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

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

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

Hosts of Viruses
Most only infect particular kinds
of hosts cells
Due to affinity of viral surface
proteins or glycoproteins (antireceptors) 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

Viral
Hosts

Human Immunodeficiency virus

Figure 13.3d

Sizes of
Viruses

Capsid
Morphology
Capsids protein coats that
provide protection for viral
nucleic acid and means of
attachment to hosts cells
Capsid composed of
proteinaceous subunits called
capsomeres
Some capsids composed of
single type of capsomere; others
are composed of multiple types

Viral Shapes

Helical

Figure 13.5a

Viral Shapes

Polyhedral

Figure 13.5b

Viral Shapes

Complex

Figure 13.5c

Viral Shapes

Complex
Bullet shaped
Figure 13.5d

Complex
Viruses

Bacteriophage T4
Figure 13.6a

The Viral
Envelope

Coronavirus

Figure 13.7a

The Viral
Envelope

Togavirus

Figure 13.7b

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)
Envelopes proteins and
glycoproteins often play role in
host recognition

DNA Viruses

RNA Viruses

Viral Replication
Dependent on hosts
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

Lytic
Replication
of
Bacteriopha
ges

Figure 13.8

Lytic Phage
Replication Cycle

Figure 13.9

Lysogeny

Lambda

Figure 13.11

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

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

Entry and Uncoating of Animal

Viruses

Figure 13.12ab

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
hosts chromosome

Table 13.4

The Role of Viruses

in Cancer
Normally, animals 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

Oncog
ene
Theory

Figure 13.15

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
hosts repressor gene
20-25% of all human cancers
Burkitts lymphoma
Hodgkins disease
Kaposis 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)

Culturing Viruses in
Bacteria

Figure 13.16

Viruses
in
Embryon
ated
Chicken
Eggs

Figure 13.17

Culturing Viruses in Cell

(Tissue) Culture

Figure 13.18

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

Stanley Prusiner
American Neurologist 1942
Nobel Prize 1997

http://
www.theguardian.com/science/2014/may/25/stanley-prusiner-neurologist-nobel-doesnt-wipe-scepticism-away#i
mg-1

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 helices called cellular PrP
Disease-causing form with sheets called prion PrP

Prion PrP converts cellular PrP

into prion PrP by inducing
conformational change

Stable Structures of PrP

Figure 13.21

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

Prions:
(Spongiform
All involve fatal
Encephalopathies)

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)

Scrapie in Sheep

Figure 13.22

New Guinea tribeswomen in the

Amyloid fibrils in the brain
early stages of kuru
of a Creutzfeld-Jakob patient