Cielo Anne P.

SanJuan

Viruses

General Characteristics and Viral Structures

General Characteristics
of Viruses
VIRAL MORPHOLOGY
In general, the shapes of viruses are classified into four groups:
filamentous, isometric (or icosahedral), enveloped, and head
and tail.
Filamentous viruses are long and cylindrical. Many plant viruses
are filamentous, including TMV (tobacco mosaic virus).
Isometric viruses have shapes that are roughly spherical, such
as poliovirus or herpesviruses.
Enveloped viruses have membranes surrounding capsids. Animal
viruses, such as HIV, are frequently enveloped.
Head and tail viruses infect bacteria. They have a head that is
similar to icosahedral viruses and a tail shape like filamentous
viruses.
In the lytic phase virus particles
infect host cells and are replicated.

In the lysogenic phase, however,

viral genetic material that has
entered the host cell becomes
incorportated in the cell and lies
dormant. It is then passed on to the
progeny of the infected cells.

Eventually, the lytic phase will start

again, and cells that were never
infected themselves, but carry the
viral genetic material will begin to
produce new virus particles.
Example of a virus attaching to
its host cell:

The KSHV virus binds the xCT

receptor on the surface of
human cells. This attachment
allows for later penetration of
the cell membrane and
replication inside the cel
Classification of Viruses
Classification of Viruses

Adenovirus
 Classification of Viruses

Transmission
electron
micrograph
of viruses
Classification of Viruses
Classification of Viruses

Example
of viruses
classified by
caspid design
Classification of Viruses
VIRUS CORE STRUCTURE
The Structure of a Virus
Viruses come in a variety of shapes that are specialized in attacking
their target cell. The two major components of all viruses are the viral
genome and its protective protein coat, known as the capsid. The viral
genome is made up of single or double-stranded RNA or DNA, and it
encodes the proteins that make up the capsid. Together, the viral
genome and the capsid are known as the nucleocapsid.

A unique feature of many eukaryotic viruses is the presence of a

phospholipid membrane, known as the envelope that surrounds the
capsid. This envelope typically originates from the membranes of
previously infected host cells, but can also include viral proteins
(called envelope proteins) attached to it. Finally, some animal viruses
have a cluster of virus-encoded proteins, the viral tegument, in the
space between the envelope and capsid.
Thank you for
listening!
TAXONOMY OF
VIRUSES
By: Jerie Mae S. Reyes
Taxonomy of Viruses
• Virus taxonomy is a virology subspecialty that addresses the
grouping (classification) of viruses (physical entities) into
categories (concepts) called taxa and the development and
implementation of a standardized system of naming (nomenclature)
for taxa.
Learning Objectives

Define viral species

Give an example of family, genus, and common

name of a virus
For your information:
• 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 don’t
infect humans.
For your information:
• Viruses are now grouped according to how their mRNA is produced.
• New, fast DNA sequencing allows further classification of viruses
into families based on genomics and structure.
• The suffix -virus is used for genus names; family names end in -
viridae; and order names end in -ales.
• In formal usage, the family and genus names are used in the
following manner: Family Herpesviridae, genus Simplexvirus, human
herpesvirus-2.
Viral Classification starts at the level of orders and
continue as follows, with the taxon suffixes given.

• Order (-virales)
• Family (-viridae)
Subfamily (-virinae)
• Genus (-virus)
• Species
Species names generally take the form of (Disease) virus.
Example:
• Rabies virus
Rabies virus, scientific name Rabies lyssavirus, is a
neurotropic virus that causes rabies in humans and animals. Rabies
transmission can occur through the saliva of animals and less
commonly through contact with human saliva.
• Rabies virus
• Family: Rhabdoviridae
• Order: Mononegavirales
• Genus: Lyssavirus
• Species: Rabies lyssavirus
Viral species
• A viral species is a group of viruses sharing the same genetic
information and ecological niche (host range). Specific epithets
for viruses aren’t 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).
Families of Viruses That
Affect Humans
Envelope Virus
• A virus that has an outer wrapping or envelope. This envelope
comes from the infected cell, or host, in a process called
"budding off." During the budding process, newly formed virus
particles become "enveloped" or wrapped in an outer coat that is
made from a small piece of the cell's plasma membrane. The
envelope may play a role in helping a virus survive and infect
other cells.
Nonenveloped Virus
• Non-enveloped viruses do not have a lipid covering, but their
effects on humans can be just as devastating. These
“naked” viruses only need their protein-based capsid and host
detector proteins to infect host cells.
Nonenveloped
Enveloped
THANKS FOR LISTENING!
God Bless ☺
ISOLATION,CULTIVATION
AND
DE NTI
I DEN TIFFIIC
CA TI ON
ATI
OF
VIRUSES

Eanha Daenniel Obligado

 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 con tains
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.
 Growing Bacteriophages in the
Laboratory

In the laboratory, three These methods involve using

methods are commonly used living animals, embryonated
for culturing animal viruses. eggs, or cell cultures.
In Living Animals
Most experiments to study Animal inoculation may be
Some animal viruses can be
the immune system’s used as a diagnostic
cultured only in living
response to viral infections procedure for identifying and
animals, such as mice,
must also be performed in isolating a virus from a
rabbits, and guinea pigs. clinical specimen.
virally infected live animals.

Some human viruses can’t be grown

After the animal is inoculated in animals or can be grown but don’t
with the specimen, the animal is cause disease. .
observed for signs of disease or
is killed so that infected tissues
can be examined for the virus.
In Living Animals
Chimpanzees can be infected with
one subspecies of human
immunodeficiency virus
(HIV-1, genus Lentivirus), but because
they don’t show symptoms of the
disease, they can’t be used to study the
effects of viral growth and disease
treatments.
 AIDS vaccines are presently being tested in humans,
but the disease progresses so slowly in humans that it
can take years to determine the effectiveness of these
vaccines.

In 1986, simian AIDS (an immunodeficiency disease of

green monkeys) was reported, followed in 1987 by feline
AIDS (an immunodeficiency disease of domestic cats).

These diseases are caused by The mice provide a reliable

In 1990, a way to infect mice with
lentiviruses, which are closely model for studying viral
HIV was found when
related to HIV, and the diseases
immunodeficient mice were replication, although they don’t
develop within a few months, thus
grafted to produce human T cells provide models for vaccine
providing a model for studying
and human gamma globulin. development.
viral growth in different tissues.
In Embryonated Eggs If the virus will grow in an
embryonated egg, this can
be a fairly convenient and
inexpensive form of host for
many animal viruses.
A hole is drilled in the shell of the
embryonated egg, and a viral
suspension or suspected virus-
containing tissue is injected into the
egg’s fluid.
There are several membranes in an
egg, and the virus is injected near the
one most appropriate for its growth

Viral growth is signaled by

the death of the embryo, by
embryo cell damage, or by
the formation of typical pocks
or lesions on the egg
membranes.
 In Cell Cultures

Cell cultures have replaced Cell cultures consist of

embryonated eggs as the
cells grown in culture
preferred type of growth
medium for many viruses. media in the
laboratory.
 Cytopathic Effect (CPE)

CPE can be detected and counted in much the

same way as plaques caused by bacteriophages
on a lawn of bacteria and reported as PFU/ml.
 Viruses may be grown in
primary or continuous cell lines
PRIMARY CELL LINES CONTINUOUS CELL LINES
Primary cell When viruses are routinely
grown in a laboratory,
lines, continuous cell lines are
used.
derived from
These are transformed
tissue slices, tend (cancerous) cells that can be
maintained through an
to die out after indefinite number of
only a few generations, and they’re
sometimes called immortal
generations. cell lines.
HeLa cell line, was isolated from the cancer of a woman (Henrietta Lacks)
who died in 1951. After years of laboratory cultivation, many such cell
lines have lost almost all the original characteristics of the cell, but these
changes haven’t interfered with the use of the cells for viral propagation.
In spite of the success of cell culture in viral isolation and growth, there
are still some viruses that have never been successfully cultivated in cell
culture.
The idea of cell culture dates back to the end of the 19th century, but it
wasn’t a practical laboratory technique until the development of
antibiotics in the years following World War II.
 The maintenance of cell culture lines requires trained technicians with
considerable experience working on a full-time basis.
Because of these difficulties, most hospital laboratories and many state
health laboratories don’t isolate and identify viruses in clinical
work.

Instead, the tissue or serum samples are sent to central

laboratories that specialize in such work.
Viral
Identification Virologists can identify and
characterize viruses by using such
modern molecular methods as use
Viruses can’t be seen of restriction fragment length
without the use of an polymorphisms and the
electron microscope. polymerase chain reaction.

Serological methods, such as PCR was used to amplify viral

Western blotting, are the most
commonly used means of
identification
RNA to identify the West Nile
virus in 1999 in the United
States and the SARS-
associated coronavirus in
China in 2002.
 The
Webstern
Blot
Viral Multiplication
Salvatierra, Jonas V.
Parts of a Virus
Virus!
 Virus Multiplication

Introduction
The nucleic acid in a virion contains only a
few of the genes needed for the synthesis
of new viruses. These include genes for the
virion’s structural components, such as the
capsid proteins, and genes for a few of the
enzymes used in the viral life cycle.
 Virus Multiplication

Introduction
A single virion can give rise to several or
even thousands of similar viruses in a
single host cell. This process can
drastically change the host cell and usually
causes its death. In a few viral infections,
cells survive and continue to produce
viruses indefinitely.
 Multiplication of
Bacteriophages
Although the means by which a virus
enters and exits 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.
 1. The Lytic Cycle
• The virions of T-even bacteriophages are large,
complex, and nonenveloped, with a characteristic
head-and-tail structure.
• The length of DNA contained in these
bacteriophages is only about 6% of that contained
in E. coli, yet the phage 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.
After a chance collision between phage
particles and bacteria, attachment, or
absorption, occurs. During this process,
an attachment site on the virus attaches
to a complementary receptor site on the
Attachment
To join.
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.
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.
During the process of penetration, the Penetration
tail sheath of the phage contracts, and
succeed in forcing a way into or
the tail core is driven through the cell
through (a thing)
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.
Once the bacteriophage DNA
has reached the cytoplasm of
the host cell, the biosynthesis of
viral nucleic acid and protein
occurs. Host protein synthesis
Biosynthesis
the production of complex
is stopped by virus induced molecules within living
degradation of the host DNA, organisms or cells.
viral proteins that interfere with
transcription, or the repression
of translation.
Initially, the phage 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 Biosynthesis
cell’s ribosomes, enzymes, and amino the production of complex
acids are used for translation. Genetic molecules within living
controls regulate when different regions organisms or cells.
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. Only
separate components— DNA Biosynthesis
and protein—can be detected. the production of complex
molecules within living
The period during viral organisms or cells.
multiplication when complete,
infective virions aren’t yet
present is called the eclipse
period.
In the next sequence of events,
maturation occurs. In this
process, bacteriophage DNA
and capsids are assembled into
complete virions. The viral
components essentially Maturation
assemble into a viral particle having reached the most
spontaneously, eliminating the advanced stage in a process
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.
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 Release
(lyses). Lysozyme, which is
allow or enable to escape from
encoded by a phage gene, is
confinement; set free
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.
 The Lysogenic Cycle
In contrast to T-even bacteriophages, some
viruses don’t cause lysis and death of the host cell
when they multiply. These lysogenic phages (also
called temperate phages) may indeed proceed
through a lytic cycle, but they are also capable of
incorporating their DNA into the host cell’s DNA to
begin a lysogenic cycle. In lysogeny, the phage
remains latent (inactive). The participating bacterial
host cells are known as lysogenic cells.
 There are three important results
of lysogeny:

1.) 2.) 3.)

First, the lysogenic
The second result The third result of
cells are immune to
of lysogeny is lysogeny is that it
reinfection by the same
phage conversion; makes specialized
phage. (However, the
that is, the host transduction
host cell isn’t immune
cell may exhibit possible.
to infection by other
new properties.
phage types.)
THANK YOU!
GOD BLESS
STAY SAFE
Multiplication of Animal
Viruses

PAULINE REYES
BSN1B
• Animal viruses differ from phages in their
mechanism of entering the host cell.
• Virus needs live host cells but must stop
synthesis of host proteins, so the viral genes
are translated. Research currently indicates
that viruses use several mechanisms to inhibit
expression of host cell genes.
• There are processes that are shared by both
DNA- and RNA-containing animal viruses.
These processes are attachment, entry,
uncoating, and release.
 Attachment
• Like bacteriophages, animal viruses have
attachment sites that attach to complementary
receptor sites on the host cell’s surface.
• The receptor sites of animal cells are proteins and
glycoproteins
• The attachment sites of animal viruses are
distributed over the surface of the virus, and the
sites themselves vary from one group of viruses
to another
• ADENOVIRUSES
- the attachment sites are
small fibers at the corners of
the icosahedron
• INFLUENZA VIRUS
- the attachment sites are
spikes located on the
surface of the envelope
 Entry
• Entry Following attachment, entry occurs. Many
viruses enter into eukaryotic cells by receptor-
mediated endocytosis.
• A cell’s plasma membrane continuously folds
inward to form vesicles. These vesicles contain
elements that originate outside the cell and are
brought into the interior of the cell to be
digested. If a virion attaches to the plasma
membrane of a potential host cell, the host cell
will enfold the virion and form a vesicle.
 Entry
• Enveloped viruses can enter by an alternative
method called fusion, in which the viral
envelope fuses with the plasma membrane
and releases the capsid into the cell’s
cytoplasm
 Uncoating
• Uncoating Viruses disappear during the
eclipse period of an infection because they are
taken apart inside the cell. Uncoating is the
separation of the viral nucleic acid from its
protein coat. This process varies with the type
of virus. These enzymes degrade the proteins
of the viral capsid
BIOSYNTHESIS OF DNA VIRUSES
• DNA-containing viruses replicate their DNA in
the nucleus of the host cell by using viral
enzymes, and they synthesize their capsid and
other proteins in the cytoplasm by using host
cell enzymes.
• Then the proteins migrate into the nucleus
and are joined with the newly synthesized
DNA to form virions. These virions are
transported along the endoplasmic reticulum
to the host cell’s membrane for release.
 DNA VIRUSES:
• Adenoviridae Named after adenoids, from
which they were first isolated, adenoviruses
cause acute respiratory diseases— the
common cold
• Poxviridae- All diseases caused by poxviruses,
including smallpox and cowpox, include skin
lesions. Pox refers to pus-filled lesions. Viral
multiplication is started by viral transcriptase;
the viral components are synthesized and
assembled in the cytoplasm of the host cell.
• Herpesviridae- Nearly 100 herpesviruses are known.
They are named after the spreading (herpetic)
appearance of cold sores. Species of human
herpesviruses (HHV) include HHV-1 and HHV-2, both in
the genus Simplexvirus, which cause cold sores; HHV-3,
Varicellovirus, which causes chickenpox; HHV-4,
Lymphocryptovirus, which causes infectious
mononucleosis; HHV-5, Cytomegalovirus, which causes
CMV inclusion disease; HHV-6, Roseolovirus, which
causes roseola; HHV-7, Roseolovirus, which infects
most infants, causing measleslike rashes; and HHV-8,
Rhadinovirus, which causes Kaposi’s sarcoma, primarily
in AIDS patients.
• Papovaviridae Papovaviruses are named for
papillomas (warts), polyomas (tumors), and
vacuolation (cytoplasmic vacuoles produced by
some of these viruses). Warts are caused by
members of the genus Papillomavirus. Some
Papillomavirus species are capable of
transforming cells and causing cancer. Viral DNA
is replicated in the host cell’s nucleus along with
host cell chromosomes. Host cells may
proliferate, resulting in a tumor.
• Hepadnaviridae - Hepadnaviridae are so
named because they cause hepatitis and
contain DNA. The only genus in this family
causes hepatitis B. Hepadnaviruses differ from
other DNA viruses because they synthesize
DNA by copying RNA, using viral reverse
transcriptase. This DNA is the template for
viral mRNA and the virus’s DNA genome.
 The
Biosynthesis
of RNA
Viruses
YNEL A.
WEDINGCO
members in team

Mimops Mimops

Mimops Mimops
 *The multiplication of RNA viruses is essentially the
same as that of DNA viruses, except RNA viruses multiply in
the host cell’s cytoplasm.
*The major differences among the multiplica- tion
processes lie in how mRNA and viral RNA are produced.
*These viruses have RNA-dependent RNA polymerase.
 *The multiplication of RNA viruses is essentially the
same as that of DNA viruses, except RNA viruses multiply in
the host cell’s cytoplasm.
*The major differences among the multiplica- tion
processes lie in how mRNA and viral RNA are produced.
*These viruses have RNA-dependent RNA polymerase.
 Picornaviruses
*Picornaviruses, such as *RNA within the virion is called a
enteroviruses and polio virus are sense strand (+ strand)
single-stranded RNA viruses *One inhibits the host cell’s
*They are the smallest viruses; synthesis of RNA,and the other
and the prefix pico- (small) plus is RNA-dependent RNA
RNA gives these viruses their polymerase.
name.
 Togaviridae
*Togaviruses are enveloped
viruses; their name is from the
Latin word for covering, toga.
 Rhabdoviridae
*rhabdoviruses, such as rabies *They contain a single - strand of
virus RNA.
*Rhabdo- is from the Greek word
for rod, which isn’t really an
accurate description of their mor-
phology.
 Reoviridae
*Reoviruses were named for their *Viral mRNA is produced in the
habitats: the respi- ratory and enteric cytoplasm, where it’s used to
(digestive) systems of humans. synthesize more viral proteins.

*The capsid containing the double-

stranded RNA is digested upon
entering a host cell. mor- phology.
 Reoviridae
*Reoviruses were named for their *Viral mRNA is produced in the
habitats: the respi- ratory and enteric cytoplasm, where it’s used to
(digestive) systems of humans. synthesize more viral proteins.

*The capsid containing the double-

stranded RNA is digested upon
entering a host cell. mor- phology.
The formation of mRNA and RNA for new
retrovirus virions is shown in Figure 13.19.
These viruses carry reverse transcrip- tase,
which uses the viral RNA as a template to
produce complementary double-stranded
DNA. This enzyme also degrades the original
viral RNA. The name retrovirus is derived
from the first letters of reverse
transcriptase. The viral DNA is then inte-
grated into a host cell chromosome as a
provirus. Unlike a pro- phage, the provirus
never comes out of the chromosome. As a
provirus, HIV is protected from the host’s
immune system and antiviral drugs.
Maturation and Release
The first step in viral maturation is the
assembly of the pro- tein capsid; this
assembly is usually a spontaneous process.
The capsids of many animal viruses are
enclosed by an enve- lope consisting of
protein, lipid, and carbohydrate, as noted
earlier. Examples of such viruses include
orthomyxoviruses and paramyxoviruses. The
envelope protein is encoded by the viral
genes and is incorporated into the plasma
membrane of the host cell. The envelope
lipid and carbohydrate are encoded by host
cell genes and are present in the plasma
membrane. The envelope actually develops
around the capsid by a process called
budding (Figure 13.20).
thank u !!
VIRUS and
CANCER
Objectives
● Define oncogene and ● Discuss the relationship
transformed cell. between DNA- and RNA-
containing viruses and
cancer

2
Several types of cancer are now
known to be caused by viruses.
Molecular biological research
shows that the mechanisms of
the diseases are similar, even
when a virus doesn’t cause the
cancer

3
The relationship between cancers and viruses was first demonstrated in 1908, when
virologists Wilhelm Ellerman and Olaf Bang, working in Denmark, were trying to isolate the
causative agent of chicken leukemia. They found that leukemia could be transferred to
healthy chickens by cell-free filtrates that contained viruses.
Three years later, F. Peyton Rous, working at the Rockefeller Institute in New York, found
that a chicken sarcoma (cancer of connective tissue) can be similarly transmitted. Virus-
induced adenocarcinomas (cancers of glandular epithelial tissue) in mice were discovered
in 1936. At that time, it was clearly shown that mouse mammary gland tumors are
transmitted from mother to offspring through the mother’s milk. The cancer-causing SE
polyoma virus was discovered and isolated in 1953 by American scientists Bernice Eddy and
Sarah Stewart

4
The viral cause of cancer can often go unrecognized for several
reasons.
● First, most of the particles of some viruses infect cells but
don’t induce cancer.
● Second, cancer might not develop until long after viral
infection.
● Third, cancers, even those caused by viruses, don’t seem to
be contagious, as viral diseases usually are.

5
The Transformation
of Normal Cells into
Tumor Cells
• Almost anything that can alter the genetic material of a eukaryotic cell has the
potential to make a normal cell cancerous.

• These cancer-causing alterations to cellular DNA affect parts of the genome called
oncogenes.

• Oncogenes were first identified in cancer-causing viruses and were thought to be a

part of the normal viral genome. However, American microbiologists J. Michael
Bishop and Harold E. Varmus received the 1989 Nobel Prize in Medicine for proving
that the cancer-inducing genes carried by viruses are actually derived from animal
cells.

7
• Oncogenes can be activated to abnormal functioning by a variety of agents, including
mutagenic chemicals, high-energy radiation, and viruses.

• Viruses capable of inducing tumors in animals are called oncogenic viruses, or

oncoviruses.

• A defining feature of all oncogenic viruses is that their genetic material integrates into the
host cell’s DNA and replicates along with the host cell’s chromosome. This mechanism is
similar to the phenomenon of lysogeny in bacteria, and it can alter the host cell’s
characteristics in the same way.

• Tumor cells undergo transformation; that is, they acquire properties that are distinct from
the properties of uninfected cells or from infected cells that don’t form tumors. After being
transformed by viruses, many tumor cells contain a virus specific antigen on their cell
surface, called tumor-specific transplantation antigen (TSTA), and transformed cells tend
to be irregularly shaped, compared to normal cells.

8
DNA ONCOGENIC
VIRUSES

9
Oncogenic viruses are found within several families of DNAcontaining
viruses. These groups include the Adenoviridae, Herpesviridae, Poxviridae,
Papovaviridae, and Hepadnaviridae.

Virtually all cervical and anal cancers are caused by human papillomavirus
(HPV).

10
Epstein-Barr (EB) virus was isolated from Burkitt’s lymphoma cells in 1964 by Michael
Epstein and Yvonne Barr. The proof that EB virus can cause cancer was accidentally
demonstrated in 1985 when a 12-year-old boy known only as David received a bone
marrow transplant. Several months after the transplant, he died of cancer. An autopsy
revealed that the virus had been unwittingly introduced into the boy with the bone
marrow transplant.

Another DNA virus that causes cancer is hepatitis B virus (HBV). Many animal studies have
been performed that have clearly indicated the causal role of HBV in liver cancer. In one
human study, virtually all people with liver cancer had previous HBV infections.

11
RNA ONCOGENIC
VIRUSES
Among the RNA viruses, only the oncoviruses in the family Retroviridae cause cancer. The human T
cell leukemia viruses (HTLV-1 and HTLV-2) are retroviruses that cause adult T cell leukemia and
lymphoma in humans. (T cells are a type of white blood cell involved in the immune response.)

Sarcoma viruses of cats, chickens, and rodents, and the mammary tumor viruses of mice, are also
retroviruses. Another retrovirus, feline leukemia virus (FeLV), causes leukemia in cats and is
transmissible among cats. There is a test to detect the virus in cat serum

The ability of retroviruses to induce tumors is related to their production of a reverse transcriptase by
the mechanism described earlier. The provirus, which is the double-stranded DNA molecule
synthesized from the viral RNA, becomes integrated into the host cell’s DNA; new genetic material is
thereby introduced into the host’s genome and is the key reason retroviruses can contribute to cancer.
Some retroviruses contain oncogenes; others contain promoters that turn on oncogenes or other
cancer-causing factors.

13
 VIRUSES TO
TREAT CANCER

14
In the early 1900s, physicians observed that tumors regressed in patients with
concurrent viral infections. Experimentally induced viral infections in cancer patients
during the 1920s suggested that viruses might have antitumor activity. These tumor-
destroying viruses, or oncolytic viruses, selectively infect and kill tumor cells or cause
an immune response against tumor cells. Several viruses are known to selectively
infect cancer cells, and these are being genetically modified to remove virulence
genes and add colony-stimulating factor genes to promote white blood cells.

Imlygic, is a herpesvirus to treat melanoma.

15
Latent Viral Infection

16
A virus can remain in equilibrium with the host and not actually produce disease for a long
period, often many years. The oncogenic viruses just discussed are examples of such latent
infections. All of the human herpes viruses can remain in host cells throughout the life of an
individual.
When herpes viruses are reactivated by immunosuppression (for example, AIDS), the resulting
infection may be fatal. The classic example of such a latent infection is the infection of the skin
by Simplexvirus, which produces cold sores. This virus inhabits the host’s nerve cells but causes
no damage until it is activated by a stimulus such as fever or sunburn—hence the term fever
blister.

In some individuals, viruses are produced, but symptoms never appear. Even though a large
percentage of the human population carries Simplexvirus, only 10–15% of people carrying the
virus exhibit the disease.

17
The chickenpox virus (Varicellovirus) can aso exist in a latent state. Chickenpox (varicella) is a
skin disease that is usually acquired in childhood. The virus gains access to the skin via the
blood. From the blood, some viruses may enter nerves, where they remain latent. Later,
changes in the immune (T cell) response can activate these latent viruses, causing shingles
(zoster). The shingles rash appears on the skin along the nerve in which the virus was latent.
Shingles occurs in 10–20% of people who have had chickenpox.

18
19
Thanks!
20



 Persistent Viral Infection

Also known as chronic viral infection,

which gradually occurs over a long
period. Typically, persistent viral
infections are fatal.

A number of persistent viral infections

have in fact been shown to be caused by
conventional viruses.
 Plant Viruses and
Viroids

Plant Viruses are viruses that affect plants. They are morphologically
similar to animal viruses, and they have similar types of nucleic acid.

These can cause color change, deformed growth, wilting, and stunted
growth in their plant hosts.

Some plant diseases are caused by viroids, short pieces of naked RNA,
only 300 to 400 nucleotides long, with no protein coat.

Some viroids, called virusoids, are enclosed in a protein coat.

Classification of Some Major Plant Viruses

1. Caulimorividae
Double-stranded DNA

Viral Genus: Cauliflower mosaic

virus

Mode of transmition: Aphids

2. Bunyaviridae
Single-stranded RNA

Viral Genus: Watermelon wilt

Mode of Transmission: Whiteflies

3. Virgaviridae
Single-stranded DNA

Viral Genus: Tobamovirus

Mode of Transmission: Wounds

4. Rhabdoviridae
Single-stranded DNA

Viral Genus: Potato yellow drawf

virus

Mode of Transmission:
Leafhoppers and aphids
5. Rheoviridae
Double-stranded DNA

Viral Genus: Wound tumor virus

Mode of transmition: Leafhoppers

 Prions

It is an infectious agent composed only of protein in a

misfolded form that is inherited and transmissible by
ingestion, transplant, & surgical instruments.

In 1982, American neurologist Stanley Prusiner proposed

that infectious proteins caused a neurological disease in
sheep called scrapie.

Prusiner coined the name Prion for proteinaceous

infectious particle.

Nine neurological animal diseases and four human diseases

now fall in this category called Transmissible spongiform
encephalopathies.
 Animal diseases Human diseases
1. Scrapie
2. Transmissible mink 1. Kuru
encephalopathy (TME)
3. Chronic wasting disease 2. Creutzfeldt–Jakob disease
4. Bovine spongiform
(CJD)
encephalopathy (BSE)
commonly known as "Mad Cow
Disease“ 3. Gerstmann-Sträussler-
5. Feline spongiform Scheinker syndrome
encephalopathy (FSE)
6. Exotic ungulate encephalopathy
4. Fatal familial insomnia
(EUE)
7. Camel spongiform
encephalopathy (CSE)
Thank you po