MICROBIOLOGY

Course Pack

Michael Jay O. Mesa

Instructor
 Bio 101 – Microbiology: Course Pack

MODULE 7: VIRUSES,
LearningVIROIDS,
OutcomesAND PRIONS

Lesson 1: Characteristics, Structure, and Classification

of Viruses

Learning Outcomes

At the end of this module, learners will be able to:

• Describe the general characteristics of viruses.
• Explain viral structure and morphology.
• Identify the diversity of viral genetic material.
• Understand virus classification criteria.
• Discuss virus host range and specificity.

Time Frame 1.5 hours

Introduction

Viruses are unique acellular infectious agents that diSer fundamentally from cellular
organisms. This lesson explores their characteristics, structure, genetic diversity, classification,
and host specificity, emphasizing their biological relevance and the challenges they pose in
microbiology and medicine.

Activity

Quiz
Multiple Choice. Choose the letter of the correct answer.
1. What is the primary characteristic that distinguishes a virus from other microorganisms?
a) It can replicate on its own without a host
b) It lacks a cellular structure and can only replicate inside a host cell
c) It has a cellular membrane
d) It can undergo photosynthesis
2. Which of the following is a component of the viral structure?
a) Ribosomes c) Nucleic acid (DNA or RNA)
b) Mitochondria d) Chloroplasts

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3. Viruses that infect bacteria are called:

a) Phages c) Viroids
b) Retroviruses d) Prions
4. Which of the following best describes the role of a viral capsid?
a) It provides energy for viral replication
b) It encodes viral proteins
c) It protects the viral genome and aids in host cell recognition
d) It synthesizes RNA from the viral DNA
5. What type of virus replication cycle involves the incorporation of viral DNA into the host cell’s
genome?
a) Lytic cycle c) Reverse transcription
b) Lysogenic cycle d) Budding cycle

Analysis

Imagine a patient presents with symptoms of fatigue, fever, and muscle aches, and laboratory
tests reveal the presence of a virus. The virus is found to have an outer protein shell (capsid) and
a central core containing either RNA or DNA. The virus is able to attach to specific receptors on
the surface of human cells, enter the cell, and hijack the host’s machinery for replication.

Question:
Given this viral structure, how does the capsid function in the virus’s ability to infect host cells,
and what role does the viral genetic material (RNA or DNA) play once inside the host cell? What
are the potential eSects of this viral infection on the host cell’s normal function and overall
health?

Abstraction
Viruses are acellular infectious agents that rely entirely on host cellular machinery for
replication. They exist as virions in the extracellular state and consist of nucleic acid (DNA or
RNA) enclosed in a protein coat called the capsid, sometimes surrounded by an envelope
derived from host membranes.

Characteristics of Viruses
• General Overview
o Viruses are responsible for many diseases in the industrialized world, such as
common colds, influenza, herpes, and AIDS.
o Despite immunizations and treatments for symptoms, finding cures for viral
diseases is challenging due to their unique characteristics and methods of host
invasion.
• Basic Characteristics
o Viruses are minuscule and acellular infectious agents.
o They contain nucleic acid (either DNA or RNA) as their genetic material
(genome).
o Lack cytoplasmic membranes, cytosol, and functional organelles.

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o Cannot perform metabolic activities independently; rely on the host cell’s

metabolism for replication.
o Similar to a computer virus in that they are inactive and harmless until they
infect a host, at which point they can be destructive.
• States of Viruses
o Extracellular State:
§ Referred to as a virion.
§ Composed of a protein coat (capsid) surrounding a nucleic acid core.
§ The combination of viral nucleic acid and capsid is called a
nucleocapsid.
§ Some virions possess a phospholipid membrane (envelope)
surrounding the nucleocapsid.
§ The outer layer provides protection and recognition sites for binding to
specific host cells.
o Intracellular State:
§ Initiated once the virus enters a host cell.
§ The capsid (and envelope, if present) is removed, leaving only the nucleic
acid, which still retains the designation of a virus.
• Distinguishing Characteristics
o Genetic Material: Variability in DNA or RNA content.
o Host Cell Specificity: DiSerent viruses target diSerent types of cells.
o Size: Viruses vary in size.
o Capsid Structure: DiSerences in the nature of their protein coats.
o Shape: Viruses can have various shapes.
o Envelope Presence: Some viruses have envelopes while others do not.

Genetic Material of Viruses

• Variety in Viral Genomes
o Viruses exhibit greater diversity in genetic material compared to cells.
o Unlike cells, which have genomes composed solely of double-stranded DNA
(dsDNA), viral genomes can be:
§ Double-stranded DNA (dsDNA)
§ Single-stranded RNA (ssRNA)
§ Single-stranded DNA (ssDNA)
§ Double-stranded RNA (dsRNA)
• Classification and Categorization
o The primary method for categorizing and classifying viruses is based on the type
of genetic material in their genomes.
• Examples of Viral Genomes
o Double-stranded DNA Viruses:
§ Examples include herpesvirus and smallpox virus.
o Single-stranded RNA Viruses:
§ Influenza virus: composed of eight linear segments of ssRNA.
§ Poliovirus: consists of a single molecule of ssRNA.
o Single-stranded DNA and Double-stranded RNA:
§ These forms are rarely found in cellular organisms.
• Structure of Viral Genomes
o Viral genomes can be:
§ Linear: Composed of multiple molecules of nucleic acid (similar to
eukaryotic cells).
§ Circular: Usually singular, as found in most prokaryotic cells.

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• Genome Size Comparison

o Viral genomes are generally smaller than cellular genomes.
§ Example: The smallest bacterium (Chlamydia species) has
approximately 1,000 protein-encoding genes.
§ In contrast, the MS2 virus genome contains only three protein-encoding
genes.
o A comparison of the physical size of a virus's genome to that of its bacterial host
(Escherichia coli) illustrates this size diSerence.

Hosts of Viruses and Their Characteristics:

• Host Specificity
o Most viruses infect specific host cells due to the precise aSinity of viral
attachment molecules (proteins or glycoproteins) for complementary host cell
surface proteins.
o Viruses can be highly specific, targeting not just a particular host but also
specific cell types within that host.
§ Example: HIV specifically attacks helper T lymphocytes in humans but
does not aSect muscle or bone cells.
o Some viruses are generalists and can infect multiple cell types or hosts.
§ Example: West Nile virus can infect humans, various bird species,
several mammals, and some reptiles.
• Types of Organisms Arected by Viruses
o All organisms are susceptible to viral infections, including:
§ Archaeal cells
§ Bacterial cells
§ Plant cells
§ Protozoan cells
§ Fungal cells
§ Animal cells
o Certain viruses are known to infect larger viruses as well.
• Bacteriophages
o Viruses that specifically infect bacteria are called bacteriophages or simply
phages.
o The number of bacteriophages is greater than the combined total of all bacteria,
archaea, and eukaryotes.
o Research on bacteriophages and animal viruses is extensive.
• Plant Viruses
o Plant viruses are less studied compared to bacterial and animal viruses but were
the first viruses identified (e.g., tobacco mosaic virus).
o They infect major food crops (corn, beans, sugarcane, tobacco, potatoes),
causing significant economic losses.
o Entry into plant cells occurs through cell wall abrasions or by vectors like
nematodes and aphids.
o Once inside, plant viruses follow a replication cycle similar to that of animal
viruses.
• Fungal Viruses
o Fungal viruses have been minimally studied and appear to exist only within host
cells, lacking an extracellular state.
o They cannot penetrate the thick fungal cell wall; however, infections can spread
through cell fusion, common in fungal life cycles.
• Size of Viruses

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o Viruses are typically much smaller than bacteria; for example, 100 million
polioviruses can fit side by side on a period.
o Virus diameters can range from as small as 17 nm to larger viruses like
Megavirus at about 500 nm, comparable to many bacterial cells.
o The discovery of viruses dates back to the late 1800s when scientists proposed
that diseases like polio and smallpox were caused by agents smaller than
bacteria, which they named “viruses” (Latin for “poison”).
• Historical Experiments
o In 1892, Dmitri Ivanowski demonstrated that viruses are acellular by filtering
infected tobacco plant sap through a fine porcelain filter that trapped cells,
allowing the infectious agents (viruses) to pass through.
o The tobacco mosaic virus (TMV) was later isolated and characterized by Wendell
Stanley in 1935, marking significant progress in virology.
o The advent of electron microscopy enabled scientists to visualize TMV and other
viruses directly.

Capsid Morphology
• Definition: The capsid is the protein coat of a virus, providing protection for the viral
nucleic acid and aiding in attachment to host cells.
• Composition:
o Made up of protein subunits called capsomeres (or capsomers).
o Capsomeres can consist of a single type of protein or multiple types.
Viral Shapes
• Classification: Viruses are classified based on the shape of their capsids into three
basic types:
o Helical Viruses:
§ Capsid forms a tube around the nucleic acid.
§ Capsomeres bond in a circular arrangement.
o Polyhedral Viruses:
§ Roughly spherical shape, resembling a geodesic dome.
§ The most common polyhedral capsid is the icosahedron, which has 20
sides.
o Complex Viruses:
§ Have diverse shapes that do not fit into helical or polyhedral categories.
§ Example: Smallpox virus, which has multiple covering layers (including
lipid) and an indistinct capsid.
§ Many bacteriophages are complex, with icosahedral heads (containing
the genome) and helical tails with tail fibers.
The Viral Envelope
• Definition: Some viruses, especially animal viruses, possess an envelope that
resembles a cell membrane surrounding their capsids.
• Structure:
o Composed of a phospholipid bilayer and proteins, including virally coded
glycoproteins that appear as spikes on the surface.
o Matrix proteins fill the space between the capsid and the envelope.
• Acquisition:
o Enveloped viruses acquire their envelope from the host cell during replication or
release, making it a portion of the host's membrane system.
• Function of Envelope:
o Plays a crucial role in the recognition of host cells.

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o Provides protection from the immune system, as enveloped viruses are

chemically similar to host cells.
• Stability:
o Enveloped viruses are more fragile than naked viruses due to susceptibility to
detergents, alcohol, and drying.
o Naked (nonenveloped) viruses are more stable outside a host but expose more
viral proteins to the environment, making them more recognizable by the
immune system.
Summary of Properties
• A summary table (Table 13.1) compares the unique properties of viruses with the
characteristics of cells, highlighting their diSerences.

Classification of Viruses
• International Committee on Taxonomy of Viruses (ICTV)
o Established in 1966.
o Aims to provide a unified taxonomic scheme for viral classification and
identification.
• Criteria for Classification
o Type of nucleic acid (DNA or RNA).
o Presence of an envelope (enveloped or non-enveloped).
o Shape and size of the virus.
• Current Taxonomic Status
o Families established
for all viral genera.
o Only seven viral orders
described.
o No kingdoms,
divisions, or classes
defined due to unclear relationships among viruses.
o Some researchers propose viruses as a fourth domain of life, alongside Bacteria,
Archaea, and Eukarya.
• Family Naming Conventions
o Derived from unique characteristics or significant members of the family.
§ Example:
§ Picornaviridae: Very small RNA viruses.
§ Hepadnaviridae: DNA virus causing hepatitis B.
§ Herpesviridae: Named after herpes simplex virus causing
genital herpes.
• Nomenclature of Viruses
o Specific epithets are common English names written in italics.
o Viruses generally known by their English names.

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o Examples of viral pathogen nomenclature:

§ HIV
§ Rabies virus.
• Major families of human viruses are grouped by the type of nucleic acid in Table 13.2.

Application

Virus Explorer
Access the Virus Explorer by clicking the link: [Link]
resources/virus-explorer.

Download and answer the worksheet from the Materials or by clicking this link:
[Link]
[Link].

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References

Tortora, G. J., Funke, B. R., & Case, C. L. (2019). Microbiology: An Introduction (13th ed.).
Pearson.
International Committee on Taxonomy of Viruses (ICTV): [Link]
Centers for Disease Control and Prevention: [Link]

Good job! That ends the Lesson 1 of Module 6. Are you

ready to learn more? Let’s go!

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Lesson 2: Viral Replication and Culturing

Learning Outcomes

At the end of this module, learners will be able to:

• Describe the general steps of viral replication.
• DiSerentiate between lytic and lysogenic cycles.
• Explain mechanisms of animal virus replication.
• Identify methods used to culture viruses.
• Discuss the relationship between viruses and cancer.

Time Frame 1.5 hours

Introduction
Viral replication is a highly specific process dependent on host cells, and understanding it is
essential for microbiology, virology, and medical research. This module explores replication
cycles, animal virus replication mechanisms, culturing techniques, and the link between
viruses and cancer.

Activity

Parts of the Virus

Label the viral structures indicated here. Write your answers on the space provided.

A. F.
B. G.

C.
H.

D. I.
E.

Influenza virus Bacteriophage

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Analysis

Answer this:
Analyze the structural and functional diSerences between a bacteriophage and the influenza
virus. How do these diSerences influence their replication mechanisms and the type of host
they infect? Discuss the implications of these diSerences on the strategies used for developing
antiviral treatments.

Abstraction
Viruses replicate by hijacking host cellular machinery, following a sequence of attachment,
entry, synthesis, assembly, and release. The lytic cycle results in immediate destruction of the
host cell, while the lysogenic cycle allows long-term integration into the host genome (lysogenic
conversion). Animal viruses diSer from bacteriophages in entry mechanisms and replication
strategies based on their nucleic acid types and presence of envelopes.

Viral Replication
• Dependence on Host Cells
o Viruses cannot reproduce independently due to:
§ Lack of genes for necessary enzymes for replication.
§ Absence of functional ribosomes for protein synthesis.
o They rely on host cell enzymes and organelles to produce new virions.
• Control of Host Cell
o Once a viral genome enters a host cell, the cell is compelled to:
§ Replicate viral genetic material.
§ Translate viral proteins, including capsomeres and enzymes.
• Lytic Replication Cycle
o Typically results in the death and lysis of the host cell.
o Consists of five stages:
1. Attachment: The virion attaches to the host cell.
2. Entry: The virion or its genome enters the host cell.
3. Synthesis: Host cell's enzymes and ribosomes synthesize new nucleic
acids and viral proteins.
4. Assembly: New virions are assembled within the host cell.
5. Release: New virions are released from the host cell.
• Types of Replication
o The section will explore:
§ Lytic replication in bacteriophages.
§ Lysogenic replication (a modified replication cycle).
§ Replication of animal viruses.

Lytic Replication of Bacteriophages

• Importance of Bacteriophages
o Serve as excellent models for studying viral biology.
o Easier and less expensive to culture than animal or human cells.
o Potential alternative to antibiotics (as noted in "Beneficial Microbes: Prescription
Bacteriophages?").
• Case Study: Bacteriophage T4

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o A well-studied double-stranded DNA (dsDNA) phage of E. coli.

o Complex structure with polyhedral heads and helical tails.
Stages of Lytic Replication
1. Attachment
o Phages are nonmotile; contact with bacteria occurs through random collisions.
o Tail fibers facilitate attachment to the host bacterium.
o Attachment proteins on tail fibers fit complementary receptor proteins on E. coli
cell walls.
o Specificity of attachment can lead to infection of only certain bacterial strains,
useful for bacterial identification (phage typing).
2. Entry
o After attachment, T4 must penetrate the bacterial cell wall and cytoplasmic
membrane.
o T4 releases lysozyme to weaken the peptidoglycan in the cell wall.
o The tail sheath contracts, allowing a hollow tube to penetrate the cell wall and
membrane, injecting the viral genome into the bacterium.
o The empty capsid remains outside the cell.
3. Synthesis
o Bacterial DNA is degraded by viral enzymes, leading to the cessation of bacterial
molecule synthesis.
o The bacterium synthesizes viral parts under the control of the viral genome.
o For dsDNA viruses like T4, mRNA is transcribed from viral DNA, and host
ribosomes translate this into viral proteins (capsomeres, tail components, DNA
polymerase, lysozyme).
4. Assembly
o Capsomeres spontaneously attach to form new capsid heads.
o Tails assemble and attach to capsid heads, and tail fibers attach to tails to form
mature virions.
o Some viruses pump their genomes into assembled capsids under high pressure.
o Occasionally, capsids may assemble around leftover host DNA, resulting in
virions that can transfer host DNA to new bacteria (transduction).
5. Release
o Newly assembled virions are released as lysozyme destroys the bacterial cell
wall, causing disintegration.
o Disintegrating cells appear as plaques in bacterial cultures, leading to the name
"bacteriophage," meaning "bacterial eater."
o The lytic replication process for T4 takes about 25 minutes, producing 100 to 200
new virions per lysed bacterial cell.
o Burst time: Time from attachment to release.
o Burst size: Number of new virions released from each lysed bacterial cell.

Lysogenic Replication of Bacteriophages

• Overview of Lysogenic Replication
o Not all bacteriophages follow the lytic replication pattern (e.g., T4).
o Some have a modified cycle where infected host cells reproduce normally for
many generations before lysing.
o This cycle is known as the lysogenic replication cycle or lysogeny, and these
phages are termed temperate phages or lysogenic phages.
• Case Study: Lambda Phage
o A well-studied temperate phage that infects E. coli.

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o Has a linear double-stranded DNA (dsDNA) molecule in a complex capsid with

an icosahedral head and a tail lacking tail fibers.
Stages of Lysogenic Replication
1. Attachment
o The virion randomly contacts an E. coli cell and attaches via its tail.
2. Entry
o The viral DNA enters the host cell.
o Unlike lytic cycles, the host cell's DNA is not destroyed, and the phage genome
does not immediately control the cell.
o The viral genome remains inactive, referred to as a prophage.
3. Prophage Activity
o The prophage remains inactive by producing a protein that suppresses prophage
genes.
o This repressor protein makes the bacterium resistant to additional infections by
other viruses of the same type.
4. Integration
o The prophage integrates into the bacterial chromosome, becoming a physical
part of it.
o The integration is achieved by fusing the viral DNA with the bacterial DNA.
o Every time the bacterium replicates its chromosome, the prophage is also
replicated, leading to all daughter cells being infected.
5. Long-Term Presence
o The prophage can remain part of the bacterial chromosome for generations or
even indefinitely.
o Lysogenic phages can change a bacterium's phenotype, a process called
lysogenic conversion.
o This conversion can turn harmless bacteria into pathogens, as seen in diseases
caused by toxins and proteins from lysogenic phage genes (e.g., diphtheria,
cholera).
6. Induction
o At some point, a prophage may be excised from the chromosome through
recombination or other genetic events, re-entering the lytic cycle.
o The process of excision from the host chromosome is called induction.
o Inductive agents include physical and chemical factors that damage DNA (e.g.,
ultraviolet light, X-rays, carcinogenic chemicals).
7. Resuming Lytic Cycle
o After induction, the lytic steps of synthesis, assembly, and release resume from
the last point of activity.
o The host cell fills with new virions and ultimately breaks open.
• Comparison of Replication Strategies
o Bacteriophages like T4 and lambda illustrate two typical replication strategies
for DNA viruses.
o Variations in replication exist for RNA viruses and enveloped viruses, which will
be explored in subsequent sections.

Replication of Animal Viruses

• Basic Steps in Replication
o Animal viruses follow the same five basic steps in their replication pathways as
bacteriophages:
1. Attachment
2. Entry

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3. Synthesis
4. Assembly
5. Release
o DiSerences arise due to the presence of envelopes on some viruses and the
eukaryotic nature of animal cells, which lack a cell wall.
Attachment of Animal Viruses
• Mechanism of Attachment
o Attachment depends on chemical attraction and the fit between viral
attachment molecules and complementary receptors on the host cell's surface.
o Animal viruses lack tails and tail fibers. Instead, they often have glycoprotein
spikes on their capsids or envelopes.
Entry and Uncoating of Animal Viruses
• Mechanisms of Entry
o Animal viruses enter host cells through three primary mechanisms:
1. Direct Penetration:
§ Some naked viruses, like poliovirus, penetrate directly. The viral
capsid sinks into the cytoplasmic membrane, creating a pore for
the genome to enter, leaving the empty capsid outside.
2. Membrane Fusion:
§ Enveloped viruses, such as the measles virus, fuse their
envelope with the host's cytoplasmic membrane. This releases
the capsid into the cytoplasm while retaining the viral
glycoproteins in the cell membrane.
3. Endocytosis:
§ Naked and enveloped viruses can trigger endocytosis, where the
host cell engulfs the entire virus after attachment to surface
receptors. Examples include adenoviruses (naked) and
herpesviruses (enveloped).

• Uncoating Process
o After entry, the viral capsid must be removed to release the genome, a process
known as uncoating.
o Uncoating mechanisms vary:
§ Some viruses are uncoated within vesicles by cellular enzymes.
§ Others are uncoated by enzymes in the cytosol.
Synthesis of DNA Viruses in Animals
• General Synthesis Process
o The synthesis of animal viruses diSers from that of bacteriophages, depending
on the nucleic acid type (DNA or RNA) and its structure (single-stranded or
double-stranded).
o Some DNA viruses enter the nucleus for replication, while most RNA viruses
replicate in the cytoplasm.
o Enveloped viruses may have viral proteins inserted into cellular membranes,
forming the viral envelope and its spikes.
• Questions to Consider:
o How is mRNA synthesized for viral protein translation?
o What molecule serves as a template for nucleic acid replication?
• dsDNA Viruses
o The synthesis of new double-stranded DNA (dsDNA) virions resembles normal
cellular DNA replication and protein translation.

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o The dsDNA genome typically enters the nucleus, where cellular enzymes
replicate it as they do host DNA, using each strand as a template.
o Messenger RNA is transcribed from viral DNA in the nucleus and transported to
the cytoplasm for ribosomes to produce capsomere proteins.
o Capsomeres then return to the nucleus to spontaneously assemble new virions.
o An exception is the hepatitis B virus, which replicates its genome using an RNA
intermediary through a process mediated by reverse transcriptase.
• ssDNA Viruses
o An example of a virus with a single-stranded DNA (ssDNA) genome is
parvovirus.
o Cellular RNA polymerase synthesizes complementary mRNA from the viral
ssDNA, allowing for the translation of viral proteins.
o To replicate ssDNA viruses, the ssDNA forms a hairpin loop, functioning as
double-stranded DNA for cellular DNA polymerase to replicate.
o The newly synthesized strand is released as ssDNA and is packaged into a viral
capsid.
Summary of Key Direrences from Bacteriophages
• Entry Mechanisms: Animal viruses utilize membrane fusion and endocytosis, unlike the
direct injection used by bacteriophages.
• Uncoating: This process varies significantly in animal viruses and is often more
complex.
• Nucleic Acid Synthesis: Strategies diSer between DNA and RNA viruses, and the
involvement of cellular machinery is more pronounced in animal viruses.

Replication of Animal Viruses

• Basic Steps: Animal viruses follow five basic steps in their replication pathways, similar
to bacteriophages:
o Attachment
o Entry
o Synthesis
o Assembly
o Release
• Direrences from Bacteriophages:
o Envelopes: Some animal viruses have envelopes, while bacteriophages do not.
o Eukaryotic Cells: Animal cells lack cell walls, influencing the entry and
replication mechanisms.
Attachment of Animal Viruses
• Mechanism:
o Attachment relies on the interaction between viral attachment molecules and
cell surface receptors.
o Animal viruses lack tails and tail fibers; instead, they often have glycoprotein
spikes.
Entry and Uncoating
• Mechanisms of Entry:
1. Direct Penetration: Naked viruses like poliovirus penetrate by attaching and
sinking into the membrane, creating a pore for the genome to enter.
2. Membrane Fusion: Enveloped viruses like the measles virus fuse their envelope
with the host cell membrane, releasing the capsid into the cytoplasm.
3. Endocytosis: Many viruses trigger endocytosis, where the entire virus is
engulfed by the host cell (e.g., adenoviruses and herpesviruses).

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• Uncoating:
o The capsid is removed to release the viral genome. This process varies, with
some viruses being uncoated by cellular enzymes and others by cytosolic
enzymes.

Synthesis of DNA Viruses

• Types of DNA Viruses:
o dsDNA Viruses:
§ Enter the nucleus, where cellular enzymes replicate the viral genome like
cellular DNA.
§ mRNA is transcribed in the nucleus and translated in the cytoplasm
(e.g., herpes and papilloma viruses).
o Hepatitis B Virus:
§ Replicates its genome using an RNA intermediary through reverse
transcriptase.

o ssDNA Viruses:
§ Example: Parvovirus.
§ Cellular RNA polymerase synthesizes mRNA from the ssDNA, and a
unique DNA replication method allows for the creation of dsDNA, which
is then released as ssDNA.

Synthesis of RNA Viruses

• Types of RNA Viruses:
1. +ssRNA Viruses:
§ Function as mRNA, enabling direct translation into proteins.
§ Examples include poliovirus; often contain RNA polymerase for
synthesizing complementary -ssRNA.
2. Retroviruses:
§ Convert their +ssRNA genome into a dsDNA intermediary using reverse
transcriptase.
§ This DNA serves as a template for further +ssRNA synthesis (e.g., HIV).
3. -ssRNA Viruses:
§ Carry RNA-dependent RNA transcriptase to transcribe +ssRNA from their
-ssRNA genome, allowing for translation and additional -ssRNA
synthesis.
§ Examples include rabies and flu viruses.
4. dsRNA Viruses:
§ Use the positive strand as mRNA for protein synthesis.

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§ One protein synthesized is RNA polymerase, which transcribes the

dsRNA to produce more viral RNA (e.g., rotaviruses).

Assembly and Release

• Assembly:
o Most DNA viruses assemble in the nucleus and are released into the cytosol,
while RNA viruses typically assemble in the cytoplasm.
• Release Methods:
o Budding: Enveloped viruses are released through budding, acquiring part of the
cellular membrane as their envelope.
o Lysis: Naked viruses may cause cell lysis or be released via exocytosis, without
acquiring an envelope.
Latency of Animal Viruses
• Definition: Some viruses can remain dormant within cells for extended periods, known
as latency.
o Examples: HIV, chickenpox, hepatitis B, herpes viruses.
• Direrences from Lysogeny:
o Latency involves permanent incorporation of the virus into the host's DNA,
making it a part of the chromosome.
o Retroviruses like HIV utilize reverse transcriptase to integrate their RNA into the
host's genome.

Here's a detailed summary of the role of viruses in cancer development, focusing on key
concepts, mechanisms, and examples:
Role of Viruses in Cancer
• Normal Cell Division Control:
o In healthy multicellular animals, cell division is tightly regulated by genetic
mechanisms.
o Genes can either inhibit division (tumor suppressor genes) or promote it
(protooncogenes).
o Neoplasia: Disruption of this genetic control leads to uncontrolled cell division,
resulting in neoplasia, where neoplastic cells form tumors.
• Types of Tumors:
o Benign Tumors: Non-invasive, remain localized; can still cause discomfort or
resource competition for adjacent cells.
o Malignant Tumors (Cancers): Invasive, can spread (metastasis) to other parts
of the body, robbing normal cells of space and nutrients, ultimately impairing
function and potentially leading to death.
Theories on Viruses and Cancer Development
• Oncogenes and Protooncogenes:

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o Protooncogenes: Genes that normally promote cell growth and division; if

dysregulated, they become oncogenes (active form associated with cancer).
o Multiple genetic mutations (referred to as "multiple hits") are typically necessary
for cancer to develop, highlighting the complexity of the process.
• Environmental Contributors:
o Factors like ultraviolet light, radiation, carcinogenic chemicals, and viruses can
disrupt the regulation of oncogenes and tumor suppressor genes.
Viruses and Cancer Statistics
• Viruses are implicated in 20-25% of human cancers, contributing through various
mechanisms:
1. Carrying Oncogenes: Some viruses have oncogenes as part of their genetic
material.
2. Insertional Mutagenesis: Viruses can insert themselves near existing
oncogenes in the host genome, promoting their expression.
3. Interference with Tumor Suppression: Some viruses can disrupt the function
of tumor suppressor genes when integrated into the host's DNA as latent
proviruses.
Historical Context
• F. Peyton Rous: In the early 1900s, he demonstrated that viruses could induce cancer in
chickens, establishing a foundational understanding of viral oncology.
Viruses Linked to Human Cancers
• Although it's challenging to definitively prove causation in human cancers, several
viruses are established as contributors to specific cancers:
o Burkitt’s Lymphoma: Associated with Epstein-Barr virus (EBV).
o Hodgkin’s Disease: Also linked to EBV.
o Kaposi’s Sarcoma: Associated with human herpesvirus 8 (HHV-8).
o Cervical Cancer: Primarily linked to human papillomavirus (HPV).
Viruses and Cancer Families
• Certain families of viruses have been implicated in cancer development:
o DNA Viruses:
§ Adenoviridae: Linked to various tumors.
§ Herpesviridae: Associated with lymphomas and other cancers.
§ Hepadnaviridae: Related to liver cancer (hepatitis B virus).
§ Papillomaviridae: Strongly associated with cervical cancer (HPV).
§ Polyomaviridae: Can contribute to certain types of tumors.
o RNA Viruses:
Retroviridae: Involvement in various leukemias and lymphomas.

Culturing Viruses in the Laboratory

• Importance of Virus Culturing:
o Essential for research, vaccine development, and treatment studies.
o Viruses cannot be cultured using standard microbiological methods due to their
inability to metabolize or replicate independently.
• Methods of Culturing Viruses:
o Virologists have developed three primary methods:
1. Mature Organisms (Bacteria, Plants, Animals)
2. Embryonated Eggs
3. Cell Cultures

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1. Culturing Viruses in Mature Organisms

A. Bacteria
• Bacteriophages (viruses that infect bacteria):
o Easier to Culture: Bacteriophages can be cultured in bacteria grown in liquid
media or on agar plates.
o Plaque Assay Technique:
§ Bacteria and phages are mixed in liquid nutrient agar and poured onto an
agar plate.
§ After incubation, phages infect and lyse bacteria, creating clear zones
called plaques, where bacteria have been killed.
§ The number of plaques helps estimate the number of phages in the
original sample.
B. Plants and Animals
• Plant Viruses:
o First virus discovered: Tobacco mosaic virus in tobacco plants.
• Animal Viruses:
o Cultured in various laboratory animals (rats, mice, guinea pigs, etc.).
o Ethical and logistical challenges associated with animal maintenance and the
use of human-only viruses.
2. Culturing Viruses in Embryonated Chicken Eggs
• Advantages:
o Inexpensive, free of contaminants, and have nourishing yolk for virus growth.
o Ideal for culturing viruses due to large size and suitable embryonic tissues.
• Process:
o Researchers inject virus samples into specific sites in fertilized chicken eggs
where the virus can replicate.
o Vaccines for some viruses can be produced using this method, leading to
potential egg protein contamination, which may prompt allergy inquiries before
vaccination.
3. Culturing Viruses in Cell (Tissue) Culture
• Definition: Cells isolated from an organism are grown on a medium or in broth.
• Advancements:
o The introduction of antibiotics allows for the limitation of contaminating
bacterial growth, making cell culture a practical method.
o Advantages:
§ Less expensive than maintaining live animals, plants, or eggs.
§ Mitigates ethical concerns related to animal testing.
Types of Cell Cultures:
• Diploid Cell Culture:
o Derived from embryonic cells; typically lasts around 100 generations before cell
death.
• Continuous Cell Culture:
o Derived from tumor cells that can divide indefinitely.
o HeLa Cells:
§ A famous continuous cell line derived from Henrietta Lacks, who died of
cervical cancer in 1951.
§ HeLa cells have lost many original characteristics and are no longer
diploid, making them a semistandard human tissue culture for various
studies, including viral infection.

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Application

Identification-Type Questions
Read each statement carefully and write the correct answer in the space provided.
1. The process in which viruses use host cell machinery to produce new virions.
2. The stage of the lytic cycle where the viral genome is introduced into the host cell.
3. A type of viral replication cycle that integrates viral DNA into the host genome for long-
term persistence.
4. The protein subunits that make up the viral capsid.
5. The enzyme released by bacteriophage T4 to weaken the bacterial cell wall during entry
and release.
6. The process of viral capsid removal to release the genome inside the host cell.
7. The replication cycle in bacteriophages that results in immediate destruction of the host
cell.
8. The method by which enveloped viruses such as the measles virus enter the host cell by
merging with its membrane.
9. The bacterial virus used as a model organism for studying lytic replication in E. coli.
10. The laboratory method that uses clear zones on a bacterial lawn to estimate the number
of bacteriophages.

References

Tortora, G. J., Funke, B. R., & Case, C. L. (2019). Microbiology: An Introduction (13th ed.).
Pearson.
National Institutes of Health (NIH): [Link]
International Committee on Taxonomy of Viruses (ICTV): [Link]
Influenza virus.
[Link]
viruses/
Bacteriophage. [Link]
microbiology/chapter/viruses/

Good job! That ends the Lesson 2 of Module 6. Are you

ready to learn more? Let’s go!

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Lesson 3: Viroids, Prions, and Nontraditional Infectious Agents

Learning Outcomes

At the end of this module, learners will be able to:

• Describe the structure and characteristics of viroids and their
pathogenicity.
• Explain the nature, discovery, and replication mechanism of
prions.
• Identify key prion diseases and their implications.
• Discuss the debate surrounding the status of viruses as living
organisms.

Time Frame 1.0 hour

Introduction

Viroids and prions are infectious agents distinct from viruses, lacking traditional cellular or viral
structures. This module explores their structures, mechanisms of pathogenicity, their roles in
diseases, and the ongoing debate about the nature of viruses and life itself.

Activity

What are Viroids?

Access the video about viroids through this link: [Link]
Ds. Answer the question below.

Analysis

Answer this question:

Viroids are unique infectious agents that consist solely of RNA, lacking the typical protein coat
(capsid) seen in most viruses. Given their structure, how do viroids manage to cause infection in
plants, and what mechanisms allow their RNA to disrupt the plant's normal gene expression?

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Abstraction

Imagine you're a researcher investigating plant diseases and discover they're caused
by viroids—tiny, circular RNA molecules that hijack plant genes, disrupting growth. In your
research, you also encounter prions, infectious proteins that misfold normal proteins, causing
fatal diseases like mad cow disease and Creutzfeldt-Jakob disease. These prions resist
sterilization methods, posing public health challenges. Meanwhile, the debate continues about
whether viruses—which lack metabolic processes but possess genomes—should be
considered alive. In this lesson, we'll explore viroids, prions, and the complexities of viral life,
delving into their structures, behaviors, and the diseases they cause.

Characteristics of Viroids
• Definition:
o Viroids are small, circular pieces of single-stranded RNA (ssRNA) that are
infectious and pathogenic, primarily aSecting plants.
• Characteristics:
o Size: As small as 239 nucleotides long.
o Lack of Capsids: Unlike viruses, viroids do not have a protein coat (capsid).
o Non-coding RNA: Viroid RNA does not code for proteins.
• Pathogenic Mechanism:
o Viroids cause disease by binding to complementary sequences of plant mRNA,
forming double-stranded RNA (dsRNA).
o A plant enzyme degrades this dsRNA as if it were from a dsRNA virus, leading to
the degradation of the plant's own mRNA, which contributes to disease
symptoms.
• Plant Diseases Caused by Viroids:
o Several plant diseases are associated with viroids, including those aSecting:
§ Coconut palms
§ Chrysanthemums
§ Potatoes
§ Cucumbers
§ Avocados
• Viroidlike Agents:
o Infectious RNA particles that lack capsids but do not infect plants can aSect
some fungi. These are not classified as viroids because they do not have plant
hosts.
o No known animal diseases are attributed to viroidlike molecules, but there is a
possibility that infectious RNA may play a role in certain human diseases.

Characteristics of Prions
• Definition:
o Prions are proteinaceous infectious agents identified by Stanley Prusiner in
1982, characterized by their lack of nucleic acid (RNA or DNA).
• Discovery Context:
o Prior to Prusiner's research, prion diseases were believed to be caused by "slow
viruses" due to the long incubation period (up to 60 years) before symptoms
appeared.
• Controversy:

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o The concept of prions challenges the universal rule of protein synthesis, which
states that proteins are synthesized from mRNA. The replication mechanism of
prions remains a subject of debate since they lack nucleic acids.
• Protein Structure:
o All mammals produce a protein called PrP (prion protein), which is found in brain
cells:
§ Cellular PrP (c-PrP): Normal, functional form with multiple α-helices.
§ Prion PrP (p-PrP): Abnormal form characterized by β-pleated sheets,
leading to disease.
• Replication Mechanism:
o Prion PrP induces misfolding of normal c-PrP into the disease-causing p-PrP
through a process known as templating.
o This misfolding propagates throughout the brain, leading to neuronal
dysfunction and death, resulting in spongiform encephalopathies (characterized
by a spongy appearance of the brain tissue).
• Factors Arecting Prion Development:
o Prions do not develop in all mammals because surrounding proteins and
polysaccharides typically maintain PrP in its normal shape.
o Human susceptibility to prion diseases can depend on the presence of
methionine at the 129th amino acid position in PrP, with about 40% of humans
carrying this variant.
Types of Prion Diseases
• Inheritance Forms:
o Inherited: Caused by mutations in the c-PrP gene leading to the initial formation
of p-PrP.
o Sporadic: Arises from random misfolding of normal c-PrP without genetic
changes.
o Infectious: Results from ingestion of infected tissue, tissue transplants, or
contact with infected tissues.
• Examples of Prion Diseases:
o Bovine Spongiform Encephalopathy (BSE): Mad cow disease, transmissible to
humans.
o Scrapie: ASects sheep.
o Kuru: A historical human prion disease that has been eliminated.
o Chronic Wasting Disease (CWD): ASects deer and elk.
o Variant Creutzfeldt-Jakob Disease (vCJD): A human disease linked to BSE.
• Potential Connections to Other Diseases:
o Some scientists propose that noninfectious prions may also be involved in
Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS),
and certain types of cancer.

Resistance and Treatment

• Resistance to Deactivation:
o Prions are resistant to standard cooking and sterilization methods. ESective
deactivation requires:
§ Heating to 482°C for four hours.
§ Autoclaving at 132°C in concentrated sodium hydroxide for one hour.
§ Treatment with a 10% phenolic compound solution for one hour.
• Potential Treatments:
o While there is no standard treatment for prion diseases, several drugs show
promise in animal studies:

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§ Quinacrine: An antimalarial drug.

§ Chlorpromazine: An antipsychotic drug.
§ Astemizole: An antihistamine.
§ Antibodies against p-PrP.
• Inter-Species Transmission:
o Prion proteins diSer between species, making transmission unlikely; however,
the BSE epidemic in the 1980s led to the spread of prions from cattle to humans
via infected beef.
o To prevent inter-species transmission, many countries have banned animal-
derived protein in animal feed.

Are Viruses Alive?

• Key Characteristics of Life:
o Traditional criteria for defining life include:
1. Growth: Organisms can grow and develop.
2. Self-reproduction: Organisms can reproduce independently.
3. Responsiveness: Organisms respond to environmental stimuli.
4. Metabolism: Organisms can metabolize nutrients to produce energy.
5. Cellular Structure: Living things are composed of cells.
• Viruses' Status:
o Lack of Living Qualities: Viruses do not exhibit the above characteristics
outside of a host cell:
§ They cannot grow or reproduce on their own.
§ They do not have cellular structures or metabolic processes.
o Perspective of Some Scientists: Some consider viruses mere complex
pathogenic chemicals due to their inability to meet the criteria of living
organisms.
• Arguments for Viruses as Living Entities:
o Complex Invasion: Viruses have sophisticated mechanisms to invade host
cells.
o Control Over Host Cells: Once inside a host, they can take control of cellular
processes.
o Genetic Material: Viruses contain genomes with instructions for self-
replication.
o Evolution: Viruses can evolve over time, adapting to their environments.
o Ultimate Parasites: They depend on host cells for replication, leading some to
view them as the least complex living entities.

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Application

Journal Review
Access the journal article in this link: [Link] The article
discusses the distinct features and behaviors of viroids and prions, contrasting them with more
traditional pathogens like bacteria and viruses, and emphasizes the complexities in detecting,
preventing, and treating diseases caused by these infectious agents.

Answer the following questions and submit it to your instructor:

1. How do viroids and prions challenge traditional concepts of biological pathogens, and what
does this imply about the complexity of infectious agents?
2. Considering the pathogenic mechanisms of viroids and prions, how do their respective
replication processes influence their potential for causing diseases in plants and animals?
3. In what ways do the distinct structural and replication features of viroids and prions impact
the strategies used for their detection, prevention, and treatment?

References

Centers for Disease Control and Prevention (CDC): [Link]

National Human Genome Research Institute: [Link]
glossary/Viroid
Steger, G., Riesner, D., & Prusiner, S. B. (2024). Viroids, Satellite RNAs and Prions: Folding of
Nucleic Acids and Misfolding of Proteins. Viruses, 16(3), 360.
Tortora, G. J., Funke, B. R., & Case, C. L. (2019). Microbiology: An Introduction (13th ed.).
Pearson.

Good job! That ends the Module 6 of our Microbiology

Course Pack. Let’s learn more. Are you ready for the
challenge?

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