VIROLOGY LECTURE

2ND YEAR BSC (HONS), PHARMACY

ALFRED MUSLIC CONTEH
B.Pharm (Hons) COMAHS
MPH, NJALA
Msc Bio-Tox UNILAG
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INTRODUCTION
 Virology is the study of viruses, their structure, classification,
evolution, and interactions with host organisms. Viruses
stand at the intersection of mystery and marvel in the realm
of microbiology.
 Viruses, while simple in structure, wield immense power in

their ability to infect virtually every form of life on Earth. From

the smallest bacteria to the largest mammals, viruses have
shaped evolutionary paths, driven ecological dynamics, and
challenged human existence.

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ORIGIN AND HISTORY OF VIROLOGY
 The germ theory of disease was formulated over 100 years
ago, and pathologists believed that a causative
microorganism would be found for each infectious disease.
These agents could be seen with a microscope, cultivated on
a nutrient medium, and retained by filters. However, in 1892,
Dmitri Iwanowski discovered that the causal agent of a
mosaic disease of tobacco plants, manifesting as a
discoloration of the leaf, passed through a bacteria-proof
filter and could not be seen or cultivated.

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 Viruses of other animals were soon discovered, such as cell-
free transmission of chicken leukemia in 1908 and solid
tumors of chickens transmitted by cell-free filtrates in 1911.
 Beijerinck repeated the experiments in 1898, and Beijerinck

became convinced this represented a new form of infectious

agent, which he termed contagium vivum fluidum, what we
now know as a virus. Loeffler and Frosch concluded that foot-
and-mouth disease could not be passed from animal to
animal, so the causative agent had to be reproducing and
thus could not be a bacterial toxin.

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 In 1915, Twort published an account of a glassy
transformation of micrococci, suggesting that the existence
of a bacterial virus or the secretion by bacteria of an enzyme
could lyse the producing cells. This idea of self-destruction by
secreted enzymes proved a controversial topic over the next
decade. In 1917, d’Hérelle observed a similar phenomenon in
dysentery bacilli, and upon noting the lysis of broth cultures
of pure dysentery bacilli by filtered emulsions of feces, he
realized he was dealing with a bacterial virus.

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DEFINITION OF VIRUS
 Viruses are microscopic infectious agents that can only
replicate inside the living cells of organisms. They consist of
genetic material
(DNA or RNA) enclosed in a protein coat called a capsid. Some
viruses also have an outer lipid envelope derived from the host
cell
membrane.

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ECONOMIC IMPORTANCE OF VIRUSES
 Viruses play significant roles in both recombinant DNA
technology
and vaccine development, leveraging their unique biological
properties for beneficial applications. Here’s an overview of
their roles in these fields:
 Vectors for Gene Delivery: Viruses, particularly

retroviruses and adenoviruses, are used as vectors to deliver

recombinant DNA into host cells.
 Viral Promoters and Enhancers: Viruses have strong

promoters and enhancers that can drive high levels of gene

expression in host cells.
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 Genetic Engineering Tools: Viral enzymes such as
integrases (e.g., HIV integrase) and polymerases are used in
molecular biology to manipulate DNA sequences and
construct recombinant DNA molecules
 Viral Vector Vaccines: Viral vectors are used to deliver

antigen genes from pathogens into host cells, stimulating

immune responses against specific diseases
 Vaccine Platforms and Development: Advances in viral

genomics and molecular biology have accelerated vaccine

development by allowing rapid identification of viral antigens,
design of vaccine constructs, and evaluation of vaccine
candidates in preclinical and clinical trials. 8
 Cancer Treatment: Oncolytic viruses are designed to
specifically infect and kill cancer cells while sparing normal
cells.
 Diagnostic Tools: Viruses are used in diagnostic assays to

detect the presence of specific pathogens or to study host

immune responses, aiding in the rapid diagnosis of diseases.
 Industrial Applications: viruses are used in the production

of nanomaterials and in the synthesis of specific proteins and

enzymes that have industrial applications.
 Education and Training: Viruses are used in educational

settings to teach students about microbiology, immunology,

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and virology, contributing to the training of the next
generation of scientists and healthcare professionals.
 DIFFERENCES BETWEEN BACTERIA AND VIRUSES
Character Typical bacteria Viruses

Intracellular parasite Absent Present

Plasma membrane Present Absent
Growth on inanimate media Present Absent
Possess both DNA and RNA Present Absent
Replication by binary fission Present Absent
Sensitive to antibiotics Yes No
ATP-generating metabolism Yes No

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MORPHOLOGY AND STRUCTURE
 Viruses may be classified into several different morphological
types base on the basis of their capsid architecture.

 The structure of these capsids has been revealed by electron

microscopy and a technique called X-ray crystallography.

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SIZE

 The clinically important viruses vary widely in their size. They

are much smaller than bacteria, range from as small as 20-
nm to as large as 300-nm viruses. Except for some giant
viruses, like the Mimivirus, can reach up to 1,000 nm.
 The collodion membrane filter with different pore sizes was

the earliest method of determining the size of virus.

Subsequently, ultracentrifugation method was used to
determine the size of the viruses by calculating from the rate
of sedimentation of virus in the ultracentrifuge.
 Electron microscopy is the most recent method for

determining the size as well as the shape of the virus.

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1.HELICAL VIRUSES
 Helical viruses resemble long rods that may be rigid or
flexible.
 The viral nucleic acid is found within a hollow, cylindrical

capsid that has a helical structure .

 Example-Rabies virus

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2. POLYHEDRAL VIRUSES
 Bacterial/plant/animal viruses are many sided or polyhedral.
 The capsid of most polyhedral virus of an icosahedron, a

regular polyhedron with 20 triangular faces and 12 corners is

in the shape.
 Example- Adenovirus

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3. ENVELOPED VIRUSES
 The capsid of some viruses is covered by an envelope.
 Enveloped viruses are roughly spherical .

 When helical or polyhedral viruses are enclosed by envelopes,

they are called enveloped helical or enveloped polyhedral

viruses.
 Example- Influenza virus

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4. COMPLEX VIRUSES
 Some viruses, particularly bacterial viruses, have
complicated structures and are called complex viruses.
 the capsid (head) is polyhedral and that the tail sheath is

helical
 The head contains the nucleic acid.

 Example- variola virus

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GENERAL STRUCTURE OF VIRUS

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STRUCTURAL COMPONENTS
 The virion consists of a nucleic acid core, the genome,
surrounded by a protein coat, the capsid. The capsid together
with the enclosed nucleic acid is known as the nucleocapsid.
 Some viruses are surrounded by envelopes.

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ENVELOP
In some viruses, the capsid is covered by an envelope, such
viruses are called enveloped viruses. All of the negative-
stranded RNA viruses are enveloped. The viruses that lack
envelope are called nonenveloped or naked viruses.
 The virion envelope usually consists of lipids, proteins, and

Glycoproteins.
 The viral envelope does not contain any cellular proteins

instead uses the host membrane as it viral envelop.

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 Depending on the virus, the envelopes of the viruses may or
may not be covered by spikes.
 The structural elements of the envelope can be damaged by

drying or by exposure to acids, detergents, and solvents;

they are only biologically active in aqueous solutions.
 Most of the enveloped viruses are usually transmitted

through body fluids, such as blood, respiratory droplets,

tissue exudates,

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VIRAL NUCLEIC ACID
 In contrast of prokaryotic and eukaryotic cells viruses can
have either DNA/RNA i.e contains only single nucleic acid.
The nucleic acid of viruses only the genetic material present.
 It may be single or double stranded.

 The percentage of nucleic acid in relation to protein ranges

from about 1% - 50%.

 Nucleic acid may be circular or linear or separate molecules.

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CAPSID
 The Nucleic acid of viruses is surrounded by a protein coat is
called capsid.
 The determination of structure of capsid depends on viral

nucleic acid.
 Each capsid is composed of protein subunits called

capsomers and it may be single or multiple type.

 Functions:

 Protect the viral nucleic acid.

 Participate in the viral infection.

 Share the antigenicity

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SPIKES
 Depending on viruses the envelope may or may not be
covered by spikes which are carbon protein complex.
 The spikes are glycoprotein-like projections on the outer
surface of the envelope. Most spikes act as viral attachment
protein (VAP).
 Some viruses attach to host cell by means of spikes.
 This characteristics used for identification purpose.
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 Ability to clump with RBC( Influenza) – heamagglutination.
CLASSIFICATION
Virus are mainly classified by phenotypic characteristics ,
such as
Morphology, nucleic acid type , mode of replication , Host
organisms and the type of disease the cause.
 Two main methods are used for the classification of viruses -

1. ICTV ( International Committee On Taxonomy of

Viruses ).
2. Baltimore.

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BALTIMORE CLASSIFICATION SYSTEM
 Viruses are classed into 7 types of genes……
 Class 1: Double Stranded DNA Viruses

 Class 2: Single-stranded DNA viruses

 Class 3: Double-stranded RNA viruses

 Class 4: Single-stranded RNA viruses - Positive-sense

 Class 5: Single-stranded RNA viruses - Negative-sense

 Class 6: Positive-sense single-stranded RNA viruses that

replicate through a DNA intermediate

 Class 7: Double-stranded DNA viruses that replicate through

a single-stranded RNA intermediate

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ON THE BASIS OF NUCLEIC ACID
 virus are two types:
 1. RNA viruses eg. Rhinovirus

 2. DNA Viruses eg. Papiloma virus

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CLASSIFICATION ON THE BASIS OF HOST

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REPLICATION
 Replication of virus is very complicated process
 Viruses never reproduce by division
 They are replicated by a process in which all components of
virus are produced separately and are assembled into intact
virons.
 For replication of virus host is necessary
 Viruses are host specific
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 Host may be a bacteria, plant or an animal
 There are 2 types of life cycle commonly seen in viruses
 They are: i Lytic Cycle ii Lysogenic Cycle

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LYTIC CYCLE

 When the lytic phages ( Bacteriophages) infect cells, the cell

responds by producing large number of few viruses i.e. at the
end of incubation period the host cell burst or lysis, releasing
new phage to infect other host cells. These is called lytic
cycle.

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STAGES
1 Attachment (adsorption) of the virion to the host cell
 2 Penetration (entry, injection) of the virion nucleic acid
into the host cell
 3 Synthesis of virus nucleic acid and protein by the host cell

machinery as redirected by the virus

 4 Assembly of capsids and Packaging of viral genomes into

new virions
 5 Release of new virions from the cell

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GROWTH CURVE OF VIRUS

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DESCRIPTIONS OF GROWTH CURVE
 Following adsorption, the infectivity of the virus particles
disappears, a phenomenon called eclipse. This is due to the
uncoating of the virus particles.
 During the latent period, replication of viral nucleic acid and

protein occurs.
 The maturation period follows, when virus nucleic acid and

protein are assembled into mature virus particles. At this

time, if the cells are broken open, active virus can be
detected.
 Finally, release occurs, either with or without cell lysis.

 The timing of the one-step growth cycle varies with the virus
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and host. 20-60min in many bacterial viruses. 8-40h in most
animal hosts
COMMON DISEASES CAUSED BY VIRUSES
 Hepatitis is the inflammation of the liver, commonly caused
by viral infections, toxins, alcohol abuse, autoimmune
diseases, or certain medications. It can lead to liver damage
and death.

TYPES
 Viral Hepatitis: Caused by viruses (Hepatitis A, B, C, D, and

E).
 Alcoholic Hepatitis: Due to excessive alcohol consumption.

 Toxic Hepatitis: Caused by drugs, chemicals, or toxins.

 Autoimmune Hepatitis: When the immune system over 37

actively attacks liver cells.

HEPATITIS B
 It is caused by hepatitis B virus.
 Viral hepatitis B is a global public health problem, causing

significant morbidity and mortality, it can cause both acute

and chronic infection, leading to liver damage.
General mode of Transmission:
 Unprotected Sex

 Blood Transfusion

 Sharing Needles and Sharp Objects

 Contact with infected Blood or Body Fluid (semen, virginal

discharge etc…).
 Mother to Child (mostly leads to chronic stage). 38
REPLICATION OF HEPATITIS B VIRUS
 Its replication takes place in the nucleus and the cytoplasm
 HBV attaches to hepatocytes and enters via endocytosis. The

partially double-stranded DNA (dsDNA) enters the nucleus.

The viral DNA is converted into covalently closed circular DNA
(cccDNA), which serves as a template for viral replication.
 Viral RNA transcripts are synthesized and translated into

proteins. Reverse transcription converts RNA back into DNA

for packaging into new virions.
 New virions are released into the bloodstream, allowing

transmission.
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DIAGRAMMATIC ILLUSTRATION

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TREATMENT
 Acute HBV: No specific treatment; supportive care only.
Chronic HBV:
 Antiviral medications (reduce viral load and prevent liver

damage):
 Tenofovir
 Entecavir

 Pegylated Interferon-alpha (IFN-α) (used in some cases)

 Liver transplantation (for end-stage liver disease or liver failure).

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HIV/AIDS
 HIV (Human Immunodeficiency Virus) is a virus that attacks the
body's immune system, specifically the CD4+ T cells, leading to
immune suppression. HIV progresses to AIDS when left untreated.
HIV can be divided into HIV 1 and HIV 2, type one is mostly
common and widely distributed globally.
 HIV is transmitted through:

1. Sexual contact (most common route)

2. Blood and blood products (e.g., sharing needles, transfusions)
3. Mother-to-child transmission (MTCT) (during pregnancy, childbirth,
or breastfeeding)
4. Needlestick injuries (healthcare workers at risk)
 Note: HIV is NOT spread through casual contact, air, water, or 42
insect bites.
REPLICATION OF HIV
1. Attachment – HIV binds to CD4+ receptors on T cells.
2. Fusion – The virus fuses with the host cell membrane and
releases RNA.
3. Reverse Transcription – Viral RNA is converted into DNA
using reverse transcriptase.
4. Integration – Viral DNA integrates into the host genome via
integrase enzyme.
5. Transcription & Translation – Viral genes are transcribed and
translated into proteins.
6. Assembly – New viral particles are assembled
7. Budding & Maturation – The new virus leaves the host cell 43

and matures, ready to infect other cells.

PREVENTION
1. Safe Sex Practices – Condom use, reducing multiple partners.
2. Pre-Exposure Prophylaxis (PrEP) – Daily medication for high-
risk individuals.
3. Post-Exposure Prophylaxis (PEP) – Emergency ART after
potential exposure.
4. Needle Exchange Programs – Prevents spread among drug
users.
5. HIV Testing & Early Diagnosis – Helps prevent transmission.
6. Mother-to-Child Transmission Prevention – ART during
pregnancy and no breastfeeding.
7. Vaccine Research – No approved HIV vaccine yet, but 44
ongoing studies.
RABIES
 Rabies is a viral zoonotic disease that affects the CNS,
leading to fatal encephalitis in mammals, including humans.

 Rabies vaccine is transmitted through:

 Bites, scratches, or saliva of infected animals.

 Mucosal exposure or rare cases like organ transplants.

 Primary vectors: dogs, bats, raccoons, foxes.

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 Early Symptoms include:
 Fever, headache, general weakness or discomfort, Pain,

tingling, or itching at the site of the bite.

 Advanced Symptoms include:

 Confusion, anxiety, agitation, hallucinations, and difficulty

swallowing, Difficulty swallowing water, and difficulty

breathing and death.

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REPLICATION

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TREATMENT
 No effective treatment once symptoms appear (nearly 100%
fatality).
Post-exposure prophylaxis (PEP) includes:
 Immediate wound washing

 Rabies vaccination

 Rabies immune globulin (RIG) for unvaccinated individuals.

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INFLUENZA VIRUS
 Part of the Orthomyxoviridae family, which also includes
other types of influenza viruses
 ~100-nm enveloped particles with a spherical or oblong

capsid
 Segmented (–)ssRNA genome of ~13,500 bp, consisting of

eight segments
 Infects birds and mammals including humans and pigs

 It causes flu, a respiratory illness that affects the nose,

throat, and sometimes the lungs

 Vaccine produced for new seasonal subtypes each year

 Causative Agents: Influenza A Influenza B, influenza C and 49

influenza D
 The influenza virus is transmitted via:
 Airborne droplets (coughing, sneezing).

 Direct contact with infected people or contaminated surfaces.

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REPLICATION
 Attachment (binding to host cell)
 Entry(endocytosis or fusion)

 Transport to Nucleus and Replication

 Translation and Protein synthesis

 Assembly and packaging

 Release( budding and exit from cell)

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TREATMENT
Antiviral Drugs
Supportive care
 Rest

 stay hydrated

 pain relief

 stay warm

 avoid contact

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COMMON COLD VIRUS
 Common cold is a viral infection of the upper respiratory tract
(also called an upper respiratory infection or URI).
 Colds usually last less than a week and are caused by

different respiratory viruses.

 Many viruses can cause a common cold.

 Rhinoviruses are the most common cause.

 Symptoms

 Most often, symptoms start 1 to 3 days after exposure to the

virus. Symptoms vary. They can include:

 Runny or stuffy nose.

 Sore or scratchy throat. 54

 Cough.
 Sneezing.

 Generally feeling unwell.

 Slight body aches or a mild headache.

 Low-grade fever.

 Transmission

 The common cold is easily spread to others. It's often spread

through airborne droplets that are coughed or sneezed into

the air by infected person.
 Colds can also be spread when an infected person touches

you or a surface (like a doorknob) that you then touch. 55

REPLICATION
 Entry and uncoating
 Viral RNA Translation

 Viral RNA replication

 Assembly and maturation

 cell lysis

 Temperature dependence

 Transmission

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TREATMENT
 There's no cure for the common cold virus. Most cases of the
common cold get better without treatment within 7 to 10
days. But a cough may last a few more days.
 Rest.

 Drink plenty of liquids.

 Humidify the air.

 Use saline nasal rinses.

 Pain relievers, Decongestant nasal sprays, Cough syrups can

help stuffy nose and cough.

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EBOLA VIRUS
 Ebola virus disease (EVD), formerly known as Ebola
hemorrhagic fever, It causes severe inflammation and tissue
damage throughout the body
 Ebola virus belongs to a type of virus called the

orthoebolavirus
 Orthoebolaviruses are found primarily in sub-Saharan Africa.

And can cause serious and often deadly disease, with a

mortality rate as high as 80 to 90 percent. They were
discovered in 1976 in the Democratic Republic of Congo.

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SIGNS AND SYMPTOMS

 People with Ebola disease may experience symptoms early in

the course of illness.
 These symptoms may include fever, aches, and fatigue. As

the person becomes sicker, the illness typically progresses to

symptoms such as diarrhea, vomiting, and unclassified
bleeding.
 Incubation period start from 2 to 21 days, However, on

average, symptoms begin 8 to 10 days after exposure to the

virus.

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TRANSMISSION
 Humans and animals can become infected with the Ebola
virus from an infected animal.
 People can also get Ebola disease through contact with the

body fluids of an infected person or contaminated objects.

 Even after someone recovers from Ebola disease, the virus

can remain in areas of the body that are shielded from the
immune system.

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REPLICATION
 Attachment
 viral entry(penetration)

 Replication and Transpiration

 Assembly and budding

 Release

 Lytic cycle

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VIRAL REPLICATION OF EBOLA

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TREATMENT
 Anti-viral drugs
 Supportive care:

 Fluids and electrolytes (body salts) by mouth or intravenous.

 Medicine to support blood pressure, reduce vomiting and

diarrhea, and to manage fever and pain.

 Treatment for other infections, if any.

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VIRAL PROTEIN SYNTHESIS
 Viral protein synthesis refers to the process by which viruses
produce the proteins necessary for their replication and
assembly within a host cell.
 Since viruses lack the cellular machinery required for protein

synthesis, they hijack the host cell's ribosomes, enzymes,

and other components to produce their own proteins.

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STEPS IN PROTEIN SYNTHESIS
1. Attachment and Entry:-the virus attaches to the host cell
and enters it, often by fusing with the cell membrane or
being endocytosed.
2. Release of Viral Genome:- Once inside the host cell, the
viral genome (DNA or RNA) is released into the cytoplasm
or nucleus.
3. Transcription and Translation:- If the virus has a DNA
genome, it typically uses the host cell's RNA polymerase to
transcribe viral mRNA, which is then translated into viral
proteins by the host cell's ribosomes. And If the virus has an
RNA genome, it may directly use the host cell's ribosomes
to translate viral proteins. 65
4. Replication of Viral Genome:- The viral genome is
replicated using viral or host enzymes, depending on the type
of virus.
5. Assembly of Viral Proteins:- Viral proteins, including
structural proteins (e.g., capsid proteins) and non-structural
proteins (e.g., enzymes), are synthesized and assembled.
6. Virion Assembly:- New viral particles (virions) are
assembled by packaging the replicated viral genome into the
newly synthesized viral proteins.
7. Release:- The newly formed virions are released from the
host cell, often by budding or cell lysis, to infect other cells.
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IMPORTANCE
 It is essential for the production of viral components,
including capsid proteins, envelope proteins, and enzymes
required for replication.
 It is a key target for antiviral drugs, which aim to inhibit viral

replication by blocking steps like transcription, translation, or

protein processing.

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HOST CELL REACTION
 This refers to the cellular responses triggered when a virus
infects a host cell.
 When a host cell is infected by a virus, it initiates a series of

reactions to detect, defend against, and eliminate the viral

threat. These reactions are part of the host's innate and
adaptive immune responses.
STEPS
1. Detection of Viral Infection:- Host cells recognize viruses
through pattern recognition receptors (PRRs), which detect
viral components such as: Viral nucleic acids (e.g., dsRNA,
ssRNA, or DNA).
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Viral proteins or other molecular patterns associated with the
virus.
STEPS CONT…..
Key PRRs include:-
Toll-like receptors (TLRs): Detect viral RNA or DNA in
endosomes or on the cell surface.
RIG-I-like receptors (RLRs): Detect viral RNA in the
cytoplasm.
cGAS-STING pathway: Detects viral DNA in the cytoplasm
2. Activation of Innate Immune Responses
Upon detecting a virus, the host cell activates innate
immune defenses to limit viral replication and spread. Key
responses include:
-Production of interferons (IFNs) 69

-Inflammatory Response
STEPS CONT…
3. Adaptive Immune Response:- If the innate immune
response is insufficient to clear the infection, the adaptive
immune system is activated.
4. Viral Evasion Strategies:- Viruses have evolved
mechanisms to evade or suppress host immune responses,
such as:-
-Inhibiting interferon production or signaling.
- Blocking antigen presentation.
- Preventing apoptosis to prolong viral replication.

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OUTCOMES OF HOST CELL REACTION
The host cell's reaction can lead to several outcomes.
1. Clearance of Infection: The immune system
successfully eliminates the virus.
2. Persistent Infection: The virus evades immune
detection and establishes a long-term infection.
3. Cell Death: The infected cell undergoes apoptosis or
necrosis, limiting viral spread.
4. Transformation: Some viruses (e.g., HPV, EBV) can
cause uncontrolled cell growth, leading to cancer.

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THANK YOU
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