Republic of the Philippines
UNIVERSITY OF EASTERN PHILIPPINES
University Town, Catarman, Northern Samar
COLLEGE OF EDUCATION
Secondary Teacher Education Department
2nd Semester SY: 2020-2021
Module in Major 7a: GENETICS
This module is prepared by:
Christine M. Adlawan, LLB, MPA
STEd Faculty
Module in GENETICS
Module
Prof. Christine M. Adlawan
7
VIRUSES
OVERVIEW
‗Viruses are everywhere‘ describes the ‗virosphere‘ — the virus
biomass of enormous variety and complexity in the environment. Viruses are
the most numerous microbes on Earth with an estimated 100 million different
types. The largest virus, mimivirus, is thought to fall into an evolutionary
position at a point before the animal and plant kingdoms split and indicate the
long history of viruses.
Humans have been battling viruses since before our species had even
evolved into its modern form. For some viral diseases, vaccines and antiviral
drugs have allowed us to keep infections from spreading widely, and have
helped sick people recover. For one disease — smallpox — we've been able
to eradicate it, ridding the world of new cases. This module will discuss
everything that we want to know about virus including its prevention and
treatment.
.
LEARNING PLAN
At the completion of this lesson, you should be able to:
1. Describe how viruses were first discovered and how they are detected;
2. Identify the general characteristics of viruses as pathogens;
3. Discuss viral genomes;
4. Explain the general characteristics of viral life cycles;
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5. Describe the characteristics used to identify viruses as obligate
intracellular parasites;
6. Explain the detailed steps of viral replication; and
7. Describe how vaccines are used in prevention and treatment of viral
diseases
ACTIVITY
Clinical Focus: Joaquim
Joaquim, a 45-year-old journalist, has just returned to the U.S. from
travels in Russia, China, and Africa. He is not feeling well, so he goes to his
general practitioner complaining of weakness in his arms and legs, fever,
headache, noticeable agitation, and minor discomfort. He thinks it may be
related to a dog bite he suffered while interviewing a Chinese farmer. He is
experiencing some prickling and itching sensations at the site of the bite
wound, but he tells the doctor that the dog seemed healthy and that he had
not been concerned until now. The doctor ordered a culture and sensitivity
test to rule out bacterial infection of the wound, and the results came back
negative for any possible pathogenic bacteria.
In your own understanding, based on this information above, what
additional tests should be performed on the patient? What type of treatment
should the doctor recommend?
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ABSTRACTION
A
virus
can
be
simply
defined as an obligate intracellular
parasite. Each viral particle, or
virion, consists of a single nucleic
acid, RNA or DNA, encoding the
viral genome surrounded by a
protein coat, and is capable of
replication only within the living
cells of bacteria, animals or plants.
Viruses
are
classified
into
different
orders
and
families
by
consideration of the type of nucleic acid present (RNA or DNA), whether the
nucleic acid is single- or double-stranded, and the presence or absence of an
envelope.
History of Viruses
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No one knows exactly when viruses emerged or from where they
came, since viruses do not leave historical footprints such as fossils. Modern
viruses are thought to be a mosaic of bits and pieces of nucleic acids picked
up from various sources along their respective evolutionary paths.
Viruses are acellular, parasitic entities that are not classified within any
domain because they are not considered alive. They have no plasma
membrane, internal organelles, or metabolic processes, and they do not
divide. Instead, they infect a host cell and use the host‘s replication processes
to produce progeny virus particles. Viruses infect all forms of organisms
including bacteria, archaea, fungi, plants, and animals. Living things grow,
metabolize, and reproduce. Viruses replicate, but to do so, they are entirely
dependent on their host cells. They do not metabolize or grow, but are
assembled in their mature form.
Viruses are diverse. They vary in their structure, their replication
methods, and in their target hosts or even host cells. While most biological
diversity can be understood through evolutionary history, such as how
species have adapted to conditions and environments, much about virus
origins and evolution remains unknown. Despite their small size, which
prevented them from being seen with light microscopes, the discovery of a
filterable component smaller than a bacterium that causes tobacco mosaic
disease (TMD) dates back to 1892?
At that time, Dmitri Ivanovski, a Russian botanist, discovered the
source of TMD by using a porcelain filtering device first invented by Charles
Chamberland and Louis Pasteur in Paris in 1884. Porcelain Chamberland
filters has a pore size of 0.1 µm, which is small enough to remove all bacteria
≥0.2 µm from any liquids passed through the device. An extract obtained from
TMD-infected tobacco plants was made to determine the cause of the
disease. Initially, the source of the disease was thought to be bacterial. It was
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surprising to everyone when Ivanovski, using a Chamberland filter, found that
the cause of TMD was not removed after passing the extract through the
porcelain filter. So if a bacterium was not the cause of TMD, what could be
causing the disease? Ivanovski concluded the cause of TMD must be an
extremely small bacterium or bacterial spore. Other scientists, including
Martinus Beijerinck, continued investigating the cause of TMD. It was
Beijerinck, in 1899, who eventually concluded the causative agent was not a
bacterium but, instead, possibly a chemical, like a biological poison we would
describe today as a toxin.
As a result, the word virus, Latin for poison, was used to describe the
cause of TMD a few years after Ivanovski‘s initial discovery. Even though he
was not able to see the virus that caused TMD, and did not realize the cause
was not a bacterium, Ivanovski is credited as the original discoverer of viruses
and a founder of the field of virology.
Today, we can see viruses using electron microscopes and we know
much more about them. Viruses are distinct biological entities; however, their
evolutionary origin is still a matter of speculation. In terms of taxonomy, they
are not included in the tree of life because they are acellular (not consisting of
cells). In order to survive and reproduce, viruses must infect a cellular host,
making them obligate intracellular parasites. The genome of a virus enters a
host cell and directs the production of the viral components, proteins and
nucleic acids, needed to form new virus particles called virions. New virions
are made in the host cell by assembly of viral components. The new virions
transport the viral genome to another host cell to carry out another round of
infection.
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Figure 1:
(a) Tobacco mosaic virus (TMV) viewed with transmission electron microscope.
(b) Plants infected with tobacco mosaic disease (TMD), caused by TMV. (credit a:
modification of work by USDA Agricultural Research Service—scale-bar data from Matt
Russell; credit b: modification of work by USDA Forest Service, Department of Plant
Pathology Archive North Carolina State University)
Characteristics of Viruses
 Infectious, acellular pathogens;
 Obligate intracellular parasites with host and cell-type specificity;
 DNA or RNA genome (never
both);
 Genome is surrounded by a
protein capsid and, in some
cases,
a
phospholipid
membrane studded with viral
glycoproteins;
 Lack
genes
products
successful
for
many
needed
for
reproduction,
requiring exploitation of hostcell genomes to reproduce
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Hosts and Viral Transmission
Viruses can infect every type of host cell, including those of plants,
animals, fungi, protists, bacteria, and archaea. Most viruses will only be able
to infect the cells of one or a few species of organism. This is called the host
range. However, having a wide host range is not common and viruses will
typically only infect specific hosts and only specific cell types within those
hosts.
The viruses that infect bacteria are called bacteriophages, or simply
phages. The word phage comes from the Greek word for devour. Other
viruses are just identified by their host group, such as animal or plant viruses.
Once a cell is infected, the effects of the virus can vary depending on the type
of virus. Viruses may cause abnormal growth of the cell or cell death, alter the
cell‘s genome, or cause little noticeable effect in the cell.
Viruses can be transmitted through direct contact, indirect contact with
fomites, or through a vector: an animal that transmits a pathogen from one
host to another.
In humans, a wide variety of viruses are capable of causing various
infections and diseases. Some of the deadliest emerging pathogens in
humans are viruses, yet we have few treatments or drugs to deal with viral
infections, making them difficult to eradicate.
Viruses that can be transmitted from an animal host to a human host
can cause zoonoses. For example, the avian influenza virus originates in
birds, but can cause disease in humans. Reverse zoonoses are caused by
infection of an animal by a virus that originated in a human.
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Viral Structures
In general, virions (viral particles) are small and cannot be observed
using a regular light microscope. They are much smaller than prokaryotic and
eukaryotic cells; this is an adaptation allowing viruses to infect these larger
cells (see Figure 2).
The size of a virion can range from 20 nm for small viruses up to 900
nm for typical, large viruses (see Figure 3). Recent discoveries, however,
have identified new giant viral species, such as Pandoravirus salinus and
Pithovirus sibericum, with sizes approaching that of a bacterial cell.
Figure 2:
(a) In this transmission electron micrograph, a bacteriophage (a virus that infects
bacteria) is dwarfed by the bacterial cell it infects.
(b) An illustration of the bacteriophage in the micrograph. (credit a: modification of
work by U.S. Department of Energy, Office of Science, LBL, PBD)
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Figure 3. The size of a virus is small relative to the size of most bacterial and
eukaryotic cells and their organelles.
In 1935, after the development of the electron microscope, Wendell
Stanley was the first scientist to crystallize the structure of the tobacco mosaic
virus and discovered that it is composed of RNA and protein. In 1943, he
isolated Influenza B virus, which contributed to the development of an
influenza (flu) vaccine. Stanley‘s discoveries unlocked the mystery of the
nature of viruses that had been puzzling scientists for over 40 years and his
contributions to the field of virology led to him being awarded the Nobel Prize
in 1946.
As a result of continuing research into the nature of viruses, we now
know they consist of a nucleic acid (either RNA or DNA, but never both)
surrounded by a protein coat called a capsid (see Figure 4). The interior of
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the capsid is not filled with cytosol, as in a cell, but instead it contains the bare
necessities in terms of genome and enzymes needed to direct the synthesis
of new virions. Each capsid is composed of protein subunits called
capsomeres made of one or more different types of capsomere proteins that
interlock to form the closely packed capsid.
Figure 4. Click for a larger image. (a) The naked atadenovirus uses spikes made of
glycoproteins from its capsid to bind to host cells. (b) The enveloped human
immunodeficiency virus uses spikes made of glycoproteins embedded in its envelope to bind
to host cells (credit a ―micrograph‖: modification of work by NIAID; credit b ―micrograph‖:
modification of work by Centers for Disease Control and Prevention)
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There are two categories of viruses based on general composition.
Viruses formed from only a nucleic acid and capsid are called naked viruses
or nonenveloped viruses. Viruses formed with a nucleic-acid packed capsid
surrounded by a lipid layer are called enveloped viruses (see Figure 4). The
viral envelope is a small portion of phospholipid membrane obtained as the
virion buds from a host cell. The viral envelope may either be intracellular or
cytoplasmic in origin.
Extending
outward
and
away from the capsid on some
naked viruses and enveloped
viruses are protein structures
called spikes. At the tips of
these spikes are structures that
allow the virus to attach and
enter a cell, like the influenza
virus hemagglutinin spikes (H) or enzymes like the neuraminidase (N)
influenza virus spikes that allow the virus to detach from the cell surface
during release of new virions. Influenza viruses are often identified by their H
and N spikes.
For example, H1N1 influenza
viruses
were
responsible
for
the
pandemics in 1918 and 2009, H2N2
for the pandemic in 1957, and H3N2
for the pandemic in 1968.
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Viruses vary in the shape of their capsids, which can be helical,
polyhedral, or complex. A helical capsid forms the shape of tobacco mosaic
virus (TMV), a naked helical virus, and Ebola virus, an enveloped helical
virus.
The capsid is cylindrical or rod shaped, with the genome fitting just
inside the length of the capsid. Polyhedral capsids form the shapes of
poliovirus and rhinovirus, and consist of a nucleic acid surrounded by a
polyhedral (many-sided) capsid in the form of an icosahedron.
An icosahedral capsid is a three-dimensional, 20-sided structure with
12 vertices. These capsids somewhat resemble a soccer ball. Both helical
and polyhedral viruses can have envelopes.
Viral shapes seen in certain types of bacteriophages, such as T4
phage, and poxviruses, like vaccinia virus, may have features of both
polyhedral and helical viruses so they are described as a complex viral shape
(see Figure 5).
In the bacteriophage complex form, the genome is located within the
polyhedral head and the sheath connects the head to the tail fibers and tail
pins that help the virus attach to receptors on the host cell‘s surface.
Poxviruses that have complex shapes are often brick shaped, with intricate
surface characteristics not seen in the other categories of capsid.
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Figure 5. Viral capsids can be (a) helical, (b) polyhedral, or (c) have a complex
shape. (credit a ―micrograph‖: modification of work by USDA ARS; credit b ―micrograph‖:
modification of work by U.S. Department of Energy)
Classification and Taxonomy of Viruses
Although viruses are not classified in the three domains of life, their
numbers are great enough to require classification. Since 1971, the
International Union of Microbiological Societies Virology Division has given
the task of developing, refining, and maintaining universal virus taxonomy to
the International Committee on Taxonomy of Viruses (ICTV). Since viruses
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can mutate so quickly, it can be difficult to classify them into a genus and a
species epithet using the binomial nomenclature system. Thus, the ICTV‘s
viral nomenclature system classifies viruses into families and genera based
on viral genetics, chemistry, morphology, and mechanism of multiplication.
To date, the ICTV has classified known viruses in seven orders, 96
families, and 350 genera. Viral family names end in –viridae (e.g,
Parvoviridae) and genus names end in −virus (e.g., Parvovirus). The names
of viral orders, families, and genera are all italicized. When referring to a viral
species, we often use a genus and species epithet such as Pandoravirus
dulcis or Pandoravirus salinus.
The Baltimore classification system is an alternative to ICTV
nomenclature. The Baltimore system classifies viruses according to their
genomes (DNA or RNA, single versus double stranded, and mode of
replication). This system thus creates seven groups of viruses that have
common genetics and biology.
Aside from formal systems of nomenclature, viruses are often
informally grouped into categories based on chemistry, morphology, or other
characteristics they share in common. Categories may include naked or
enveloped structure, single-stranded (ss) or double-stranded (ds) DNA or ss
or ds RNA genomes, segmented or nonsegmented genomes, and positivestrand (+) or negative-strand (−) RNA. For example, herpes viruses can be
classified as a dsDNA enveloped virus; human immunodeficiency virus (HIV)
is a +ssRNA enveloped virus, and tobacco mosaic virus is a +ssRNA virus.
Other characteristics such as host specificity, tissue specificity, capsid shape,
and special genes or enzymes may also be used to describe groups of similar
viruses.
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The Table below lists some of the most common viruses that are
human pathogens by genome type.
Common Pathogenic Viruses
Genome
dsDNA,
enveloped
dsDNA,
naked
ssDNA,
naked
Family
Poxviridae
Example Virus
Orthopoxvirus
Poxviridae
Herpesviridae
Parapoxvirus
Simplexvirus
Adenoviridae
Atadenovirus
Papillomaviridae
Papillomavirus
Reoviridae
Reovirus
Parvoviridae
Reoviridae
Adeno-associated
dependoparvovirus A
Adeno-associated
dependoparvovirus B
Rotavirus
Picornaviridae
Picornaviridae
Enterovirus C
Rhinovirus
Picornaviridae
Togaviridae
Hepatovirus
Alphavirus
Togaviridae
Retroviridae
Rubivirus
Lentivirus
Parvoviridae
dsRNA,
naked
+ssRNA,
naked
+ssRNA,
enveloped
−ssRNA,
enveloped
Filoviridae
Zaire Ebolavirus
Orthomyxoviridae Influenzavirus A, B, C
Rhabdoviridae
Lyssavirus
Clinical Features
Skin papules, pustules,
lesions
Skin lesions
Cold sores, genital
herpes, sexually
transmitted disease
Respiratory infection
(common cold)
Genital warts, cervical,
vulvar, or vaginal
cancer
Gastroenteritis severe
diarrhea (stomach flu)
Respiratory tract
infection
Respiratory tract
infection
Gastroenteritis
Poliomyelitis
Upper respiratory tract
infection (common cold)
Hepatitis
Encephalitis,
hemorrhagic fever
Rubella
Acquired immune
deficiency syndrome
(AIDS)
Hemorrhagic fever
Flu
Rabies
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How Viruses Replicate
Viral replication is the term used that indicates the formation of
biological viruses during the infection process in the target host cells. Viruses
must first penetrate and enter the cell before viral replication can occur. From
the perspective of the virus, the purpose of viral replication is to allow
reproduction and survival of its kind. By generating abundant copies of its
genome and packaging these copies into viruses, the virus is able to continue
infecting new hosts.
Replication between viruses is varied and depends on the type of
genes involved. Most DNA viruses assemble in the nucleus; most RNA
viruses develop solely in cytoplasm. Viral populations do not grow through
cell division, because they are acellular. Instead, they hijack the machinery
and metabolism of a host cell to produce multiple copies of themselves, and
they assemble inside the cell.
The life cycle of viruses differs greatly between species but there are
six (6) common basic stages:
1. Attachment is a specific binding between viral capsid proteins and
specific receptors on the host cellular surface. This specificity determines
the host range of a virus.
For example, HIV can infect only a limited range of human leukocytes.
Its surface protein, gp120, specifically interacts only with the CD4 molecule –
a chemokine receptor – which is most commonly found on the surface of
CD4+ T-Cells. This mechanism has evolved to favor those viruses that infect
only cells within which they are capable of replication. Attachment to the
receptor can fore the viral envelope protein to undergo either changes that
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result in the fusion of viral and cellular membranes, or changes of nonenveloped virus surface proteins that allow the virus to enter.
2. Penetration follows attachment. Virions enter the host cell through
receptor-mediated endocytosis or membrane fusion. This is often called
viral entry.
The infection of plant and fungal cells is different from that of animal
cells. Plants have a rigid cell wall made of cellulose, and fungi one of chitin,
so most viruses can get inside these cells only after trauma to the cell wall.
However, nearly all plant viruses (such as tobacco mosaic virus) can also
move directly from cell to cell, in the form of single-stranded nucleoprotein
complexes, through pores called plasmodesmata. Bacteria, like plants, have
strong cell walls that a virus must breach to infect the cell. However, since
bacterial cell walls are much less thick than plant cell walls due to their much
smaller size, some viruses have evolved mechanisms that inject their genome
into the bacterial cell across the cell wall, while the viral capsid remains
outside.
3. Uncoating is a process in which the viral capsid is removed: This may be
by degradation by viral or host enzymes or by simple dissociation. In
either case the end-result is the release of the viral genomic nucleic acid.
4. Replication - Replication of viruses depends on the multiplication of the
genome. This is accomplished through synthesis of viral messenger RNA
(mRNA) from ―early‖ genes (with exceptions for positive sense RNA
viruses), viral protein synthesis, possible assembly of viral proteins, then
viral genome replication mediated by early or regulatory protein
expression. This may be followed, for complex viruses with larger
genomes, by one or more further rounds of mRNA synthesis: ―late‖ gene
expression is, in general, of structural or virion proteins.
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Hepatitis C virus: A simplified diagram of the Hepatitis C virus replication cycle.
5. Assembly - Following the structure-mediated self-assembly of the virus
particles, some modification of the proteins often occurs. In viruses such
as HIV, this modification (sometimes called maturation) occurs after the
virus has been released from the host cell.
6. Release - Viruses can be released from the host cell by lysis, a process
that kills the cell by bursting its membrane and cell wall if present. This is a
feature of many bacterial and some animal viruses. Some viruses undergo
a lysogenic cycle where the viral genome is incorporated by genetic
recombination into a specific place in the host‘s chromosome. The viral
genome is then known as a provirus or, in the case of bacteriophages a
prophage. Whenever the host divides, the viral genome is also replicated.
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The viral genome is mostly silent within the host; however, at some point
the provirus or prophage may give rise to active virus, which may lyse the
host cells. Enveloped viruses (e.g., HIV) typically are released from the
host cell by budding. During this process the virus acquires its envelope,
which is a modified piece of the host‘s plasma or other internal membrane.
The genetic material within virus particles, and the method by which the
material is replicated, varies considerably between different types of
viruses.
COVID-19 and inhibiting viral replication
COVID-19 has become a recent focus of viral replication studies. So
far, over 300 human proteins have been found to interact with severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2) during infection. It is
believed that by blocking certain interactions between human and viral
proteins, the viral replication can be stopped, thereby stopping transmission.
Similar therapeutic methods have been suggested for other diseases,
such as HIV. When similar studies on interactions between human and viral
proteins were done for HIV, they took a few years. Despite this, the
interaction mapping for COVID-19 is progressing much quicker and many
existing drugs that may be useful in stopping or slowing COVID-19 have been
identified. However, many of these drugs have now been found to be
ineffective.
There is some opposition to this method. Drugs targeting human
protein function, which would then stop viral replication, might also produce
side effects that are highly deleterious to already vulnerable patients. Some
short-term drugs are seen as more applicable for COVID-19, but the wisdom
and efficacy of this are still disputed.
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Steps of Virus Infections
A virus must ―take over‖ a cell to replicate. The viral replication cycle
can produce dramatic biochemical and structural changes in the host cell,
which may cause cell damage. These changes, called cytopathic effects, can
change cell functions or even destroy the cell. Some infected cells, such as
those infected by the common cold virus (rhinovirus), die through lysis
(bursting) or apoptosis (programmed cell death or ―cell suicide‖), releasing all
the progeny virions at once.
The symptoms of viral diseases result from the immune response to
the virus, which attempts to control and eliminate the virus from the body, and
from cell damage caused by the virus. Many animal viruses, such as HIV
(human immunodeficiency virus), leave the infected cells of the immune
system by a process known as budding, where virions leave the cell
individually. During the budding process, the cell does not undergo lysis and
is not immediately killed. However, the damage to the cells that HIV infects
may make it impossible for the cells to function as mediators of immunity,
even though the cells remain alive for a period of time. Most productive viral
infections follow similar steps in the virus replication cycle: attachment,
penetration, uncoating, replication, assembly, and release.

Attachment
A virus attaches to a specific receptor site on the host cell membrane
through attachment proteins in the capsid or via glycoproteins embedded in
the viral envelope. The specificity of this interaction determines the host (and
the cells within the host) that can be infected by a particular virus. This can be
illustrated by thinking of several keys and several locks where each key will fit
only one specific lock.
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Entry
The nucleic acid of bacteriophages enters the host cell naked, leaving
the capsid outside the cell. Plant and animal viruses can enter through
endocytosis, in which the cell membrane surrounds and engulfs the entire
virus. Some enveloped viruses enter the cell when the viral envelope fuses
directly with the cell membrane. Once inside the cell, the viral capsid is
degraded and the viral nucleic acid is released, which then becomes available
for replication and transcription.
Pathway to viral infection: In influenza virus infection, glycoproteins attach to a host
epithelial cell. As a result, the virus is engulfed. RNA and proteins are made and assembled
into new virions.
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Replication and Assembly
The replication mechanism depends on the viral genome. DNA viruses
usually use host cell proteins and enzymes to make additional DNA that is
transcribed to messenger RNA (mRNA), which is then used to direct protein
synthesis. RNA viruses usually use the RNA core as a template for synthesis
of viral genomic RNA and mRNA. The viral mRNA directs the host cell to
synthesize viral enzymes and capsid proteins, and to assemble new virions.
Of course, there are exceptions to this pattern. If a host cell does not provide
the enzymes necessary for viral replication, viral genes supply the information
to direct synthesis of the missing proteins. Retroviruses, such as HIV, have
an RNA genome that must be reverse transcribed into DNA, which then is
incorporated into the host cell genome.
To convert RNA into DNA, retroviruses must contain genes that
encode the virus-specific enzyme reverse transcriptase, which transcribes an
RNA template to DNA. Reverse transcription never occurs in uninfected host
cells; the needed enzyme, reverse transcriptase, is only derived from the
expression of viral genes within the infected host cells. The fact that HIV
produces some of its own enzymes not found in the host has allowed
researchers to develop drugs that inhibit these enzymes. These drugs,
including the reverse transcriptase inhibitor AZT, inhibit HIV replication by
reducing the activity of the enzyme without affecting the host‘s metabolism.
This approach has led to the development of a variety of drugs used to treat
HIV and has been effective at reducing the number of infectious virions
(copies of viral RNA) in the blood to non-detectable levels in many HIVinfected individuals.
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Egrees
The last stage of viral replication is the release of the new virions into
the host organism, where they are able to infect adjacent cells and repeat the
replication cycle. Some viruses are released when the host cell dies and other
viruses can leave infected cells by budding through the membrane without
directly killing the cell.
Vaccines for Prevention
While we do have limited numbers of effective antiviral drugs, such as
those used to treat HIV and influenza, the primary method of controlling viral
disease is by vaccination, which is intended to prevent outbreaks by building
immunity to a virus or virus family. A vaccine may be prepared using
weakened live viruses, killed viruses, or molecular subunits of the virus. In
general, live viruses lead to better immunity, but have the possibility of
causing disease at some low frequency. Killed viral vaccine and the subunit
viruses are both incapable of causing disease, but in general lead to less
effective or long-lasting immunity.
Weakened live viral vaccines are designed in the laboratory to cause
few symptoms in recipients while giving them immunity against future
infections. Polio was one disease that represented a milestone in the use of
vaccines. Mass immunization campaigns in the U.S. in the 1950s (killed
vaccine) and 1960s (live vaccine) essentially eradicated the disease, which
caused muscle paralysis in children and generated fear in the general
population when regional epidemics occurred. The success of the polio
vaccine paved the way for the routine dispensation of childhood vaccines
against measles, mumps, rubella, chickenpox, and other diseases.
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Live vaccines are usually made by attenuation (weakening) of the
―wild-type‖ (disease-causing) virus by growing it in the laboratory in tissues or
at temperatures different from what the virus is accustomed to in the host. For
example, the virus may be grown in cells in a test tube, in bird embryos, or in
live animals. The adaptation to these new cells or temperature induces
mutations in the virus‘ genomes, allowing them to grow better in the
laboratory while inhibiting their ability to cause disease when reintroduced into
the conditions found in the host.
These attenuated viruses thus still cause an infection, but they do not
grow very well, allowing the immune response to develop in time to prevent
major disease. The danger of using live vaccines, which are usually more
effective than killed vaccines, is the low but significant risk that these viruses
will revert back to their disease-causing form by back mutations. Back
mutations occur when the vaccine undergoes mutations in the host such that
it readapts to the host and can again cause disease, which can then be
spread to other humans in an epidemic. This happened as recently as 2007 in
Nigeria where mutations in a polio vaccine led to an epidemic of polio in that
country.
Some vaccines are in continuous development because certain
viruses, such as influenza and HIV, have a high mutation rate compared to
other viruses or host cells. With influenza, mutation in genes for the surface
molecules helps the virus evade the protective immunity that may have been
obtained in a previous influenza season, making it necessary for individuals to
get vaccinated every year. Other viruses, such as those that cause the
childhood diseases measles, mumps, and rubella, mutate so little that the
same vaccine is used year after year.
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Module in GENETICS
Prof. Christine M. Adlawan
SUMMARY
Viruses are acellular entities that can usually only be seen with an
electron microscope. Their genomes contain either DNA or RNA, and they
replicate using the replication proteins of a host cell. Viruses are diverse,
infecting archaea, bacteria, fungi, plants, and animals. Viruses consist of a
nucleic-acid core surrounded by a protein capsid with or without an outer lipid
envelope.
Viral replication within a living cell always produces changes in the cell,
sometimes resulting in cell death and sometimes slowly killing the infected
cells. There are six basic stages in the virus replication cycle: attachment,
penetration, uncoating, replication, assembly, and release. A viral infection
may be productive, resulting in new virions, or nonproductive, meaning the
virus remains inside the cell without producing new virions.
Viruses cause a variety of diseases in humans. Many of these
diseases can be prevented by the use of viral vaccines, which stimulate
protective immunity against the virus without causing major disease. Viral
vaccines may also be used in active viral infections, boosting the ability of the
immune system to control or destroy the virus. Antiviral drugs that target
enzymes and other protein products of viral genes have been developed and
used with mixed success. Combinations of anti-HIV drugs have been used to
effectively control the virus, extending the lifespan of infected individuals.
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Module in GENETICS
Prof. Christine M. Adlawan
APPLICATION
Name each labeled part of the illustrated bacteriophage.
ASSESSMENT
1. Discuss the geometric differences among helical, polyhedral, and
complex viruses.
2. What was the meaning of the word ―virus‖ in the 1880s and why
was it used to describe the cause of tobacco mosaic disease?
3. In terms of evolution, which do you think arises first? The virus or
the host? Explain your answer.
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Module in GENETICS
Prof. Christine M. Adlawan
4. Do you think it is possible to create a virus in the lab? Imagine that
you are a mad scientist. Describe how you would go about creating
a new virus?
FEEDBACK
Do you have any question relative to our topic? Write them below.
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REFERENCES

Goulding, J., 2020. Virus Replication. [online] Immunology.org.
Available
at:
<https://www.immunology.org/public-
information/bitesized-immunology/pathogens-and-disease/virusreplication>.

H. Lecoq. "[Discovery of the First Virus, the Tobacco Mosaic
Virus: 1892 or 1898?]." Comptes Rendus de l‘Academie des
Sciences – Serie III – Sciences de la Vie 324, no. 10 (2001): 929–
933.
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Module in GENETICS

Prof. Christine M. Adlawan
US Department of Health and Human Services, Centers for
Disease Control and Prevention. "Antibiotic Resistance Threats in
the United States, 2013."

http://www.cdc.gov/drugresistance/pdf/ar-threats-2013-508.pdf
(accessed September 22, 2015).

M. Clokie et al. "Phages in Nature." Bacteriophage 1, no. 1
(2011): 31–45. ↵

Marks, R., 2020. Unveiling How Coronavirus Hijacks Our Cells to
Help Rush New Drugs to Patients. [online] UCSF.edu. Available
at:
<https://www.ucsf.edu/news/2020/03/416986/unveiling-how-
coronavirus-hijacks-our-cells-help-rush-new-drugs-patients>.

US Food and Drug Administration. "FDA Approval of Listeriaspecific Bacteriophage Preparation on Ready-to-Eat (RTE) Meat
and Poultry Products."

Reece, JB., Campbell, N.A, Urry, L.A, et.al., Campbell Biology.
11th edition.

Wang, W., Wu, C., Amarasinghe, G., and Leung, D., 2019. Ebola
Virus Replication Stands Out. Trends in Microbiology, 27(7), pp.
565-566.
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