VIROLOGY :

INTRODUCTION TO VIROLOGY,
ITS’ PATHOGENESIS & ERADICATION

Lisa T. Muslich
2019 Microbiology Department, Faculty of Medicine, Hasanuddin University
Learning Objectives

1. Viral general characteristic,

structure and classification
2. Viral multiplication
3. Pathogenesis of viral infection
4. Viral eradication
5. Microbiology diagnostic methods
of viral infection
 History

-rabies vaccine-

17th century
light microscope
Foot and Mouth Disease
Introduction
 Pathogenic microorganism : virus,
bacteria, fungi, parasite
 Viral division based on :

1. Type and structure of nucleic acid

2. Replication strategy

3. Capsid symmetry

4. Enveloped
Properties of viruses
 Obligate intracellular parasites (Inactive outside the
host cell and active only inside host cells)
 Ultramicroscopic size (20 nm – 450 nm in diameter)
 Basic structure (capsid & nucleic acid)
 Nucleic acid (DNA or RNA) : dsDNA, ssDNA, ssRNA,
or dsRNA
 Surface molecules  high specificity for attachment to
the host cell
 Multiply by taking control of host cell’s genetic material
and regulating the synthesis and assembly of new
viruses
 Lack enzymes
 Lack machinery for synthesizing proteins
Size comparison of viruses with
eukaryotic cells (yeast) and bacteria

Foundations in Microbiology,
2012.
 1 2

https://www.uwyo.edu/virtual_edge/units/direct_stain.html http://people.upei.ca/jlewis/html/lab_1.html

3 4

https://cmr.asm.org/content/22/4/552
Hierarchical classification

 Order – family – subfamily – genus – species

 Order  -virales; e.g. Herpesvirales
 Family  -viridae; e.g. Herpesviridae.
 Subfamily  -virinae; e.g. Alphaherpesvirinae.
 Genus  -virus; e.g Simplexvirus.
 Species  e.g. Herpes simplex 1 virus (HSV-
1) & Herpes simplex 2 virus (HSV-2)
 Structure
Positive-sense
a. Genome
Single stranded

RNA Negative-sense

Double stranded

Single stranded
DNA
Double stranded
RNA vs DNA
 Viral genome
The Baltimore classification :
1. dsDNA: these viruses make mRNA and replicate their genomes just
as cell do.
2. ssDNA: these viruses must first replicate their genome to dsDNA,
which is then used for transcription to mRNA.
3. dsRNA: the negative strand is used to produce +ssRNA that acts as
mRNA. Both strands are used as templates for genome replication.
4. +ssRNA: the genome acts as messenger RNA.
5. -ssRNA: these viruses synthesize +ssRNA from the genome that
acts as mRNA and as a template for genome replication.
6. +ssRNA reverse transcription: retroviruses are capable of using an
RNA template to make dsDNA, incorporate into the host genome and
becomes latent.
7. dsDNA reverse transcription: virus replicate through a single-
stranded RNA intermediate
https://viralzone.expasy.org/254
Structure

Practical Handbook of Microbiology, 2015.

Capsid
• Morphological subunit  capsomer
• Structural subunit  protomer
• Capsomer composed of 5 protomer
(pentamer) or 6 protomer
Capsid
 Capsid function :
a. Protect the genome
b. Receptor attachment
c. Elicit antibody production
d. Antigenic determinant for serologic evaluation
Antigenic Determination
 Envelope glycoproteins and naked virus
capsid spikes  antigenic variation  viral
serotype
 Viral serotype  cross-reactivity, little cross-
protection
Basic types of viral morphology

Foundations in Microbiology, 2012.

Classification of Important Virus

Lippincott’s Illustrated Review. 2012

Medical Microbiology and Infection at a glance.
2012
Virus families, genera, common
names, and types of diseases

Foundations in Microbiology,
2012.
 Foundations in
Microbiology, 2012.
DNA vs RNA virus
DNA virus :
 Double-strand DNA (except Parvovirus)
 Naked-virus (except herpes, poxvirus, &
hepadnavirus)
 Icosahedron capsid and replication
inside the nucleus (except poxvirus)
RNA virus :
 Single-strand RNA (except reovirus)
 Enveloped (except Calicivirus,
Picornavirus, & Reovirus)
 Helical capsid (except Picornavirus,
Calicivirus, Flavivirus, Retrovirus,
Reovirus, & Togavirus)
 Cytoplasmic replication (except
Orthomyxovirus & Retrovirus have both
cytoplasmic and nucleic phase)
 Positive, negative or both sense of RNA
strand
DNA viruses
A. Parvoviridae  Eg. JC virus (leukoencephalopathy); BK virus
(nephropathy in transplant recipients); Merkel cell
 size : 18–26 nm. virus (Merkel cell skin carcinomas)
 cubic symmetry (32 capsomeres), no envelope  SV40, a primate virus, can also infect humans
 single-stranded DNA (5 kb) D. Papillomaviridae
 Replication only in actively dividing cells; capsid  8 kb, size 55–60 nm
assembly in the nucleus
 Certain types of human papillomaviruses are
 Human B19 replicates in immature erythroid cells causative agents of genital cancers in humans
(aplastic crisis, fifth disease, and fetal death)
 cannot be grown in cultured cells in vitro.
B. Anelloviridae (from Latin anello meaning ring)
E. Adenoviridae
 ~30 nm in diameter
 70–90 nm
 icosahedral virions, no envelope.
 Nonenveloped, cubic symmetry (fiber spikes)
 negative sense, circular, single-stranded DNA (2–4 kb)
 linear, doublestranded DNA (26–48 kb)
 Anelloviruses include the torque tenoviruses, and are
globally distributed in the human population and many  Replication in the nucleus.
animal species. No specific disease associations have
been proven.  At least 57 types infect humans, (mucous
membranes, lymphoid tissue)
C. Polyomaviridae
 cause acute respiratory diseases, conjunctivitis, and
 45 nm, nonenveloped, gastroenteritis
 heat-stable, solubilization-resistant viruses
 cubic symmetry (72 capsomeres)
 produce tumors in infected hosts.
 circular, double-stranded DNA (5 kb)
 replicate within the nucleus.
DNA viruses… (cont.)
F. Hepadnaviridae  Eg. herpes simplex types 1 and 2 (oral and
genital lesions), varicella-zoster virus
 40–48 nm, enveloped viruses (chickenpox and shingles), cytomegalovirus,
 circular, partially double-stranded DNA Epstein-Barr virus (infectious mononucleosis
molecules (3.2 kbp) and association with human neoplasms),
human herpesviruses 6 and 7 (T cell
 Replication involves repair of the single- lymphotropic), and human herpesvirus 8
stranded gap in the DNA, transcription of (associated with Kaposi sarcoma)
RNA, and reverse transcription of the RNA to
make genomic DNA. H. Poxviridae
 27-nm icosahedral nucleocapsid core  brick-shaped or ovoid viruses 220–450 nm
long × 140–260 nm wide × 140–260 nm thick
 The surface protein  overproduced during
replication (liver)  bloodstream.  envelope

 e.g. Hepatitis B virus (acute and chronic  characteristic vesicular skin lesions
hepatitis); persistent infections  liver cancer.  linear, covalently closed, double-stranded
G. Herpesviridae DNA (130–375 kb)
 150–200 nm  Containing about 100 proteins

 The nucleocapsid is 100 nm in diameter, with  Replication occurs entirely within the cell
cubic symmetry cytoplasm.
 and 162 capsomeres, envelope.  Some are pathogenic for humans (smallpox,
vaccinia, molluscum contagiosum); others that
 linear, double-stranded DNA (120–240 kb) are pathogenic for animals can infect humans
 Latent infections (ganglial or lymphoblastoid (cowpox, monkeypox).
cells)
RNA viruses
A. Picornaviridae  27–40 nm
 28–30 nm, cubic symmetry  cup-shaped depressions on their surfaces
 ether-resistant viruses  single-stranded, positive-sense RNA (7.3–
 Single stranded and positive sense (7.2–8.4 8.3 kb)
kb)  No envelope
 Eg. enteroviruses (polioviruses,  Noroviruses (eg, Norwalk virus)  epidemic
coxsackieviruses, echoviruses, and acute gastroenteritis.
rhinoviruses [more than 100 serotypes D. Hepeviridae
causing common colds]) and hepatovirus
(hepatitis A)  32–34 nm
 Rhinoviruses are acid labile and have a high  ether resistant
density; other enteroviruses are acid stable
and have a lower density  single-stranded, positive-sense RNA (7.2 kb)
B. Astroviridae  It lacks a genome-linked protein (VPg)
 28–30 nm  Human hepatitis E virus
 distinctive star-shaped outline on their E. Picobirnaviridae
surfaces  35–40 nm,
 linear, positive-sense, single-stranded RNA  nonenveloped viruses
(6.8–7.0 kb)
 icosahedral
 may be associated with gastroenteritis in
humans and animals  linear, doublestranded, segmented (bipartite)
RNA (two segments), 4kb
C. Caliciviridae
RNA viruses… (cont.)
F. Reoviridae  single-stranded, positive-sense RNA (9.7–11.8 kb
 60–80 nm,  enveloped virion measures 65–70 nm
 ether-resistant,  Eg. eastern equine encephalitis virus, rubella virus
 nonenveloped, icosahedral I. Flaviviridae
 short spikes extend from the virion surface  enveloped
 linear, double-stranded, segmented RNA (10–12  40–60 nm
segments), 18–30 kbp
 single-stranded, positive-sense RNA (9.5 to 12 kb)
 Individual RNA segments 200 to 3000 bp
 Mature virions accumulate within cisternae of the
 Replication in the cytoplasm endoplasmic reticulum
 Eg. Rotaviruses (gastroenteritis), Colorado tick fever  Eg. yellow fever virus and dengue viruses, Hepatitis
virus of humans C virus
G. Arboviruses and Rodent-Borne Viruses J. Arenaviridae
 Arboviruses complex cycle involving arthropods as  pleomorphic, enveloped
vectors (dengue, yellow fever, West Nile fever, and
encephalitis viruses)  60 to 300 nm (mean, 110–130 nm)
 Rodent-borne viruses  persistent infections in  segmented, circular, negative sense, single-
rodents (hantavirus infections and Lassa fever) stranded RNA (10–14 kb)
 The viruses in these ecologic groupings belong to  Replication occurs in the cytoplasm
several virus families, including arenaviridae,  virions incorporate host cell ribosomes during
bunyaviridae, flaviviridae, reoviridae, rhabdoviridae, maturation  “sandy” appearance
and togaviridae.
 ie, the Tacaribe complex, Lassa fever virus of Africa
H. Togaviridae
 alphaviruses—as well as rubella virus
 lipid-containing envelope and are ether sensitive
RNA viruses… (cont.)
K. Coronaviridae  segments range from 890 to 2350 nucleotides each
 enveloped  Eg. influenza viruses
 120- to 160-nm N. Bunyaviridae
 positive-sense, single stranded RNA (27–32 kb)  spherical or pleomorphic
 cause mild acute upper respiratory tract illnesses—“colds”—but a new  80- to 120-nm
coronaviruses causes severe acute respiratory syndrome (SARS) and
Middle East respiratory syndrome (MERS)  enveloped
 Eg. Toroviruses (gastroenteritis)  triple-segmented, single-stranded, negative-sense or ambisense RNA
(11–19 kb)
L. Retroviridae
 three circular, helically symmetric nucleocapsids (2.5 nm in diameter
 spherical, enveloped viruses (80–110 nm) and 200–3000 nm in length
 two copies of linear, positive-sense, single-stranded RNA (7–11 kb  Replication occurs in the cytoplasm, and an envelope is acquired by
each) budding into the Golgi.
 helical nucleocapsid within an icosahedral capsid  The majority transmitted to vertebrates by arthropods (arboviruses).
Hantaviruses are transmitted not by arthropods but by persistently
 Contains a reverse transcriptase enzyme infected rodents via aerosols of contaminated excreta.
 produces a DNA copy of the RNA genome O. Bornaviridae
 DNA  circularized and integrated into host chromosomal DNA.  enveloped, spherical (70–130 nm)
 eg. Leukemia and sarcoma viruses of animals and humans, foamy  linear, single-stranded, nonsegmented, negative-sense RNA (8.5–
viruses of primates, and lentiviruses (human immunodeficiency viruses; 10.5 kb)
visna of sheep)
 nonsegmented, negative-sense RNA viruses
 Retroviruses cause acquired immunodeficiency syndrome (AIDS)
 replication and transcription of the viral genome occur in the nucleus
M. Orthomyxoviridae
 Eg. Borna disease virus is neurotropic in animals; a postulated
 80- to 120-nm association with neuropsychiatric disorders of humans is unproven.
 enveloped
 helical symmetry
 round or filamentous
 surface projections contain hemagglutinin or neuraminidase activity
 linear, segmented, negative-sense, single-stranded RNA (10–13.6 kb)
RNA viruses… (cont.)
P. Rhabdoviridae  Eg. mumps, measles,

 resembling a bullet, flat at one end

parainfluenza, metapneumo, and
and round at the other (75 × 180 respiratory syncytial viruses
nm) The envelope has 10-nm  Genetically stable
spikes R. Filoviridae
 linear, single-stranded,
 enveloped, pleomorphic (very long
nonsegmented, negative-sense and threadlike)
RNA (11–15 kb)
 80 nm wide and about 1000 nm
 Eg. Rabies virus
long
Q. Paramyxoviridae  envelope contains large
 150–300 nm peplomers
 Pleomorphic  linear, negative-sense,

 nucleocapsid measures 13–18 nm

singlestranded RNA (18–19 kb)
 Eg. Marburg and Ebola viruses 
 linear, singlestranded,
nonsegmented, negative-sense severe hemorrhagic fever in Africa
RNA (16–20 kb)
 nucleocapsid and the hemagglutinin
are formed in the cytoplasm
Viral multiplication
Basic steps:
1. Recognition and attachment.

2. Penetration.

3. Uncoating.

4. Synthesis : replication and protein

production.
5. Assembly.

6. Release.
 Viral
multiplication

Foundations in Microbiology, 2012.

 Viral multiplication
1. Attachment
a. Attachment site on
the viral surface
 Glycoprotein in
viral envelopes
 Capsid proteins

b. Host cell receptor

molecules
(spesific for each
virus family)
Lippincott’s Illustrated Review.
2012
Sherris Medical Microbiology, 2014.
Viral multiplication
2. Penetration and uncoating
a. Membrane fusion

Foundations in Microbiology, 2012.

Viral multiplication
(Penetration and uncoating, cont.)

b. Receptor-mediated endocytosis

Foundations in Microbiology, 2012.

 Viral multiplication
3. Synthesis : Replication & protein
production
a. dsDNA virus
1. Enters the nucleus
2. Transcribed  mRNA
3. Viral mRNA leaves nucleus 
translated  structural protein
4. Viral DNA replicated repeatedly
in the nucleus
5. Viral DNA & protein assembled
 mature virus
6. Some viral DNA insert itself
into host DNA (latency)
Foundations in Microbiology, 2012.
 Viral multiplication
(Synthesis: Replication & protein production, cont.)

b. +ssRNA virus
1. Penetration

2. Directly translated 
viral proteins
3. Negative genome is
synthesized
4. Negative template 
synthesize positive
replicates
5. RNA strands & protein
assemble  mature
virus
Foundations in Microbiology, 2012.
Viral multiplication
(Synthesis: Replication & protein production, cont.)

c. Retrovirus
Can reverse the order of the flow of genetic
information
Common genetic formation patterns are
DNA  DNA; DNA  RNA; RNA  RNA
In retrovirus : RNA  DNA
1. RNA template  ssDNA

2. ssDNA  dsDNA

3. Viral dsDNA enter nucleus

4. dsDNA  ssRNA

5. Retroviral DNA inserted in host’s DNA (latent

infection)
Viral transcription of each genome
Viral multiplication
5. Assembly
Generally in the host cell compartment where
viral nucleic acid replication occurs
Most RNA virus  cytoplasm
Most DNA virus  nucleus
Viral multiplication
5. Release
a. Naked virus  disintegration of the dying cell

b. Enveloped virus :

i. Glycoprotein synthesized and transported to

host cell membrane
ii. Cytoplasmic domains of membrane proteins
bind nucleocapsid
iii. Nucleocapsid enveloped by host cell
membrane
iv. “budding” of host cell membrane

v. Release of enveloped virion

Viral Pathogenesis
A. Entry & primer replication
B. Viral spread & cell tropism
C. Cell destruction & clinical manifestation
D. Recovery from infection
E. Viral release
Viral Transmission
Virus transmitted via:
 Horizontal routes

 Vertical routes

 Vector or animal routes

Common
routes of
transmission

Sherris Medical Microbiology, 2014.

Viral Pathogenesis
A. Entry & primer replication

 Attachment to body
surface (skin, respiratory
tract, urogenital tract,
conjunctiva) OR direct
inoculation within the
body (through needle
injection)

 port d’entrée replication.

 Routes of viral
infection

Jawetz, Melnick & Adelsberg Medical

Microbiology, 2016.
Routes of Infection
Virus

Port d’entree
• Skin
Through injection,
• Respiratory tract
blood transfusion,
• GI tract
mosquitos bite
• Urogenital tract

Multiplication &
Blood (primer viremia)
symptoms

Delayed
Secondary site
symptoms
Viral Pathogenesis
B. Viral spread & cell tropism

 Port d’entrée  primer replication  blood

(viremia) or lymphatic system  free in plasma or
connected to cells within blood  cell tropism
 Tropism  capability of virus to infect discrete
population of cells within a tissue or organ
 Tropism is determined by:
1. Specific interaction of viral surface protein and
cellular receptors on host cells.
2. Intracellular factors (host transcription factor,
factors necessary for viral replication)
Viral pathogenesis
C. Cell destruction & clinical manifestation

 Viral pathogenesis at the cellular level

Lippincott’s Illustrated Review.

2012
 Viral pathogenesis
C. Cell destruction & clinical manifestation

Characteristic of clinical presentation in viral

infection:
1. Acute viral infection

2. Latent infection

3. Chronic or persistent infection

Host Immune Response
A. Innate Immune Response
 largely mediated by IFNs, produced very quickly
(within hours)  inhibit viral replication  viral
production then decreases
 Several pathways appear to be involved,
including:
(1) a dsRNA-dependent protein kinase (PKR);
(2) an oligonucleotide synthetase, 2-5A
synthetase;
(3) a phosphodiesterase;
(4) nitric oxide synthetase.
Host Immune Response
A. Innate Immune Response

 Viruses mechanisms that block the inhibitory activities of IFNs

on virus replication:
(1) specific viral proteins that block induction of expression of
IFN (herpesvirus, papillomavirus, Filovirus, hepatitis C virus,
rotavirus),
(2) block the activation of the key PKR protein kinase
(adenovirus, herpesviruses),
(3) activate a cellular inhibitor of PKR (influenza, poliovirus),
(4) block IFN-induced signal transduction (adenovirus,
herpesviruses, hepatitis B virus), or
(5) neutralize IFN-γ by acting as a soluble IFN receptor
(myxoma virus).
Host Immune Response… (cont.)
B. Adaptive Immune Response
 Infiltration with mononuclear cells and lymphocytes characterizes the
inflammatory reaction of uncomplicated viral lesions.
 Virus-encoded proteins serve as targets for the immune response.

 Viral polypeptides  recognized by cell surface  cytotoxic T lymphocytes

 lysis of virus-infected cells
 Humoral immunity protects from reinfection.

 Neutralizing antibody  capsid proteins blocks the initiation of viral

infection (attachment, entry, or uncoating)
 Secretory IgA antibody  respiratory or gastrointestinal tracts.

 Some viruses infect and damage cells of the immune system  human
retrovirus HIV
 Immune response  disease exacerbation  subsequent infection with
similar strains (dengue virus hemorrhagic fever)
 Another potential adverse effect of the immune response  autoantibodies
(molecular mimicry)  host may then experience postinfectious
autoimmune disease, such as Guillain-Barre syndrome associated with
prior measles infection.
Virus mechanism to avoid immune
system
 Antigenic Variation, eg. Influenza virus, herpes
virus
 Release of antigens
 Production of antigens at sites that are
inaccessible to the immune system, eg.
Herpesvirus  neurons)
Ecology & Viral Transmission
Viral transmission include:
a. Direct transmission : person to person contact, through:
 Aerosol or droplet (Influenza, Measles, Smallpox)

 Sexual contact (Papillomavirus, Hepatitis B virus, Herpes Simplex

virus type-2, HIV)
 Hand-mouth, hand-eyes, mouth to mouth contact (Herpes Simplex
virus, Rhinovirus, Epstein-Barr virus)
 Contaminated blood (Hepatitis B virus, HIV)

b. Indirect transmission, through:

 Feco-oral transmission (Enterovirus, Rotavirus, Hepatitis A virus)

 Vomit (Norwalk virus, rhinovirus)

c. Zoonotic transmission, through:

 Bites (rabies)

 Droplet or aerosol (Arenavirus, Hantavirus)

d. Vector transmission (Togavirus, Flavivirus, Bunyavirus)

Vector Transmission of Virus
 3 patterns of arthropods transmission:
a. Human-arthropods cycle, eg. Urban yellow
fever, dengue fever
b. Lower vertebrate-arthropods cycle with
tangential infections of human, eg. Jungle
yellow fever, St. Louis encephalitis.
c. Arthropod-arthropod cycle with occasional
infections of human and lower vertebrate, eg.
Colorado tick fever, LaCrosse encephalitis.
Viral Emerging Disease
 Combined factors involved in viral emerging disease:
1. Environmental changes (deforestation, flooding, drought, famine)
2. Human behavior (sexual behavior, drug abuse, outdoor
recreation)
3. Socio-economic & demographic phenomena (war, poverty,
population growth & migration, urban decay)
4. Traveling & trading (highway, international flight)
5. Food production (food supply globalization, food processing &
packing method)
6. Health services (new medical tools, blood transfusion, organ &
tissue transplant, immunosuppressive drugs, antibiotic use)
7. Microbial adaptation (virulence alteration, drugs resistance,
chronic disease cofactor)
8. Society health procedure (inadequate sanitation procedure and
vector control, insufficient prevention program, lack of trained
health workers)
Viral Eradication and Prevention
1. Antiviral chemotherapy

a. Nucleoside and nucleotide analog

b. Reverse transcriptase inhibitors
c. Protease inhibitor
d. Integrase inhibitors
e. Fusion inhibitor
f. Other antiviral 
1. Amantadine & rimantadine

2. Oseltamivir

3. Foscarnet

4. Acyclovir

5. Ganciclovir
Viral Eradication and Prevention
2. Viral vaccine

 General principles
Viral infection  specific antigen  immune
response  immunity
 Killed-virus vaccine

• made by purifying viral preparations to a

certain extent and then inactivating viral

infectivity in a way that does minimal damage
to the viral structural proteins; mild formalin
treatment is frequently used
• prepared from whole virions
Viral Eradication and Prevention
2. Viral vaccine… (cont.)

 Attenuated live virus vaccine

• use virus mutants that antigenically overlap
with wild-type virus but are restricted in some
step in the pathogenesis of disease
• The genetic basis is not known  serial
passages in animals or cell cultures (usually
from a species different from the natural
host)
Viral Eradication and Prevention
2. Viral vaccine… (cont.)

 Subunit vaccine
• Pieces of virus
• Disadvantages: not as immunogenic (do not
create immune response as whole pathogens
and booster)
• Examples: Hepatitis B (HBV) vaccine, Human
pappillomavirus (HPV) vaccine
Jawetz, Melnick & Adelsberg Medical
Microbiology, 2016.
Clinical laboratory methods for viral
infection
 Four major methods:
1. Direct detection of the virus in clinical
specimen
2. Nucleic-acid based detection

3. Isolation of viruses in cell cultures

4. Serologic assays to detect antibodies to

virus
1. Direct detection
 Less sensitive than culture method
 Quick results

 Methods:

a. Microscopy
- Bright field light microscopy  can only
observe poxviruses
- Electron microscopy  expensive,
labor-intensive, not a very sensitive method
in detecting virus
- Direct flourescent antibody (DFA) test
Visual changes observed from cytopathic effect, e.g.: Cowdry type A
bodies (HSV & VZV), HPV-associated koilocytes (HPV), Negri bodies
(Rabies)
b. Enzyme Immunoassays (EIA)
- Less sensitive than cell cultures or IF test
2. Nucleic acid-based detection
Examples: - Detect non-culturable virus
1. Hybridization assay - Detect multiple virus
2. Polymerase Chain Reaction simultanously
(PCR) assays - Viral genetic characterization
3. Nucleic acid sequence-
based amplification
4. PCR + flow cytometry  Disadvantages:
combination
- Detect active and inactive
virus
 Advantages: - High cost
- Faster turnaround time - Specialized training and
- Better sensitivity than cell complex facilities
culture and DFA
- Quantitative
3. Viral isolation
 Cell culture
 Cytopathic effect on cell culture
 Centrifugation-enhanced shell vial culture

- Gold standard
4. Serologic testing
 Indication:
1. Diagnosis of infections with non-culturable
agents, e.g. Hepatitis virus
2. Determination of immune status in regard to
rubella, measles, VZV, HAV, and HBV
3. Monitoring of patients who are
immunosuppressed or have had transplants
4. Epidemiologic or prevalence studies
Viral Quantitation
 Hemagglutination assay
 Plaque assay
 Immunologic assay (ELISA, IFA)
 Molecular assay (PCR)

Plaque assay.
Sherris Medical Microbiology, 2014.
 Viral
detection
methods

Jawetz, Melnick & Adelsberg Medical

Microbiology, 2016.
Definitions
 Pathogenesis : means by which organism produce
disease in host.
 Pathogenicity : ability to cause disease.
 Virulence : “capacity” to produce disease.
 Virions : infectious form of a virus as it exists
outside the host cell, capable of surviving in
crystalline form, consisting of a nucleic acid core, a
protein coat, and, in some species, an external
envelope.
 Epitope : antigenic determinant, portion of a foreign
protein, or antigen, that is capable of stimulating an
immune response.
 References
1. Brooks G. F., et al. Jawetz, Melnick & Adelberg’s Medical Microbiology
(25th ed.). New York: McGraw-Hill. 2010
2. Talaro K.P., Chess B. Foundation in Microbiology (8th ed.). New York:
McGraw-Hill. 2012
3. Harvey R. A., Cornelissen C. N., & Fisher B.D. Lippincott’s Illustrated
Reviews: Microbiology (3rd ed.). Philadelphia: Two Commerce Square.
2012
4. Mishra S. K., & Agrawal D. A Concise Manual of Pathogenic
Microbiology. New Jersey: John Wiley & Sons, Inc. 2013
5. Goldman E. & Green L. H. Practical Handbook of Microbiology. (3rd
ed.). New York: CRC Press. 2015
6. Greenwood D., et al. Medical Microbiology, A Guide to Microbial
Infections. (18th ed.). Toronto: Churchill Licvingstone. 2012
7. Flint J., Racaniello V. R., Rall G. E., et al. Principles of Virology (4th
ed.). Washington D.C.: ASM Press. 2015
8. Generalov I. I. Medical Microbiology, Virology & Immunology. Belarus:
VSMU Press. 2016