Viruses

Introduction

•Viruses: infectious agents that are too small to be seen by light microscope
& are not cells.
–They have no cell nucleus, organelles or cytoplasm.
– Louis Pasteur first proposed the term virus.
–Prokaryotes & eukaryotes have DNA & RNA, virus particles contain only one
kind of nucleic acid DNA or RNA (never both).
•They display properties of living organism only when they invade host cells.
–Viruses replicate only inside living host; i.e. obligate intracellular parasites.
–Viruses don’t grow or replicate alone, they infect host cell & program it to
synthesize the components of new viruses.
•The virus infection may have little or no effect on the host cell or may result
in cell damage or death.
 Introduction

• Viruses differ from cells in important ways:

1. Prokaryotic and eukaryotic cells contain both DNA and
RNA, individual virus particles contain only one kind of
nucleic acid.
2. Cells grow and divide, but viruses do neither.
3. Viral replication requires that a virus particle to infect a
cell and program the host cell’s machinery to
synthesize the components required for the assembly
of new virus particles.
4. Do not possess genetic information for energy-
producing systems.
 Size Range

• Smallest infectious agents.

• Most are so small, they can only be seen with an electron
microscope.
• Animal viruses
– Proviruses- around 20 nm in diameter.
– Mimiviruses- up to 450 nm in length.
• Viewing viruses:
– Special stains and an electron microscope.
– Negative staining outlines the shape.
– Positive staining shows internal details.
– Shadow casting technique.
 Components of Viruses

•Viruses are made up, mainly, of a nucleic acid core surrounded by a protein coat called
capsid; together they form a nucleocapsid.
•In some viruses the nucleocapsid is also surrounded by a lipid envelope; which is a lipid-
containing membrane.
–A complete virus particle, composed of the abovementioned components is called a
‘virion’.
•Nucleic acids
–Lie in the core of virus
–Viral genome (genetic material) is either:
 DNA or RNA
 Single stranded or double stranded,
 Linear, circular or segmented
–Size of the viral genome:
•DNA: ~3 kb to more than 300 kb
•RNA: ~4 kb to 32 kb
 Components of Viruses

•Capsid:
–The protein capsid is an essential component in any virus.
–Viral capsid is composed of protein subunits called ‘capsomeres’.
•Viral capsomere may have either single type of proteins or several different
proteins.
•Number, type and arrangement of capsomeres are characteristic for each virus.
–Functions of viral proteins:
1. Protect the viral genome.
2. Provide the structural symmetry (shape) of the virus particle.
3. Participate in the attachment of the virus particle to the host cell.
4. Determine the antigenic characteristics of the virus.
–Some viruses also carry protein enzymes which are essential for the initiation of
the viral replicative cycle.
 Components of Viruses

•Envelope
–Enveloped viruses have a lipid bilayer membrane outside their capsid.
–The envelop is acquired after the virus is assembled in a host as it buds or move
through host cell membranes.
–Viruses with a nucleocapsid (viral genome & capsid) but without an envelope are called
naked or non-enveloped viruses.
–Composition of an envelope is determined by viral genome & by the substances
derived from host membranes.
– Mainly a combination of lipids, proteins & carbohydrates.
–Some viruses have spikes on their envelope which are glycoprotein projections that
may extend outside the envelope.
•They serve to attach the virions to host cell receptors.
•Determine the antigenic characteristics of the enveloped viruses.
•Some spikes cause RBCs to clump (hemagglutination), a property used to identify
viruses.
 Components of Viruses

•Envelope
–Advantages:
1. Because derived from host cell membrane, virus can be
hidden from attack by host immune system.
2. Help virus infect new cells by fusion of envelope with host
cell membrane.
–Disadvantages:
• Enveloped viruses are damaged easily by any environmental
condition that destroys biological membranes.
e.g. elevated temperature, freezing & thawing, pH below 6 or
above 8, lipid solvents and some chemical disinfectants.
Components of Viruses
 Size and Shape of Viruses

•Viruses have range of sizes, the smallest being below 30nm while the
largest is more than 300nm (10th of a human RBC).
•Most viruses have specific shape determined by their capsid or envelope:
–Viruses with an envelope have almost spherical shape.
1. Helical capsid: composed of ribbon like protein forms a spiral around the
nucleic acid.
2. Polyhedral capsid: many-sided.
•Icosahedral (20 triangular faces with 12 evenly spaced corners) is one of
the most common.
3. Complex capsid: more complicated capsid such as combination of helical
& icosahedral capsids.
•Complex viruses have more elaborate coat or capsid, e.g. bacteriophages
have special structures like head, tail & tail fibers.
Size and Shape of Viruses
 Host Range and Specificity of Viruses

•Viruses can infect all forms of life (algae, bacteria, fungi, protozoa, plants ,
animals, and even archaea.
•But for most viruses, each virus is limited to one host or even to one type
of cells or tissues of the host.
•Host range of a virus is the spectrum of hosts that the virus can infect.
–e.g. poliovirus causes infection to humans only, while rabies virus causes
infection to many warm blooded animals.
•Viral specificity refers to the specific kind of cells a virus can infect (called
tissue tropism).
–e.g. some papillomaviruses infect only skin cells (warts), while
cytomegalovirus (have lethal effects) can attack salivary glands, GIT, liver,
lungs, crosses placenta & attacks foetus.
–“one virus, one disease” concept is not necessarily true!
 Host Range and Specificity of Viruses

•Viral specificity is determined by:

1. The ability of a virus to attach to the host cell.
i.e. depends on presence of specific receptor on host cell & specific
attachment structure on viral capsid or envelope.
2. Presence of enzymes & proteins in the host that the virus needs in
order to replicate itself inside the host cell.
3. Ability of viruses to be released from the cell.
•Viruses can’t reproduce by themselves, they must infect host cells, un-
coat their genetic material and use the host’s machinery to replicate.
•Whether viruses are living or non-living is still a debate?
–Non-living: can’t reproduce alone, no metabolism.
–Living: because they have genetic material that is active after infection.
 Classification of Viruses

• International committee on taxonomy of viruses (ICTV):

• [phylum - class] – order (-virales) – family (-viridae) – subfamily (-virinae) – genus (-virus)
- species - strain/type
–Currently: the viral species (group of viruses that share the same genome & the same
relationship to organisms) is written in English not Latin.
e.g. HIV virus: family Retroviridae, genus Lentiviridae, spp. Human immunodeficiency
virus.
• As of 2017, 9 orders, 131 families, 46 subfamilies, 803 genera, and 4,853 species of
viruses have been defined by the ICTV.
–Virus families are often distinguished based on:
1. nucleic acid type,
2. capsid symmetry (shape) and number of capsomeres
3. envelope
4. size
5. Host range and target cells
 Classification of Viruses

•Nucleic acid classification

–Major groups are classified first as DNA or RNA viruses.
–Subdivisions are based on properties of nucleic acid; single stranded
(ss) or double stranded (ds).
–Since eukaryotic cells don’t have enzymes to copy viral RNA
molecules, RNA viruses must have enzymes or genes for the enzymes
that are needed to copy the viral RNA molecules.
–ssRNA viruses contain either (+)sense RNA i.e. RNA acts as mRNA
that can be translated by host ribosomes, or anti-sense /(-)sense RNA:
RNA acts as template during transcription to make complementary
(+)sense mRNA which will be translated by host ribosomes.
–(-) sense virus must carry RNA polymerase within virion.
 Classification of Viruses - Examples

•RNA viruses

–Enteroviruses
1. Non-enveloped (+)sense ssRNA viruses from the
family Picornaviridae.
2. E.g. poliovirus (which causes poliomyelitis).
3. They are resistant to chemicals & can replicate in &
pass through GIT & spread to the nervous system.
4. They spread through the fecal-oral route.
 Classification of Viruses - Examples

•RNA viruses
–Retroviridae
• Enveloped viruses having two copies of (+)sense ssRNA.
• Also contain the enzyme reverse transcriptase.
• The following pattern is followed for protein synthesis:
1. Viral RNA is reverse-transcribed into DNA by reverse transcriptase.
2.The DNA is integrated into the host’s genome by integrase enzyme,
this integrated DNA is known as a provirus.
3.The provirus (DNA) is then transcribed into RNA.
4.The resultant RNA is finally translated into polypeptides (proteins).
Retroviruses causes AIDS (HIV), tumors & leukemias (HTLV-1).
 Retroviruses - example

• Human immunodeficiency virus (HIV) is the cause of acquired

immune deficiency syndrome (AIDS).
• HIV is able to attach and invade cells bearing receptors that
the virus recognizes and the most important of these
receptors is CD₄ receptors.
• Cells possessing CD₄ receptors are called CD₄+ cells.
• The most important CD₄+ cells is; helper T cells and
macrophages.
 Classification of Viruses - Examples

•DNA viruses
–Herpesviridae (herpesviruses)
• Enveloped dsDNA viruses.
• E.g. Herpes simplex virus 1&2, varicella-zoster virus, cytomegalovirus and Epstein-Barr
virus.
• Widely distributed in nature & most animals are infected with herpesviruses (one or more
of them).
• When cells are infected with some herpesviruses, the viral DNA can become a provirus and
exhibit ‘latency’.
• Viral latency indicates the virus ability to remain in host cells, usually neurons, for long
time.
• The latent virus can be reactivated later to cause a new episode of a disease, e.g. varicella-
zoster virus: initial infection causes chickenpox, after the disease is resolved, the virus can
remain latent in neurons.
• Reactivation of the virus (due to stress or other factors) at later age causes shingles (zoster).
 Emerging Viruses

•Some viruses caused infections since 1000s of years ago.

•But microbiologists believe that many recent unexpected viral
diseases are caused by ‘emerging viruses’.
•Emerging viruses may result from:
1. Viruses that have crossed the ‘host species barrier’, i.e. an animal
virus acquiring the ability to infect humans. e.g. Influenza virus: if
a host cell is simultaneously infected by 2 different viruses (e.g.
human, swine) they can swap parts of their genomes → new
mutant type occur → resulting in “a chimeric virus or chimera”, for
example, human flu virus covered by bird or pig type capsid, that
is a new virus which is not recognized by human immune system,
another example is Covid-19.
 Emerging Viruses

• Viruses which were endemic (low level of infection in localized

area) and then spread world-wide (epidemic or even
pandemic).
• e.g. poliovirus was endemic since ancient times, but after
1900 it was spread world-wide due to urbanization and
migration.
• Note: RNA viruses mutate faster than DNA viruses, single-
stranded viruses mutate faster than double-strand virus, and
genome size appears to correlate negatively with mutation
rate (Viruses with smaller genomes tend to mutate faster).
 Classification of Viruses

• Viruses are also classified according to host range

into:

1. Bacteriophages (viruses that infect bacteria).

2. Animal viruses (viruses that infect animals and
human).
3. Plant viruses (viruses that infect plants).
 Bacteriophages (Phages)

•Bacteriophages (literally means eater of bacteria) are viruses that

infect and replicate within bacterial cells.
•Bacteriophages are highly specific in term of their host and hence
they have been used to treat bacterial diseases (phage therapy).
•Advantages of phage therapy:
1. Cheap, rapid (cures in 1-2 days) and effective in small doses.
2. Can be used to treat long term antibiotic-resistant bacterial
infections.
3. Selectivity: attacking only targeted bacteria without affecting
human cells or the beneficial normal flora.
4. Rarely cause side effects.
 Bacteriophages (Phages) - Example

•T-Even phages

–The letter ‘T’ indicates ‘type’ and the word ‘even’ indicates ‘even
number’, i.e. T2, T4 and T6.
–They are dsDNA viruses that infect E. coli cells.
–They have a characteristic structure which is made of:
1.Head: a polyhedral capsid surrounding the nucleic acid core.
2.Collar: joining the virus head to its tail.
3.Tail: a hollow helical protein used to pass the nucleic acid into
the host cell after attachment.
4.Tail fibers: serve for recognition and attachment to host cells.
 Viral Replication

•Common stages of viral replication cycle:

1.Adsorption: the attachment of viruses to host cells.
2.Penetration: the entry of virions (or their genome) into host
cells.
3.Synthesis: the synthesis of new nucleic acid molecules, capsid
proteins & other viral components using the host cell’s
machinery.
4.Maturation: assembly of newly synthesized viral components
into complete virions.
5.Release: release of new virions from host cells. Frequently
this step causes lysis of host cells.
 Replication of Bacteriophages

•Steps of bacteriophage replication: (T4 phage):

1.Adsorption: the attachment of viruses to host cells. It is a chemical

attraction process. Specific proteins found in tail fibers bind to specific
receptor sites on host cells. Some bind to cell wall, others bind to flagella
or pili.
2.Penetration: lysozyme (present in phage tail) weakens bacterial cell wall,
tail contracts, the hollow tube penetrates the cell wall & contacts cell
membrane. Viral DNA is then injected & the capsid remains outside.
3.Synthesis: phage DNA controls host cell’s metabolic machinery, bacterial
DNA is disrupted & the resulting nucleotides are used to build new phage
DNA. Phage DNA → transcribed mRNA → translated on host ribosomes →
proteins (e.g. capsid + enzymes).
 Replication of Bacteriophages

Steps of bacteriophage replication:

4.Maturation: assembly of newly synthesized viral components into

complete virions. In host cytoplasm, heads are assembled, dsDNA is
packed into each head, also phage tail & collar are assembled.
5.Release: lysozymes (coded by phage genes) breaks down cell wall
allowing viruses to escape, i.e. bacterial cell is lysed, new phages
can now infect more bacterial cells.
–Phages that lyse & destroy the host cell are called lytic phages
(virulent phage). In this case, the replication cycle is called lytic
cycle.
 Phage Growth

•Replication curve
–Eclipse period: from penetration to
biosynthesis, in this period mature virions are
not detected in host cell.
–Latent period: from penetration up to phage
release. This period includes eclipse period.
–After eclipse period the no. of released
viruses per host cell rises & then levels off.
–Eclipse period = Lag phase in bacteria.
 Estimation of Phage Numbers

•Phage assay (plaque assay) is a method used to estimate the number of

phages in a sample (phage titer).
•Procedures:
1.Prepare plates containing susceptible bacterial lawn (layer of bacteria).
2.Make serial dilution of phage suspension.
3.From each dilution take a sample (small volume) & inoculate onto the plate
containing susceptible bacterial lawn.
4.During incubation, each phage will infect a bacterial cell & the phages
produced from each bacterium will lyse the bacterium & the surrounding
bacteria, this will result in the appearance of clear zones on the bacterial
lawn called plaques.
5.After incubation, count the no. of plaques x dilution factor = no. of phages
(plaque forming units / PFU).
Estimation of Phage Numbers
 Lysogeny

•Lysogeny: a stable long-term relationship between the phage

& its host cell where phage nucleic acid is incorporated into the
host nucleic acid and becomes a prophage.
–Together, the prophage and the involved bacterial cell are
called lysogenic cell (lysogen).
•Virulent (lytic) phages: destroy their host cells.
•Temperate phages (lysogenic phage): for some time they may
undergo a lytic cycle but most of the time they exhibit lysogeny.
• The prophage remains dormant for a long time & when
bacterial cell divides, the prophage multiplies as part of the
bacterial chromosome.
 Lysogeny

•The inserted prophage may have genes that alter the phenotype of
the bacterial cell, a process known as lysogenic conversion.
•Lysogenic conversion may:
1. Repress virus replication.
2. Provide ‘immunity’ to infection by other phages, i.e. by preventing
their adsorption or biosynthesis.
3. Increase pathogenicity and/or virulence of lysogenic bacterial
cells, i.e. by exotoxins release.
E.g. Corynebacterium diphtheria & Clostridium botulinum don’t cause
disease unless they are infected by a lysogenic phage, once they have
a prophage that include genes coding for exotoxins →exotoxin
release by bacteria → tissue damage.
 Lysogeny

•Lysogenic cycle lasts as long as the bacteria is growing while the

prophage in it.
•Due to a certain stimulant (e.g. lack of nutrients or toxic
chemicals to the lysogen) or even spontaneously, the prophage
can become active & starts the lytic cycle, a process called
induction.
•Through induction the provirus removes itself from the bacterial
chromosome, phage DNA then codes for viral proteins, enzymes &
other components and the cycle is completed as a lytic cycle.
•The majority of bacteriophages are believed to undergo lysogeny.
 Replication of Animal Viruses

• Animal viruses: viruses that infect humans and animals.

1.Adsorption:
–Naked viruses have attachment sites (proteins) on the surfaces of their capsids e.g.
(canyons or depressions) that bind to specific receptors on host cells.
–Enveloped viruses have spikes that recognize a membrane protein receptor on the
surface of host cell.
2.Penetration:
–Nucleic acid & capsid penetrate animal cell (unlike phages only nucleic acid is
injected).
–Naked viruses enter cells by endocytosis (pit-like region on cell surface) & enter the
cell as vesicles.
–Enveloped viruses either fuse with host plasma membrane or enter by endocytosis.
–Once inside cell cytoplasm, un-coating (release of viral genome) from protein coat
occurs by proteolytic enzymes.
 Replication of Animal Viruses

3.Synthesis:
–DNA viruses: DNA replicates in host nucleus while capsid & other proteins are
synthesized in cytoplasm. The new viral proteins move to the nucleus & combine with
new viral DNA to form virions.
–RNA viruses: synthesis undergoes in greater variety than DNA. (RNA & RNA retroviruses).
4.Maturation:
–When viral components are available in abundant amounts, assembly into virions starts.
–Envelope lipids & glycoproteins are synthesized by host enzymes.
–If the virus is of enveloped type, the virion is incomplete until it buds through one of the
host membranes, e.g. plasma membrane, nuclear membrane, Golgi or endoplasmic
reticulum.
5.Release:
–The budding of new virions may or may not kill the host cell (herpes & pox viruses cause
lysis to cells).
 Latent Viral Infection

•Example 1: herpes simplex virus causes cold sores, can exhibit lytic cycle or
can remain latent within the cell through out the individual’s life in the nerve
cells. When activated (cold, stress, fever) they replicate resulting in lytic cycle
and another disease episode.
•Example 2: Varicella-Zoster virus may remain dormant in nerve cells, once
activated it forms rash along the nerve (shingles).
 Culturing Animal Viruses

• Viruses have to be grown in living tissue.

• First they were cultured in living animals, later in
chick embryo, recently in cell culture (tissue culture).
• Primary purposes of viral cultivation:
1. To isolate and identify viruses in clinical
specimens.
2. To prepare viruses for vaccines.
3. To do detailed research on viral structure,
multiplication cycles, genetics, and effects on
host cells.
 Culturing Animal Viruses

1. ANIMALS
2. EMBRYONATED EGGS
3. CELL CULTURE
 Culturing Animal Viruses

ANIMALS
Advantages
1. Testing new viral vaccines or new antiviral drugs.
2. Some viruses e.g. hepatitis B, papillomaviruses and other
agents e.g. prions (BSE, scrapie) will not grow in cell culture.
3. Studies on pathogenesis to model human disease (including
the use of transgenic animals). Transgenic
animals are animals (most commonly mice) that have had a
foreign gene deliberately inserted into their genome.
4. Source of primary cell cultures.
5. Production of antibodies for diagnostic and research purposes.
 Culturing Animal Viruses

ANIMALS
Disadvantages
1. Expensive.
2. Complex systems making it difficult to discern
events during the infection.
3. Have their own indigenous viruses, some of
which may interfere with the experiment or in
some cases are dangerous to humans e.g.
Marburg virus, herpes B virus, Covid-19.
 Culturing Animal Viruses

Animal models

Symptoms and signs

1. increased temperature
2. circling (Walk in circles around their longitudinal axis)
3. sneezing
4. rash
5. pustules/pocks
6. Death
 Culturing Animal Viruses

Tissues

Post-infection/post-mortem histology
1. inclusion bodies (sometimes called elementary bodies,
are nuclear or cytoplasmic aggregates of stable
substances, usually proteins. They typically represent sites
of viral multiplication in a bacterium or an eukaryotic cell
and usually consist of viral capsid proteins)
2. inflammatory response
3. cell death/necrosis
 Culturing Animal Viruses

EMBRYONATED EGGS
Advantages
1. More convenient and less expensive than animals.
2. More easily manipulated for study.

Disadvantages
3. Only susceptible to a small range of viruses.
4. Requirement for large and specialized incubator that
allows “rocking” of eggs.
5. Requirement for reliable supplies of fertilized eggs.
 Culturing Animal Viruses

Embryonated eggs

Effect on embryo
• slow growth
• death
 Culturing Animal Viruses

CELL CULTURE

Media
• Balanced salt solution + glucose
• Amino acids and vitamins
• Antibiotics
1. Penicillin/streptomycin (crystamycin)
2. Antifungal agent e.g. fungizone
• pH regulation (Sodium bicarbonate/CO₂)
 Culturing Animal Viruses

Cell culture :

• Animal cells are taken freed from surrounding tissue by enzymes, washed,
counted & dispensed into plastic flasks, tubes or bottles containing nutrients.
• Antibiotics are added to prevent microbial contamination.
• Cells will attach to plastic surface, multiply & spread to form sheets, one
cell-thick called ‘monolayers’. When the sheet of cells fill the surface area
available, the culture is said to be “confluent.”
• Monolayers can be sub-cultured; a process where cells from a culture are
transferred to new container with fresh nutrients (passage).
–Plaque assay similar to that of phages can be used on animal/human cells.
Plaque Assay of animal viruses
 Culturing Animal Viruses

Cell culture
1.Primary cultures
• A culture taken directly from an organism, often embryonic tissue e.g.
chick embryo fibroblasts.
• Composed of different cell types with differing susceptibility to viruses,
although fibroblast-like cells tend to outgrow other types.

2.Diploid cell lines

• Derived from human or animal fetal tissue. At least 75% of the cells have
the same karyotype (the number and visual appearance of the
chromosomes in the cell nuclei of an organism or species) as the
organism from which they were originally obtained e.g. human embryo
lung (HEL) cells.
 Culturing Animal Viruses

Cell culture
3.Continuous cell lines

• Derived from tumours.

• Normal cells that have acquired tumour-like
properties (“transformed” cells).
• Aneuploid (i.e. have an abnormal number of
chromosomes. (e.g. HeLa cells)).
 Culturing Animal Viruses

• Cytopathic effect (CPE) is the visible effect viruses

have on cells.
• The effect differs according to the infecting virus, e.g.
lysis, change in shape of cells, swelling, detachment
from adjacent cells or the container.
• Not all viruses produce a CPE → need to detect viral
antigens, e.g. haemadsorption.
 Viruses and Teratogenesis

•Teratogenesis is the induction of defects during embryonic development.

•Teratogen: an agent that induces such a defect.
•Some viruses act as teratogens, i.e. they can be transferred through
placenta & infect the fetus.
–The earlier the embryo is infected, the more the damage can be.
–e.g. cytomegalovirus & rubella cause teratogenic effects.
–If the damage is severe it may lead to death of fetus.
•TORCH screen: series of tests to detect teratogenic diseases in pregnant
women & new born infants.
–The test detects antibodies against Toxoplasmosis, disease-causing
viruses (usually hepatitis B, varicella), rubella virus, cytomegalovirus &
herpes simplex virus.
 Viruses and Cancer

• Cancer is an uncontrolled and/or invasive growth of

abnormal cells.
• Tumor or neoplasm (localized accumulation of cells) can
be benign, a non-cancerous growth.
• But if the cells invade and interfere with the functioning
of surrounding normal tissue, the tumor is malignant.
• Malignant tumors and their cells can metastasize, or
spread, to other tissues in the body.
• About 20% of human cancers are caused by viruses (DNA
& retro viruses) (Luo and Ou, 2015).
 Viruses and Cancer

• Although many viruses can cause various tumors in animals, only seven of
them are associated with human cancers and are currently considered
oncogenic viruses:
–Human papilloma viruses (HPV-16 and HPV-8) cause cervical cancer.
–Epstein-Bar virus affects lymphocytes, causes destruction to the jaw and is
associated with some forms of cancer such as Hodgkin's lymphoma,
Burkitt's lymphoma and nasopharyngeal carcinoma.
–Hepatitis B &C viruses potentially cause liver cancer.
– Human herpes virus 8 (HHV8) is responsible for Kaposi’s sarcoma often
found in patients with acquired immunodeficiency syndrome (AIDS).
– Merkel cell polyomavirus (MCPyV) causes Merkel cell carcinoma.
– Human T-lymphotropic virus (HTLV-1) is the causative agent of adult T-cell
lymphoma.
 Viruses and Cancer – Viral Oncogenes

• Oncogene is a gene that has the potential to cause cancer (onco =

mass).
• The proteins produced by tumor viruses that cause uncontrolled
host cell division come from segments of DNA called oncogenes.
• Oncogenes & proto-oncogenes:
• oncogenes are viral genes which cause neoplasm & also contain the
information for synthesizing viral proteins needed for viral
replication.
• proto-oncogenes are normal cellular genes that control cell division
and can act as oncogenes  as a consequence of mutations resulting
from the integration of viral DNA within or adjacent to cellular
genes.
 Virus-Like Agents

•Satellites:
–Small ssRNA molecules (enclosed in a capsid), which lack genes
required for their replication.
–They can replicate only in the presence of a helper virus.
– They are not related to (different from) the helper virus.
– Called satellite as their reproduction “revolves around” a helper
virus.
–There are 2 types of satellites:
1. Satellite viruses: code for their capsid protein.
2. Satellite nucleic acid (virusoid): whose helper virus encodes
their capsid.
 Virus-Like Agents

•Delta hepatitis (hepatitis delta virus, HDV):

–It is a defective pathogen that requires coinfection with

hepatitis B virus (HBV) to replicate, i.e. it is considered a
satellite.
–Significantly increases the severity of HBV infection (i.e.
increases the mortality rate to 20%).
–Transmitted by blood and can be prevented by vaccination
against hepatitis B as it can’t infect without its helper virus.
–It has the smallest genome of any known animal virus.
 Virus-Like Agents

•Virophages:
–Similar to satellite viruses in that they can only replicate in
presence of a helper (host) virus but they impair their helper
virus’s replication.
–e.g. Sputnik virus: it co-infects amoeba cells with a larger virus
(Mimivirus) causing the inhibition of its replication.

•Viroids:
–Infectious RNA particles smaller than a virus & don’t require a
helper virus for their replication.
–Usually cause plant diseases.
 Virus-Like Agents

•Prions:

–Small proteinaceous infectious particle, that cause neurological

degenerative diseases such as ‘mad cow disease’.
In cattle, it is called bovine spongiform encephalopathy (BSE); while in
humans, it is called Creutzfeldt–Jakob disease (CJD).
–Characteristics of prions:
1. Resistant to inactivation by heating to 90°C, which usually inactivates
viruses.
2. Prion infection is not sensitive to radiation treatment that damages virus
genomes.
3. Not destroyed by enzymes that digest DNA or RNA.
4. Sensitive to protein denaturing agents, such as phenol and urea.
 Virus-Like Agents

•Prions:
–Prions are normal proteins that become folded incorrectly, possibly as a
result of a mutation.
– The harmless normal proteins, from which prions are produced, are found
on the plasma membrane of many mammalian cells, especially brain cells.
–The prion proteins (PrP) are thought to stick together inside cells, forming
small fibers, or fibrils.
– Because the fibrils cannot be organized in the plasma membrane
correctly, such aggregations eventually kill the cell.
–Prions are believed to cause other copies of the normal protein to fold
improperly and hence spread the disease.
–Prions move easily from one species to another (by injection or ingestion
of contaminated food).
 Treatment of Animal Viral Infections

• Because they are not bacteria, antibiotics are

ineffective.
• Antiviral drugs block virus replication by targeting
one of the steps in the viral life cycle.
• Interferon shows potential for treating and
preventing viral infections.
• Vaccines stimulate immunity.
 Plant viruses

• More than 1000 different viruses cause plant diseases.

• Including diseases of citrus trees, cocoa trees, rice, barely,
tobacco, turnips, cauliflower, potatoes, tomatoes and many
fruits, vegetables, trees and grains.
• These diseases result in huge economic losses.
• Plant viruses are usually transmitted via insects (e.g. aphids,
leaf hoppers, whiteflies), mites, nematodes (i.e. round
worms), infected seeds, cuttings and tubers, and
contaminated tools (e.g. hoes, clippers and saws).