some carry copies of oncogenes as part of their genomes
– Some promote oncogenes already present in host
– Some interfere with tumor repression when inserted into host’s
repressor gene
– Specific viruses are known to cause ~15% of human cancers
– Burkitt’s lymphoma
– Hodgkin’s disease
– Kaposi’s sarcoma
– Cervical cancer
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Culturing Viruses in the Laboratory
• Culturing Viruses in Mature Organisms
– In bacteria
– In plants and animals
• Culturing Viruses in Embryonated Chicken Eggs
– Inexpensive, among the largest of cells, free of contaminating
microbes, and contain a nourishing yolk
• Culturing Viruses in Cell (Tissue) Culture
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Viral plaques in a lawn of bacterial growth on an agar plate
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Figure 13.17
Inoculation sites for the culture of viruses in eggs
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Figure 13.18
Culturing Viruses in the Laboratory
• Culturing Viruses in Cell (Tissue) Culture
– Consists of cells isolated from an organism and grown on a
medium or in a broth
– Two types of cell cultures
– Diploid cell cultures
– Continuous cell cultures
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An example of cell culture
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Figure 13.19
Are Viruses Alive?
• Some consider them complex pathogenic chemicals that lack the
characteristics of life
• Others consider them to be the least complex living entities because
they
– Use sophisticated methods to invade cells
– Have the ability to take control of their host cell
– Are able to replicate themselves
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Other Parasitic Particles: Viroids and Prions
• Characteristics of Viroids
– Extremely small, circular pieces of RNA that are infectious and
pathogenic in plants
– Similar to RNA viruses, but lack capsid
– May appear linear due to H bonding
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The RNA strand of the small potato spindle tuber viroid
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Figure 13.20
One effect of viroids on plants
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Figure 13.21
Other Parasitic Particles: Viroids and Prions
• Characteristics of Prions
– Proteinaceous infectious agents
– Cellular PrP protein
– Made by all mammals
– Normal structure with -helices called cellular PrP
– Prion PrP
– Disease-causing form with -sheets called prion PrP
– Prion PrP converts cellular PrP into prion PrP by inducing
conformational change
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Other Parasitic Particles: Viroids and Prions
Animation: Prions: Overview
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The two stable forms of prion protein (PrP)
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Figure 13.22
Other Parasitic Particles: Viroids and Prions
• Characteristics of Prions
– Normally, nearby proteins and polysaccharides force PrP into
cellular shape
– Excess PrP or PrP mutations result in formation of prion PrP
– Cause newly synthesized cellular PrP to refold into prion PrP
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Other Parasitic Particles: Viroids and Prions
Animation: Prions: Characteristics
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Other Parasitic Particles: Viroids and Prions
• Characteristics of Prions
– Prion diseases
– Fatal neurological degeneration, fibril deposits in brain, and
loss of brain matter
– Large vacuoles form in brain
– Characteristic spongy appearance
– Spongiform encephalopathies – BSE, vCJD, kuru
– Prions only destroyed by incineration or autoclaving in 1 N NaOH
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Brain with appearance typical in prion-induced diseases
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Figure 13.23
Other Parasitic Particles: Viroids and Prions
Animation: Prions: Disease
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