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