Viruses, Viroids and Prions

Viruses
Viruses are too small to be seen with a light microscope and can’t be cultured outside their
hosts.
 1886
Tobacco Mosaic Disease (TMD)
TMV (1935)
 1990
Human immunodeficiency virus (HIV)
SARS-associated coronavirus
Several different hepatitis viruses
Foodborne hepatitis A virus
Bloodborne hepatitis B virus and hepatitis C virus
 The World Health Organization’s list of the top 10 emerging pathogens likely to
cause severe outbreaks in the near future are all viral diseases.
 These include highly pathogenic human corornaviruses, chikungunya virus, Zika
virus, and thrombocytopenia syndrome virus.
Practice the following questions:
List down ten (10) dangerous viruses which are linked to public health.

General Characteristics of Viruses

One hundred years ago, researchers described the infectious agent as contagium vivum
fluidum—a contagious fluid.
By the 1930s, scientists had begun using the word virus.
In 1935 it was possible for the first time to carry out chemical and structural studies on a
purified virus. At about the same time, the invention of the electron microscope made it
possible to see viruses.

Whether viruses are living organisms???

Ambiguous answer!!!
Life can be defined as a complex set of processes resulting from the actions of proteins
specified by nucleic acids. The nucleic acids of living cells are in action all the time. Because
viruses are inert outside living host cells, in this sense they are not considered to be living
organisms.

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However, once viruses enter a host cell, the viral nucleic acids become active and viral
multiplication results. In this sense, viruses are alive when they multiply in the host cells they
infect.
From a clinical point of view, viruses can be considered alive because they cause infection
and disease, just as pathogenic bacteria, fungi, and protozoa do.
Depending on one’s viewpoint, a virus may be regarded as an exceptionally complex
aggregation of nonliving chemicals, or as an exceptionally simple living microorganism.
Infection: An infection is the invasion of an organism's body tissues by disease-causing
agents, their multiplication, and the reaction of host tissues to the infectious agents and the
toxins they produce.
Protozoa: Protozoa are single celled organisms. They come in many different shapes and
sizes ranging from an Amoeba which can change its shape to Paramecium with its fixed
shape and complex structure. They live in a wide variety of moist habitats including fresh
water, marine environments and the soil.

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 How, then, do we define virus?
Viruses were originally distinguished from other infectious agents because they are especially
small (filterable) and because they are obligatory intracellular parasites—that is, they
absolutely require living host cells in order to multiply. However, both of these properties are
shared by certain small bacteria (such as some rickettsias).
The truly distinctive features of viruses are now known to relate to their simple structural
organization and their mechanism of multiplication.

Accordingly, viruses are entities that

 Contain a single type of nucleic acid, either DNA or RNA.
 Contain a protein coat (sometimes itself enclosed by an envelope of lipids, proteins,
and carbohydrates) that surrounds the nucleic acid.
 Multiply inside living cells by using the synthesizing machinery of the cell.
 Cause the synthesis of specialized structures that can transfer the viral nucleic acid to
other cells.
 Viruses have few or no enzymes of their own for metabolism; for example, they lack
enzymes for protein synthesis and ATP generation.
 ATP: ATP – or Adenosine Triphosphate – is the primary energy carrier in all living
organisms on earth. Microorganisms capture and store energy metabolized from food
and light sources in the form of ATP. When the cell requires energy, ATP is broken
down through hydrolysis.
 To multiply, viruses must take over the metabolic machinery of the host cell.
 This fact has considerable medical significance for the development of antiviral drugs,
because most drugs that would interfere with viral multiplication would also interfere
with the functioning of the host cell and therefore are too toxic for clinical use.
Practice the following questions:
Whether viruses are dead or alive? Explain from your point of view.
Define infection, protozoa and ATP.
Simplify the distinctive features of viruses.

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 Viruses and Bacteria Compared/Comparison/ Differentiation

Interferon:
 Interferons are a group of signaling proteins made and released by host cells in
response to the presence of several viruses. In a typical scenario, a virus-infected cell
will release interferons causing nearby cells to heighten their anti-viral defenses.
 A protein released by animal cells, usually in response to the entry of a virus, which
has the property of inhibiting virus replication.
Practice the following questions:
Distinguish between viruses and bacteria.
What do you understand by interferon?

Host Range
 The host range of a virus is the spectrum of host cells the virus can infect.
 There are viruses that infect invertebrates (an animal lacking a backbone), vertebrates (an
animal of a large group distinguished by the possession of a backbone or spinal column),
plants, protists (A protist is any eukaryotic organism that is not an animal, plant, or
fungus. A single-celled organism of the kingdom Protista, such as a protozoan or simple
alga), fungi, and bacteria.
 However, most viruses are able to infect specific types of cells of only one host species.
 In rare cases, viruses cross the host-range barrier, thus expanding their host range.
 In this topic, we are concerned mainly with viruses that infect either humans or bacteria.
 Viruses that infect bacteria are called bacteriophages, or phages.

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 The particular host range of a virus is determined by the virus’s requirements for its
specific attachment to the host cell and the availability within the potential host of cellular
factors required for viral multiplication.
 For the virus to infect the host cell, the outer surface of the virus must chemically interact
with specific receptor sites on the surface of the cell.
 The two complementary components are held together by weak bonds, such as hydrogen
bonds.
 The combination of many attachment and receptor sites leads to a strong association
between host cell and virus.
 For some bacteriophages, the receptor site is part of the cell wall of the host; in other
cases, it is part of the fimbriae or flagella. For animal viruses, the receptor sites are on the
plasma membranes of the host cells.



 The potential to use viruses to treat diseases is intriguing because of their narrow host
range and their ability to kill their host cells. The idea of phage therapy—using
bacteriophages to treat bacterial infections—has been around for 100 years. Recent
advances in our understanding of virus-host interactions have fueled new studies in the
field of phage therapy. Experimentally induced viral infections in cancer patients during
the 1920s suggested that viruses might have antitumor activity. These tumor-destroying, or
oncolytic, viruses may selectively infect and kill tumor cells or cause an immune response
against tumor cells. Some viruses naturally infect tumor cells, and other viruses can be
genetically modified to infect tumor cells. At present several studies are underway to
determine the killing mechanism of oncolytic viruses and the safety of using viral therapy.

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Practice the following questions:
Interpret the following terms: host range, invertebrates, vertebrates, protists,
bacteriophages and receptor.
Summarize the factors prescribed for viral multiplication.
State a theory of tumor management by viral infection.
Viral Size
 Viral sizes are determined with the aid of electron microscopy.
 Different viruses vary considerably in size.
 Although most are quite a bit smaller than bacteria, some of the larger viruses (such as the
vaccinia virus) are about the same size as some very small bacteria (such as the
mycoplasmas, rickettsias, and chlamydias).
 Viruses range from 20 to 1000 nm in length.
Practice the following question:
Give an overview on viral size.

Viral Structure
A virion is a complete, fully developed, infectious viral particle composed of nucleic acid
and surrounded by a protein coat outside of a host cell, and is a vehicle of transmission from

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one host cell to another. Viruses are classified by their nucleic acid and by differences in the
structures of their coats.
Nucleic Acid
 In contrast to prokaryotic (Prokaryotes are single-celled organisms of the domains
Bacteria and Archaea. All prokaryotes have plasma membranes, cytoplasm,
ribosomes, a cell wall, DNA, and lack membrane-bound organelles. Many also have
polysaccharide capsules. Prokaryotic cells range in diameter from 0.1–5.0 µm) and
eukaryotic cells (Like a prokaryotic cell, a eukaryotic cell has a plasma membrane,
cytoplasm, and ribosomes, but a eukaryotic cell is typically larger than a prokaryotic
cell, has a true nucleus (meaning its DNA is surrounded by a membrane), and has
other membrane-bound organelles that allow for compartmentalization of functions.
Eukaryotic cells tend to be 10 to 100 times the size of prokaryotic cells), in which
DNA is always the primary genetic material (and RNA plays an auxiliary role)
 A virus can have either DNA or RNA—but never both.
 The nucleic acid of a virus can be single-stranded or double-stranded.

 Thus, there are viruses with the familiar double-stranded DNA, with single-stranded
DNA, with double-stranded RNA, and with single-stranded RNA.
 Depending on the virus, the nucleic acid can be linear or circular.
 In some viruses (such as the influenza virus), the nucleic acid is in several separate
segments.
 The percentage of nucleic acid in relation to protein is about 1% for the influenza
virus and about 50% for certain bacteriophages.
 The total amount of nucleic acid varies from a few thousand nucleotides (or pairs) to
as many as 250,000 nucleotides. (E. coli’s chromosome consists of approximately 4
million nucleotide pairs.)
Capsid and Envelope
 The nucleic acid of a virus is protected by a protein coat called the capsid (Figure
below).

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 a. A polyhedral virus
 The structure of the capsid is ultimately determined by the viral nucleic acid and
accounts for most of the mass of a virus, especially of small ones.
 Each capsid is composed of protein subunits called capsomeres.
 In some viruses, the proteins composing the capsomeres are of a single type; in other
viruses, several types of protein may be present.
 Individual capsomeres are often visible in electron micrographs (see figure for an
example).

b. Mastadeno virus
 The arrangement of capsomeres is characteristic of a particular type of virus.
 In some viruses, the capsid is covered by an envelope, which usually consists of some
combination of lipids, proteins, and carbohydrates.

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
 Some animal viruses are released from the host cell by an extrusion process that coats
the virus with a layer of the host cell’s plasma membrane; that layer becomes the viral
envelope.
 In many cases, the envelope contains proteins determined by the viral nucleic acid and
materials derived from normal host cell components.
 Depending on the virus, envelopes may or may not be covered by spikes, which are
carbohydrate-protein complexes that project from the surface of the envelope.
 Some viruses attach to host cells by means of spikes.
 Spikes are such a reliable characteristic of some viruses that they can be used as a
means of identification.
 The ability of certain viruses, such as the influenza virus (Figure b), to clump red
blood cells is associated with spikes.
 Such viruses bind to red blood cells and form bridges between them.
 The resulting clumping is called hemagglutination and is the basis for several useful
laboratory tests. (See Figure)

 Viruses whose capsids are not covered by an envelope are known as nonenveloped
viruses (see Figure a & b).
 The capsid of a nonenveloped virus protects the nucleic acid from nuclease enzymes
in biological fluids and promotes the virus’s attachment to susceptible host cells.

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  When the host has been infected by a virus, the host immune system is stimulated to
produce antibodies (proteins that react with the surface proteins of the virus).
 This interaction between host antibodies and virus proteins should inactivate the virus
and stop the infection.
 However, some viruses can escape antibodies because regions of the genes that code
for these viruses’ surface proteins are susceptible to mutations.
 The mutant virus can alter surface proteins, such that the antibodies are not able to
react with them.
 Influenza virus frequently undergoes such changes in its spikes.
 This is why you can get influenza more than once.
 Although you may have produced antibodies to one influenza virus, the virus can
mutate and infect you again.
Practice the following questions:
Define virion, prokaryotic and eukaryotic cells.
Compare between prokaryotic and eukaryotic cells.
What is the status of nucleic acid, capsid and envelop in the viral structure?
Briefly describe the viral structure.

General Morphology
Viruses may be classified into several different morphological types on the basis of their
capsid architecture. The structure of these capsids has been revealed by electron microscopy
and a technique called X-ray crystallography.
Helical Viruses
 Helical viruses resemble long rods that may be rigid or flexible.
 The viral nucleic acid is found within a hollow, cylindrical capsid that has a helical
structure (Figure a & b).
 The viruses that cause rabies and Ebola hemorrhagic fever are helical viruses.

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Polyhedral Viruses
 Many animal, plant, and bacterial viruses are polyhedral, or many-sided, viruses.
 The capsid of most polyhedral viruses is in the shape of an icosahedron, a regular
polyhedron with 20 triangular faces and 12 corners (see Figure).

 The capsomeres of each face form an equilateral triangle. An example of a polyhedral

virus in the shape of an icosahedron is the adenovirus (shown in figure above).
 Another icosahedral virus is the poliovirus.
Enveloped Viruses
 As noted earlier, the capsid of some viruses is covered by an envelope.
 Enveloped viruses are roughly spherical (Something spherical is like a sphere in
being round, or more or less round, in three dimensions).

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  When helical (spiral) or polyhedral
(A polyhedron (plural polyhedra or polyhedrons) is a three-dimensional shape with
flat polygonal faces, straight edges and sharp corners or vertices. The
word polyhedron comes from the Classical Greek, as poly- ("many") + -hedron (form
of "base" or "seat")) viruses are enclosed by envelopes, they are called enveloped
helical or enveloped polyhedral viruses.
 An example of an enveloped helical virus is the influenza virus (see Figure).

 An example of an enveloped polyhedral (icosahedral) virus is the herpes simplex

virus (see Figure).

Complex Viruses
 Some viruses, particularly bacterial viruses, have complicated structures and are
called complex viruses.
 One example of a complex virus is a bacteriophage.

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  Some bacteriophages have capsids to which additional structures are attached (Figure)

 In this figure, notice that the capsid (head) is polyhedral and that the tail sheath is
helical.
 The head contains the nucleic acid.
 Another example of complex viruses are poxviruses, which do not contain clearly
identifiable capsids but have several coats around the nucleic acid (Figure b).

Practice the following questions:

Classify viruses based on their capsid architecture and demonstrate them.
Skeletonize different forms of viruses.

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 Taxonomy of Viruses
 Just as we need taxonomic categories of plants, animals, and bacteria, we need viral
taxonomy to help us organize and understand newly discovered organisms.
 The oldest classification of viruses is based on symptomatology, such as for diseases
that affect the respiratory system.
 This system was convenient but not scientifically acceptable because the same virus
may cause more than one disease, depending on the tissue affected.
 In addition, this system artificially grouped viruses that do not infect humans.
 New, fast DNA sequencing allows the International Committee on Taxonomy of
Viruses to group viruses into families based on genomics and structure.
 The suffix –virus (Alphacoronavirus) is used for genus names; family names end in
–viridae (Coronaviridae); and order names end in –ales (Nidovirales).
 In formal usage, the family and genus names are used in the following manner:
Family Herpesviridae, genus Simplexvirus, human herpesvirus 2.
 A viral species is a group of viruses sharing the same genetic information and
ecological niche (host range).
 Specific epithets (characteristics) for viruses are not used.
 Thus, viral species are designated by descriptive common names, such as human
immunodeficiency virus (HIV), with subspecies (if any) designated by a number
(HIV-1).
Practice the following questions:
Illustrate the taxonomy of viruses.
Define viral species.
Table presents a summary of the classification of viruses that infect humans (at least five)
Homework????? (Summarize the classification of viruses that infect humans.)

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 Isolation, Cultivation and Identification of Viruses (Sessional)
Bacteriophages
Animal viruses
Plant viruses
 We know viruses can’t multiply outside a living host cell
 Viruses must be provided with living cells instead of a fairly simple chemical
medium.
 Living plants and animals are difficult and expensive to maintain, and pathogenic
viruses that grow only in higher primates and human hosts cause additional
complications.
 However, viruses that use bacterial cells as a host (bacteriophages) are rather easily
grown on bacterial cultures.
 This is one reason so much of our understanding of viral multiplication has come
from bacteriophages.

Growing bacteriophages in the laboratory

 Bacteriophages can be grown either in suspensions of bacteria in liquid media or in
bacterial cultures on solid media.
 The use of solid media makes it possible to use the plaque method to detect and count
viruses.
 A bacteriophage sample is mixed with host bacteria and melted agar.
 The agar containing the bacteriophages and host bacteria is then poured into a Petri
plate containing a hardened layer of agar growth medium.
 The virus-bacteria mixture solidifies into a thin top layer that contains a layer of
bacteria approximately one cell thick.
 Each virus infects a bacterium, multiplies, and releases several hundred new viruses.
 These newly produced viruses infect other bacteria in the immediate vicinity, and
more new viruses are produced.
 Following several viral multiplication cycles, all the bacteria in the area surrounding
the original virus are destroyed.
 This produces a number of clearings, or plaques, visible against a lawn of bacterial
growth on the surface of the agar (Figure).
 While the plaques form, uninfected bacteria elsewhere in the Petri plate multiply
rapidly and produce a turbid background.

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  Theoretically each plaque corresponds to a single virus in the initial suspension.
 Therefore, the concentrations of viral suspensions measured by the number of plaques
are usually expressed in terms of plaque-forming units (PFU).

Viral Identification
 Serological methods, such as Western blotting, are the most commonly used means of
identification. In these tests, the virus is detected and identified by its reaction with
antibodies
 Virologists can identify and characterize viruses by using such modern molecular
methods as use of restriction fragment length polymorphisms (RFLPs) and the
polymerase chain reaction (PCR).

Viral Multiplication

Multiplication of Bacteriophases

 The entry and exit of virus into a host cell may vary.
 The basic mechanism of viral multiplication is similar for all viruses.
 Bacteriophages can multiply by two alternative mechanisms: the lytic cycle or the
lysogenic cycle.
 The lytic cycle ends with the lysis (Breakdown of a cell caused by damage to its
plasma (outer) membrane. It can be caused by chemical or physical means (for
example, strong detergents or high-energy sound waves) or by infection with a strain
virus that can lyse cells) and death of the host cell, whereas the host cell remains
alive in the lysogenic cycle.

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  Because the T-even bacteriophages (T2, T4, and T6) have been studied most
extensively, we’ll describe the multiplication of T-even bacteriophages in their host,
E. coli, as an example of the lytic cycle.

T-Even Bacteriophages:
The Lytic Cycle
 The virions of T-even bacteriophages are large, complex, and nonenveloped, with a
characteristic head-and-tail structure shown in Figure.
 The length of DNA contained in these bacteriophages is only about 6% of that
contained in E. coli, yet the bacteriophage has enough DNA for over 100 genes.
 The multiplication cycle of these phages, like that of all viruses, occurs in five distinct
stages: attachment, penetration, biosynthesis, maturation, and release.
Stage-1: Attachment
 After a chance collision between phage particles and bacteria, attachment, or
adsorption, occurs.
 During this process, an attachment site on the virus attaches to a complementary
receptor site on the bacterial cell.


 This attachment is a chemical interaction in which weak bonds are formed between
the attachment and receptor sites.
 T-even bacteriophages use fibers at the end of the tail as attachment sites.
 The complementary receptor sites are on the bacterial cell wall.
Stage-2: Penetration
 After attachment, the T-even bacteriophage injects its DNA (nucleic acid) into the
bacterium.


 To do this, the bacteriophage’s tail releases an enzyme, phage lysozyme, which
breaks down a portion of the bacterial cell wall.

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  During the process of penetration, the tail sheath of the phage contracts, and the tail
core is driven through the cell wall.
 When the tip of the core reaches the plasma membrane, the DNA from the
bacteriophage’s head passes through the tail core, through the plasma membrane, and
enters the bacterial cell.
 The capsid remains outside the bacterial cell.
 Therefore, the phage particle functions like a hypodermic syringe to inject its DNA
into the bacterial cell.
Stage-3: Biosynthesis
 Once the bacteriophage DNA has reached the cytoplasm of the host cell, the
biosynthesis of viral nucleic acid and protein occurs.


 Host protein synthesis is stopped by virus-induced degradation of the host DNA, viral
proteins that interfere with transcription (Transcription is the process by which the
information in a strand of DNA is copied into a new molecule of messenger RNA
(mRNA)), or the repression of translation (A process occurring in the ribosome, in
which a strand of messenger RNA (mRNA) guides assembly of a sequence of amino
acids to make a protein).
 Initially, the bacteriophage uses the host cell’s nucleotides and several of its enzymes
to synthesize many copies of phage DNA.
 Soon after, the biosynthesis of viral proteins begins.
 Any RNA transcribed in the cell is mRNA transcribed from phage DNA for the
biosynthesis of phage enzymes and capsid proteins.
 The host cell’s ribosomes, enzymes, and amino acids are used for translation.
 Genetic controls regulate when different regions of phage DNA are transcribed into
mRNA during the multiplication cycle. For example, early messages are translated
into early phage proteins, the enzymes used in the synthesis of phage DNA.
 Also, late messages are translated into late phage proteins for the synthesis of capsid
proteins. For several minutes following infection, complete phages can’t be found in
the host cell.

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  Only separate components— DNA and protein—can be detected. The period during
viral multiplication when complete, infective Virions aren’t yet present is called the
eclipse period.
Stage-4: Maturation
 In this process, bacteriophage DNA and capsids are assembled into complete virions.
 The viral components essentially assemble into a viral particle spontaneously,
eliminating the need for many nonstructural genes and gene products.
 The phage heads and tails are separately assembled from protein subunits, and the
head is filled with phage DNA and attached to the tail.

Stage-5: Release
 The final stage of viral multiplication is the release of virions from the host cell.
 The term lysis is generally used for this stage in the multiplication of T-even phages
because in this case, the plasma membrane actually breaks open (lyses).
 Lysozyme, which is encoded by a phage gene, is synthesized within the cell.
 This enzyme causes the bacterial cell wall to break down, and the newly produced
bacteriophages are released from the host cell.
 The released bacteriophages infect other susceptible cells in the vicinity, and the viral
multiplication cycle is repeated within those cells.

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 The lytic cycle of a T-even bacteriophage
Practice the following question:
Describe the lytic cycle of T-even bacteriophages.
Please go to your browser, copy the following youtube link to the browser URL for
better understanding:
1. https://www.youtube.com/watch?v=WnWr12lxRO4
2. https://www.youtube.com/watch?v=tGVDYGxqtJ0
Growing bacteriophages in the laboratory
3. https://www.youtube.com/watch?v=GzNay9XRYRs
The lytic cycle of a T-even bacteriophage

Plant Viruses and Viroids

 Plant viruses are morphologically similar to animal viruses, and they have similar
types of nucleic acid (Table).
 Classification of Some Major Plant Viruses

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
 In fact, some plant viruses can multiply inside insect cells.
 Plant viruses cause many diseases of economically important crops, including beans
(bean mosaic virus), corn and sugarcane (wound tumor virus), and potatoes (potato
yellow dwarf virus).
 Viruses can cause color change, deformed growth, wilting, and stunted growth in their
plant hosts.
 Some hosts, however, remain symptomless and only serve as reservoirs of infection.
 Plant cells are generally protected from disease by an impermeable cell wall.
 Viruses must enter through wounds or be assisted by other plant parasites, including
nematodes, fungi, and, most often, insects that suck the plant’s sap.
 Once one plant is infected, it can spread infection to other plants in its pollen.
 In laboratories, plant viruses are cultured in protoplasts (plant cells with the cell walls
removed) and in insect cell cultures.
 Some plant diseases are caused by viroids, short pieces of naked RNA, only 300 to
400 nucleotides(A nucleotide is the basic building block of nucleic acids. RNA and
DNA are polymers made of long chains of nucleotides. A nucleotide consists of a
sugar molecule (either ribose in RNA or deoxyribose in DNA) attached to a
phosphate group and a nitrogen-containing base) long, with no protein coat.
 The nucleotides are often internally paired, so the molecule has a closed, folded,
three-dimensional structure that helps to protect it from destruction by cellular
enzymes.
 Some viroids, called virusoids, are enclosed in a protein coat.
 Virusoids cause disease only when the cell is infected by a virus.
 Viroids and virusoids are replicated continuously by host RNA polymerase in the cell
nucleus or chloroplasts.
 When the enzyme reaches the end of the viroid RNA, it goes to the beginning.
 The viroid RNA is a ribozyme that cuts the continuous RNA into viroid segments.
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 The RNA doesn’t code for any proteins and may cause disease by gene silencing.


 Annually, infections by viroids, such as potato spindle tuber viroid (PSTV), result in
losses of millions of dollars from crop damage (Figure).


 Current research on viroids has revealed similarities between the base sequences of
viroids and introns (An intron (for intragenic region) is any nucleotide sequence
within a gene that is removed by RNA splicing during maturation of the final RNA
product. In other words, introns are non-coding regions of an RNA transcript, or the
DNA encoding it, that are eliminated by splicing before translation).
 Introns are sequences of genetic material that don’t code for polypeptides.
 This observation has led to the hypothesis that viroids evolved from introns.
 Thus far, viroids and virusoids have been conclusively identified as pathogens only of
plants, although hepatitis D may be caused by a virusoid.
 Hepatitis D is RNA enclosed in a protein coat and requires coinfection by Hepatitis B
virus. Some researchers call HDV satellite RNA.
 Overview:

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 1. Plant viruses must enter plant hosts through wounds or with invasive parasites,
such as insects.
2. Some plant viruses also multiply in insect (vector) cells.
3. Viroids are infectious pieces of RNA that cause some plant diseases.
4. Virusoids are viroids enclosed in a protein coat.
Practice the following questions:
Classify major plant viruses.
Recall the following terms: viroids, virusoids, nucleotides and introns.
How does a plant be infected by viruses and viroids?
Prions
 A few infectious diseases are caused by prions.
 In 1982, American neurobiologist Stanley Prusiner proposed that infectious proteins
caused a neurological disease in sheep called scrapie.
 The infectivity of scrapie-infected brain tissue is reduced by treatment with
proteases(A protease (also called a peptidase or proteinase) is an enzyme that
catalyzes (increases the rate of) proteolysis, the breakdown of proteins into smaller
polypeptides or single amino acids. They do this by cleaving the peptide bonds within
proteins by hydrolysis, a reaction where water breaks bonds) but not by treatment
with radiation, suggesting that the infectious agent is pure protein.
 Prusiner coined the name prion for proteinaceous infectious particle.
 Nine animal diseases now fall into this category, including the ―mad cow disease‖ that
emerged in cattle in Great Britain in 1987.
 All nine are neurological diseases called transmissible spongiform encephalopathies
because large vacuoles develop in the brain (Figure 22.18b).


 The human diseases are kuru, Creutzfeldt-Jakob disease (CJD), Gerstmann-
SträusslerScheinker syndrome, and fatal familial insomnia.

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  These diseases often run in families, which indicates a possible genetic cause.
 However, they aren’t only inherited, because mad cow disease arose from feeding
scrapie-infected sheep meat to cattle, and the new (bovine) variant was transmitted to
humans who ate undercooked beef from infected cattle.
 Additionally, CJD has been transmitted with transplanted nerve tissue and
contaminated surgical instruments.
 These diseases are caused by the conversion of a normal host glycoprotein called
PrPC (for cellular prion protein) into an infectious form called PrPSc (for scrapie
protein).
 The gene for PrPC is located on chromosome 20 in humans.
 Recent evidence suggests that PrPC is involved in preventing cell death.
 One hypothesis for how an infectious agent that lacks any nucleic acid can reproduce
is shown in Figure 13.23.
 The actual cause of cell damage isn’t yet known.
 Fragments of PrPSc molecules accumulate in the brain, forming plaques; these
plaques are used for postmortem diagnosis, but they don’t appear to be the cause of
cell damage.
 Overview
1. Prions are infectious proteins first discovered in the 1980s.
2. Prion diseases involve the degeneration of brain tissue.
3. Prion diseases are the result of an altered protein; the cause can be a mutation in the
normal gene for PrPC or contact with an altered protein (PrPSc).
Practice the following questions:
Define protease.
How does infectious disease caused by prion?
https://www.youtube.com/watch?v=chTU792DWas
https://www.youtube.com/watch?v=qmsWOrQtj4w

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