Chapter 13
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Transcript of Chapter 13
Chapter 13
Characterizing and Classifying Viruses, Viroids,
and Prions
Viruses• Cause many infections of
humans, animals, plants, and bacteria
• Cannot carry out any metabolic pathway
• Neither grow nor respond to the environment
• Cannot reproduce independently
• Obligate intracellular parasites
Characteristics of Viruses• Cause most diseases
that plague industrialized world
• Virus are miniscule, acellular, infectious agents having one or several pieces of DNA or RNA
• No cytoplasmic membrane, cytosol, or organelles (one exception)
• Have extracellular and intracellular states
Characteristics of Viruses• Extracellular state– Called virion– Protein coat (capsid)
surrounding nucleic acid–Nucleic acid and capsid
together are called the nucleocapsid
– Some have phospholipid envelope
–Outermost layer provides protection and recognition sites for host cells
• Intracellular state– Capsid removed– Virus exists as nucleic acid
Structure of Viruses
How Viruses Are Distinguished• Type of genetic material
they contain• Kinds of cells they attack
(host range)• Size of virus• Nature of capsid coat• Shape of virus• Presence or absence of
envelope
Genetic Material of Viruses
• Show more variety in nature of their genomes than do cells
• May be DNA or RNA; never both
• Primary way to categorize and classify viruses
• Can be dsDNA, ssDNA, dsRNA, ssRNA
• May be linear and composed of several segments or single and circular
• Much smaller than genomes of cells
Hosts of Viruses• Most only infect particular kinds
of host’s cells–Due to affinity of viral surface
proteins or glycoproteins (anti-receptors) for complementary proteins or glycoproteins on host cell surface (receptors)
• Generalists – infect many kinds of cells in many different hosts
Viral Hosts
Tobacco mosaic virus
Viral Hosts
T-even Bacteriophage
Viral Hosts
HIV
Figure 13.3d
Viral Hosts
Human Immunodeficiency virus
Sizes of Viruses
Capsid Morphology
• Capsids – protein coats that provide protection for viral nucleic acid and means of attachment to host’s cells
• Capsid composed of proteinaceous subunits called capsomeres
• Some capsids composed of single type of capsomere; others are composed of multiple types
Figure 13.5a
Viral Shapes
Helical
Figure 13.5b
Viral Shapes
Polyhedral
Figure 13.5c
Viral Shapes
Complex
Figure 13.5d
Viral Shapes
Complex – Bullet shaped
Figure 13.6a
Complex Viruses
Bacteriophage T4
Figure 13.7a
The Viral Envelope
Coronavirus
Figure 13.7b
The Viral Envelope
Togavirus
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
DNA Viruses
RNA Viruses
Viral Replication• Dependent on host’s
organelles and enzymes to produce new virions
• Replication cycle usually results in death and lysis of host cell → lytic replication
• Stages of lytic replication cycle– Attachment– Entry– Synthesis– Assembly– Release
Figure 13.8
Lytic Replication
of Bacteriopha
ges
Figure 13.9
Lytic Phage Replication Cycle
Figure 13.11
Lysogeny
Lambda
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
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
Figure 13.12ab
Entry and Uncoating of Animal Viruses
Synthesis of Animal Viruses
• Each type of animal virus requires a different strategy depending on its nucleic acid
• Must consider:–How mRNA is
synthesized?–What serves as a template
for nucleic acid replication?
Synthesis of Proteins and Genomes in Animal RNA Viruses
Table 13.3
Assembly and Release of Animal Viruses• Most DNA viruses assemble in
and are released from nucleus into cytosol
• Most RNA viruses develop solely in cytoplasm
• Number of viruses produced and released depends on type of virus and size and initial health of host cell
• Enveloped viruses can cause persistent infections
• Naked viruses released by exocytosis or may cause lysis and death of host cell
Release of Enveloped Viruses by Budding
Virion Abundance in Persistent Infections
Latency of Animal Viruses• When animal viruses remain
dormant in host cells• May be prolonged for years
with no viral activity, signs, or symptoms
• Some latent viruses do not become incorporated into host chromosome (exist as episomes)
• When provirus is incorporated into host DNA, condition is permanent; becomes permanent physical part of host’s chromosome
Table 13.4
The Role of Viruses in Cancer• Normally, 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 that inhibit division “turned on”
• Neoplasia – uncontrolled cell division in multicellular animal; mass of neoplastic cells is a tumor
• Benign vs. malignant tumors–Metastasis– Cancers
Figure 13.15
Oncogene
Theory
Factors Involved in Activation of Oncogenes• Ultraviolet light• Radiation• Carcinogens• Viruses
How Viruses Cause Cancer• Some carry copies of
oncogenes as part of their genomes
• Some stimulate oncogenes already present in host
• Some interfere with tumor repression; they insert into host’s repressor gene
• 20-25% of all human cancers– Burkitt’s lymphoma–Hodgkin’s disease– Kaposi’s sarcoma– Cervical cancer
Effects of Animal Viruses on Cells:
Culturing Viruses in the Laboratory
• In Whole Organisms– Bacteria– Plants and Animals• Embryonated Chicken Eggs
• In Cell (Tissue Culture)
Figure 13.16
Culturing Viruses in Bacteria
Figure 13.17
Culturing Viruses
in Embryon
ated Chicken
Eggs
Figure 13.18
Culturing Viruses in Cell (Tissue) Culture
Characteristics of Viroids
• Extremely small (a few hundred bases), circular pieces of RNA that are infectious and pathogenic in plants
• Similar to RNA viruses, but lack capsid
• May appear linear due to hydrogen bonding and significant secondary structure
Structure of a Viroid:
Viroids
Effect of PSTVs
Prions• Proposed by Stanley
Prusiner in 1982• Prions have the following
characteristics:– resistant to inactivation by
temperatures in excess of 90 degrees C
– Resistant to radiation that would damage DNA
–Not destroyed by DNAses or RNAses
– Sensitive to protein denaturing agents such as phenol and urea
–Do not elicit inflammatory reactions or antibody formation
– Transmitted only by intimate contact with infected tissues or secretions
http://www.theguardian.com/science/2014/may/25/stanley-prusiner-neurologist-nobel-doesnt-wipe-scepticism-away#img-1
https://media.licdn.com/mpr/mpr/p/1/005/089/335/1fce0a0.jpg
Stanley PrusinerAmerican Neurologist 1942 –
Nobel Prize 1997
Characteristics of Prions• Proteinaceous infectious agents
• Composed of single protein PrP• All mammals contain a gene
that codes for the primary sequence of amino acids in PrP
• Two stable tertiary structures of PrP–Normal functional structure with
α-helices called cellular PrP–Disease-causing form with β-
sheets called prion PrP• Prion PrP converts cellular PrP
into prion PrP by inducing conformational change
Figure 13.21
Stable Structures of PrP
Characteristics of Prions• Normally, nearby proteins and
polysaccharides in lipid rafts force PrP into cellular shape
• Excess PrP production or mutations in PrP gene result in initial formation of prion PrP
• When prions are present, they cause newly synthesized cellular PrP to refold into prion PrP
Diseases Caused by Prions:
(Spongiform Encephalopathies)• All involve fatal
neurological degeneration, deposition of fibrils in brain, and loss of brain matter
• Large vacuoles form in brain; characteristic spongy appearance
• Scrapie in sheep• Mad cow disease (BSE)• Kuru in New Guinea
headhunters• Creutzfeld-Jakob disease
(CJD)
Figure 13.22
Scrapie in Sheep
New Guinea tribeswomen in the Amyloid fibrils in the brainearly stages of kuru of a Creutzfeld-Jakob patient