Virus classification

and
nomenclature
 Symmetry of viruses
Viruses are divided into three groups, based on the
morphology of the nucleocapsid and the arrangement of
capsomeres.

1-Cubic symmetry: The virus particle is icosahedral in

shape (almost spherical particle ) and the nucleic acid
contained inside the capsid. The icosahedron particle is
composed of 20 equilateral triangles , 12 vertices and has
2,3,5 rotational symmetry.
2- helical symmetry : The virus
particle is elongated or
pleomorphic (not spherical), and
the nucleic acid is spiral.
Capsomeres are arranged round
the nucleic acid.

3- complex symmetry: The virus

particle does not confirm either
cubic or helical symmetry.
• Virus classification
is the process of naming viruses and placing them into
a taxonomic system.

• Taxonomy
A Science with dynamic field, based on information -Uses
techniques and theories of: -Collating and describing; identification
and classification; grouping and naming of viruses

• Nomenclature is just naming

• there are Four main schemes used for the classification of

viruses:
1. The International Committee on Taxonomy of Viruses (ICTV)
system
2. LHT System of Virus Classification
3. Baltimore Classification – 7 classes
4. Holmes classification
Baltimore classification
 Nomenclature of Viruses
How are viruses named?
1. Named after the diseases eg. Measles virus, smallpox virus

2. geographic locations eg. Newcastle disease virus, Ebola virus,

Norwalk virus, Bunyaviridae, Sendai virus, Coxsackie virus

3. Host and signs of disease eg.Tobacco mosaic virus

4. Latin and Greek words eg. Coronaviridae – “crown” Parvoviridae –

“small”

5. Virus discovers eg. Epstein-Barr virus

6. How they were originally thought to be contracted

eg. dengue virus (“evil spirit”), influenza virus (the “influence” of bad
air)

7. Combinations of the above eg. Rous Sarcoma virus

 CLASSIFICATION OF VIRUSES

(1) Nucleic acid type: RNA or DNA; single-stranded or double-stranded;

strategy of replication.
(2) Size and morphology, including type of symmetry, number of
capsomeres, and presence of membranes.
(3) Presence of specific enzymes, particularly RNA and DNA polymerases,
and neuraminidase
(4) Susceptibility to physical and chemical agents, especially ether.
(5) Immunologic properties.
(6) Natural methods of transmission.
(7) Host, tissue, and cell tropisms.
(8) Pathology; inclusion body formation.
(9) Symptomatology.
 International Committee on Taxonomy of
Viruses (ICTV)
http://talk.ictvonline.org
• Formed and governed by the Virology Division of the
International Union of Microbiological Societies (IUMS),
established in 1966
• Update publication on taxonomy at approximately 3-year
intervals
➢ develop an internationally agreed taxonomy for viruses
➢ maintain an index of virus names
➢ maintain an ICTV database, that records the data that
characterize each named viral taxon, with their common names
in all major languages
• A minor point is that names of orders and families are italicized,
unlike in the International Code of Nomenclature for algae,
fungi, and plants and International Code of Zoological
Nomenclature.
 International Committee on
Taxonomy of Viruses (ICTV)
Viral classification starts at the level of order and
continues as follows, with the taxon suffixes given
in italics:
• Order (-virales)
• Family (-viridae)
• Subfamily (-virinae)
• Genus (-virus)
• Species
Species names generally take the form
of [Disease] virus.
 BALTIMORE CLASSIFICATION
Baltimore classification (first defined in 1971) is a classification system that
places viruses into one of seven groups depending on

• It is basically based on the method of viral synthesis.

• It groups viruses into families according to their type of genome.

• a combination of their nucleic acid (DNA or RNA),

• strandedness (single-stranded or double-stranded),
• Sense (+ or -), and
• method of replication.
Named after American Biologist David Baltimore, a Nobel Prize-winning
biologist, these groups are designated by Roman numerals.
 BALTIMORE CLASSIFICATION

1. dsDNA viruses (e.g. Adenoviruses, Herpesviruses, Poxviruses)

2. ssDNA viruses (+ strand or "sense") DNA (e.g. Parvoviruses)

3. dsRNA viruses (e.g. Reoviruses)

4. (+)ssRNA viruses RNA (e.g. Picornaviruses,Togaviruses)

5. (−)ssRNA viruses RNA (e.g. Orthomyxoviruses, Rhabdoviruses)

6. ssRNA-RT viruses RNA with DNA intermediate in life-cycle (e.g.

Retroviruses)
7. dsDNA-RT viruses (e.g. Hepadnaviruses)
Baltimore Classification of Viruses
 HOLMES CLASSIFICATION
Holmes (1948) used Carolus Linnaeus's system of binomial
nomenclature to classify viruses into 3 groups under one
order, Virales. They are placed as follows:

• Group I: Phaginae (attacks bacteria)

• Group II: Phytophaginae (attacks plants)
• Group III: Zoophaginae (attacks animals)
 LHT System (of Virus Classification

• The LHT (Lwoff, Horne, and Tournier) System of Virus

Classification is based on chemical and physical characters
like nucleic acid (DNA or RNA), Symmetry (Helical or
Icosahedral or Complex), presence of envelope, diameter of
capsid, number of capsomers.

• This classification was approved by the Provisional

Committee on Nomenclature of Virus (PNVC) of the
International Association of Microbiological Societies (1962)
 Terminology and Definition
• Virus is a broad general term for any aspect of the infectious agent and includes:
• the infectious or inactivated virus particle
• viral nucleic acid and protein in the infected cell

• Virion is the physical particle in the extra-cellular phase which is able to spread
to new host cells; complete intact virus particle

• Viroids
– Small, autonomously replicating molecules
– Single stranded circular RNA, 240-375 residues in length
– Plant pathogens

• Prions
– Infectious particles that are entirely protein
– No nucleic acid
– Highly heat resistant
– Animal disease that affects nervous tissue
– Affects nervous tissue and results in
• Bovine spongiform encephalitis (BSE) “mad cow disease”,
• Scrapie in sheep
• kuru & Creutzfeldt-Jakob Disease (CJD) in humans
• Satellite or defective viruses
– Viruses which require a second (helper) virus for replication
• Example: hepatitis delta virus requires hepatitis B
• Bacteriophage
Virus that infects prokaryotic (bacterial) cells

• Pseudovirus:
During viral replication the capsid sometimes encloses host nucleic
acid rather than viral nucleic acid. Such particles look like ordinary
virus, particles when observed by electron microscopy, but they do
not replicate. Pseudovirions contain the “wrong” nucleic acid.
Viral Pathogenesis
•Viral Pathogenesis refers to the
series of events that occur during
viral infection of a host.

•It is the sum of the effects on the

host of virus replication and of
immune response
Views of viral pathogenesis
 POSSIBLE OUTCOMES OF VIRAL INFECTIONS

Acute Infection
Symptomatic infections
Persistent infection
•Chronic
•Latent Inapparent infection
•Transformation
IS A DISEASE THE OUTCOME OF ALL VIRAL INFECTIONS?
The outcome of a viral infection depends from the
the characteristics of the virus-host interactions
and from the host defense response

Determinants of viral pathogenesis

Determinants of viral disease

IS A DISEASE THE OUTCOME OF ALL VIRAL INFECTIONS?
The hallmarks of virus-host interactions

Determinants of viral disease: nature of the

disease

•type of target tissues (replication sites);

•pathways of viral entry;
•viral spread to the replication sites;
•viral tropism;
•cells permissivity to virus replication;
•virulence of viral strain.
IS A DISEASE THE OUTCOME OF ALL VIRAL INFECTIONS?
The hallmarks of virus-host interactions

Determinants of viral disease: severity of the

disease

•cytopathogenic attitude of the virus;

•immunopathology;
•initial inoculum of the virus;
•compromised host;
•host genetic background;
•age.
IS A DISEASE THE OUTCOME OF ALL VIRAL INFECTIONS?
The hallmarks of virus-host interactions

Determinants of viral disease: severity

of the disease

The host immune conditions:

•competence of the immune system;

•previous exposure to the virus (immunity)

 VIRAL PATHOGENESIS
The process by which viruses cause disease

•Viral entry
•Viral spread
•Tissue invasion
•Tropism
•Virus shedding and
transmission

•The host defense

•Disease
Viral pathogenesis: time course of typical infection
Sites of virus entry into the host
Different routes of viral entry into the host
Incubation periods of some common viral infections
Virus infection and spread into the host

PENETRATION
PRIMARY LOCALIZED INFECTION
REPLICATION influenza, enteric viruses

PRIMARY TARGET TISSUES

VIREMIA Sensistivity and permissivity

SECONDARY
REPLICATION

DISSEMINATE
SECONDARY INFECTION
VIREMIA exhantema viruses, polio
Entry, dissemination and shedding of blood-borne viruses

Infections can be
localized, or can
spread beyond the
initial site of
replication (a
disseminate
infection)

With many organs

involved the
infection becomes
systemic
Sites of virus entry in the respiratory tract
Enterovirus pathogenesis
Rabies pathogenesis
Varicella-zoster (VZV) infection and spread

VZV enters via conjunctiva and

upper respiratory tract

Replication occurs in regional

lymph nodes

Primary viremia via infected T cells

Replication in visceral organs (liver,

spleen, etc.)

Secondary viremia and subseqeunt

acute infection of skin -”chicken
pox” rash

Latency establish in sensory

ganglia of PNS

Reactivation results in “shingles”-

postherpetic neuralgia
 Viral pathogenesis is the sum of the effects on
the host due to virus replication and the immune
response

• Direct effects of primary infection by cytolityc viruses

(e.g. virus-induced lysis of neurons in CNS by poliovirus)

• Indirect effects of noncytolytic viruses

(e.g. conseguence of the immune response)

•CD8+ T cell-mediated (HIV, HBV, Coxackievirus B)

•CD4+ T cell-mediated
Th1 (measle, HSV)
Th2 (RSV)
•Antibody-mediated (HBV, rubella)
•Immunosuppression (HIV, CMV, measle, influenza)
Measles virus infection and spread
 Kinetics of virus replication and immune responses
The kinetics of virus replication and the kinetics of the defensive response both affect the outcome

Slow localized spread

Intermediate spread

Fast disseminate spread

General patterns of infection
General patterns of infection
Acute infection followed by clearance of virus:
•productive infection
•viremia (circulating virus)
•clearance by immune system
•example: rhinovirus (common cold)
The course of typical acute infection
Some persistent viral infections of humans
Acute infection followed by latent infection and
periodic reactivation:
• initial productive infection with viremia
• viral persistence in non-infectious form
• intermittent reactivation with productive infection
• example: herpes simplex virus type 1 (HSV-1)
 HSV-1 latency and reactivation

1. Productive infection of epithelial cells

2. Virus infects sensory neurons
3. Virus travels to sensory ganglion by neuronal retrograde transport
4. Virus establishes latent infection in sensory ganglion
5. Limited expression of viral genes, latency associated transcripts (LATs),
viral genome replicates in episomal state
6. Virus may be reactivated by changes in physiological status of the
neuron
(neuron damage, immunosuppression, hormonal changes, stress, UV)
7. Changes lead to activation of viral gene expression and productive
infection
HSV-1 primary infection of a sensory ganglion
HSV-1 latency
and reactivation
Epstein-Barr virus primary and persistent infection
Acute infection followed by chronic infection:
•initial productive infection with viremia
•virus not cleared completely by immune system
•continuous, low-level productive infection
•may be "smoldering" infection (productive infection
by small fraction of cells)
•example: human immunodeficiency viruses (HIV)
HIV

•initial productive infection of permissive cells

•viremia
•apparent latent infection
•evidence for smoldering infection of population of permissive cells
•antigenic variants produced during time course of infection:
> 109 new cells infected each day; every possible point mutation occurs between
104 and 105 times per day in an infected individual
Slow, chronic infection
•seen only with unconventional infectious agents scrapie,
bovine spongiform encephalopathy (mad cow disease)
•continuous and slowing increasing production of
infectious agent with time.
MECHANISMS OF VIRAL PATHOGENESIS

CELLULAR PATHOGENESIS

HOST IMMUNE RESPONSE

EPIDEMIOLOGY, PREVENTION AND CONTROL

MECHANISMS OF VIRAL PATHOGENESIS

CELLULAR PATHOGENESIS

HOST IMMUNE RESPONSE

EPIDEMIOLOGY, PREVENTION AND CONTROL

 Cellular pathogenesis: patterns of infection

Type Viral production Cell fate

•Abortive - -
•Cytolytic + death
•Persistent
Chronic + senescence
Latent - -
Transforming
DNA viruses - immort./transfor.
RNA viruses + immort./transfor.
 MECHANISMS OF CELLULAR PATOGENESIS

Direct effects of cytolityc viruses

• Cytopathic effect
• Inclusion bodies
• Apoptosis
• Dysregulation of cell physiology

Indirect effects of non-cytolytic viruses

• Host immune response
 MECHANISMS OF CELLULAR PATHOGENESIS

Cytopathic effect(s): Virus(es)

• Inibition of host protein synthesis polio, herpes, toga, pox
• Host chromosome margination and DNA herpes
degradation
• Nuclear shrinking picorna
• Proliferation of nuclear membrane herpes
• Cell membrane alterations enveloped viruses
• Vacuoles in the cytoplasm papova
• Syncytia (cell fusion) paramyxo, herpes, HIV
• Cell Rounding up and detachment herpes, rabdo, adeno, picorna

Inclusion bodies:
• Intranuclear basophils adeno
• Virion in the cytoplasm (Negri bodies) rabdo
• “Factories” in the cytoplasm (Guarnieri bodies) pox
• “Owl eyes” in the nucleus CMV
• Perinuclear acidophils reo
Cytopathic Effects: an overview

HSV-1
Syncitia formation

RSV

Measle virus
 Inclusion bodies formation

Reovirus replicate in the cytoplasm and generate inclusion

bodies containing viral proteins stained by eosin
 Mechanisms of viral
transformation and
oncogenesis

2
MECHANISMS OF VIRAL PATHOGENESIS

CELLULAR PATHOGENESIS

HOST IMMUNE RESPONSE

EPIDEMIOLOGY, PREVENTION AND CONTROL

 HOST DEFENSES AGAINST VIRAL INFECTIONS

1. Physical barriers

2. Chemical barriers

3. Intrinsic cellular defenses

4. Innate soluble immune response: cytokines,

inflammation, fever, complement

5. Innate cellular immune response: DC, macrophages

6. Adaptive soluble immune response: antibodies

7. Adaptive cellular immune response: NK, CTL

Integration of intrinsic defense with the innate and
adaptive immune response
Intrinsic defense
responses
Apoptosis as a defense against viral infection
 PATHOGENESIS OF A VIRAL DISEASE
The kinetics of host defense mechanisms
 Immune reactions during the response to viral
infections that can cause host cell damage and disease

• Interferons and lymphokines: fever, headache,malaise.

• Delayed-Type Hypersensitivity, Complement

fixation, Immunocomplexes: cell damage and local
inflammatory responses.

• Inflammation due to the cell-mediated response:

severe tissue damages in adults.

• Immunocomplexes accumulation in the blood and

kidney: glomerulonephritis.
MECHANISMS OF VIRAL PATHOGENESIS

CELLULAR PATHOGENESIS

HOST IMMUNE RESPONSE

EPIDEMIOLOGY, PREVENTION AND CONTROL

 EPIDEMIOLOGY OF VIRAL DISEASES
The study of the occurrence, distribution and control of diseases

• Prevalence: the proportion or percentage of individuals in the

population having a disease.

• Incidence: the total number of cases of disease in a population.

• Morbidity: incidence of illness in a population.

• Mortality: incidence of death in a population.

 EPIDEMIOLOGY OF VIRAL DISEASES
The study of the occurrence, distribution and control of diseases

• Outbreak: the occurrence of a large number of cases of a

disease in a new site and in a short period of time (HAV).

• Endemic: disease constantly present, usually in low numbers.

• Epidemic: the occurrence of a disease in unusually high

numbers due to the introduction of new viral strain in a naive
population (Influenza).

• Pandemic: a worldwide epidemic due to the introduction of a

new virus (HIV, SARS, Influenza).
EPIDEMIOLOGY OF VIRAL DISEASES
Classification of disease by incidence
 EPIDEMIOLOGY OF VIRAL DISEASES
The spread of the Asian influenza pandemic of 1957
 EPIDEMIOLOGY OF VIRAL DISEASES
Recent outbreaks of emerging and reemerging infectious diseases
 EPIDEMIOLOGY OF VIRAL DISEASES

Mechanisms of viral transmission:

•aerosol, infected things, direct contact, sexual contact, transplant,
blood-transfusion, zoonosis.

Factors influencing viral transmission

•Environmental persistence of virions;
•Viral replication in body fluids

Risk factors
•Age, health, immune status, work, travels, life style

Populations characteristics
•Percentage of susceptible serum-negative individuals

Geography/Season
Prevention and control
•Quarantine, vector elimination, immunization (natural infection,
vaccination), antiviral therapy
Viral infections are transmitted among hosts in specific ways
Acute viral infections with
seasonal variation in
incidence
Effect of humidity on transmission of influenza virus
 EPIDEMIOLOGY OF VIRAL DISEASES
Prevention and control

Quarantine

Public health measures

•Directed against the reservoirs (domestic animals,
wild animal, insect, humans)
•Directed against transmission (food, water, air)
•Education (STDs)

Immunization
•Natural infection
•Vaccination

Antiviral therapy
EPIDEMIOLOGY OF VIRAL DISEASES
Prevention and control

Vaccines:
the proven best defense
against viruses

Antiviral drugs:
small molecules that block
virus replication