Study of Virus

Learning objectives
Upon completion of this chapter, the student will be able to:
1. Define virus.

2. Describe structure & properties of medically important

viruses

3. Illustrate classification of medically important viruses

4. Explain virus infectious/Replication/Multiplication cycle

5. Describe antiviral agents and their mechanism of action

6. Explain Antiviral agents and vaccine

7. Describe Virus host interaction and viral pathogenesis

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 1. Introduction to Virus

• Viruses are unicellular ultra-microscopic microorganisms.

• They differ from other micro -organism by their small size 20-300
nm (0.02-0.3µm) Viruses are the smallest infectious agents
because of these
– They cannot seen with light microscope and seen only in
electron microscope.
• They have no cellular structure (They are not a cell but they are
component of a cell and have only Genome).
• Their genome containing either deoxyribonucleic acid ( DNA) or
ribonucleic acid( RNA) but not both genome
• Viral components are assembled & do not replicate by division
• Viruses multiply by a complex process and not by binary fission.
 1. Introduction to cont

• Viruses are obligatory intracellular parasites.

• They in ability to Replicate out side of living cells or they replicate
inside living cells only because they lack enzymes necessary for
protein and nucleic acid synthesis so depend up on synthetic
machinery of host cells
• Viruses are not living and Virus must be infectious to endure in
nature
• They are sensitive to interferon but not sensitive to antibiotic.
• Viruses are neither prokaryotes nor eukaryotes cell because they
are not a cell.
 How is the size of viruses measured?
• Direct microscopy
• Filtration through graded porosity, dependent
on size and physical structure
• Sedimentation in ultracentrifuge

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2. Structure of a virus

or peplomers
 Basic virus structure

Fig. 1. From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005,

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 2. Structure of a virus
• All viruses consists of a central core of Nucleic acid (Genome) which is RNA or DNA.
• This central Nucleic acid is covered by a protein coat called CAPSID .
– The capsid is antigenic and also contains receptors which enable a virus to attach to the surface of its
specific host cells.
– The capsid itself is composed of number of sub unit is called CAPSOMERE.
– The capsomere may be arranged as under.
• Around coiled nucleic acid which is known as helical arrangement.
• As cubes around spheroidal nucleic acid known as IcosaIhedral arrangement .
• Some virus do not fit either helical or icosahedral capid symmaty is called complex symmetry.
• Finally the capsid may be covered by an ENVELOPE is called enveloped virus.
– The envelop is derived from host cells membrane when virus is released by budding, envelope is lipo
protein in nature.
– Envelope viruses compared with non-enveloped (nacked) viruses enveloped virus are more sensitive
to heat, detergent, and liquid solvents .
• Protein sub units may be seen as projecting spikes on the surface of the envelope.
• These are called peplomers. peplomers used as a receptor
complex symmetry.

IcosaIhedral

helical arrangement
 3. Classification of viruses
The main Characteristics for Classification of viruses
1. Genome or Type of Nucleic Acid
 DNA (Deoxyribovirus) or RNA (RiboVirus)
 Strands of nucleic acid (double (Ds) or single strand(Ss) )
 linear or circular
 Strategy of replication (Positive sense & negative sense RNA)
 Positive sense RNA can be translated directly into protein
or directly act as mRNA.
 Negative sense RNA can be transcribed by a virus coded,
virion packaged RNA dependent RNA polymerase
2. Size & morphology
 Type of symmetry ( Icosahedral, Helical and Complex )
 Presence or absence of envelope (envelop and non-envelop or
nacked virus) 10
3. Presence of specific enzymes
E.g: - Reverse transcriptase
4. Host tissue or cell tropism
E.g: Hepatitis viruses, HIV, etc
5.Mode of transmission e.g. Arboviruses
6. Host range E.g. Animal, bacteria, plant
7. Type of disease E.g. encephalitis

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 Classification viruses---
• Dynamic
• Universal system of virus taxonomy
• Major groups (families basis of
- Virion morphology
- Gene structure
- Strategies of replication ( Baltimore classification)

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 Classification viruses---
• By 7th ICTV report
- More than 4000 viruses →
- 3 Orders
- 63 families, 9 subfamilies, 240 genera. 100’s
unassigned
- Currently 24 families that infect humans and
animals

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 Classification viruses---
Names & typography of virus species

• Names of orders, families, subfamilies and

genera written in italics with a capital initial
letter
• The English common names of virus species
Written in italics with a capital initial letter

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 Classification of viruses---
System evolved (developed)
• 1 Viruses grouped in to families : virion
morphology, genome structure, strategis of
replication
• Suffix for Order- virales, for families - viridae (eg- Filo,
Para and rhabd--)
• 2 some large families (Herpesviridae, Parvoviridae,
paramyxovoridae)-subfamilies Suffix- --virinae for
subfamilies
• 3 Genera: physiochemical and serologic
differences- name suffix for Genera -virus
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 Classification of viruses---
Example
• Measles virus
Order Mononegavirales
Family Paramyxoviridae
Subfamily Paramyxovirinae
Genus Morbilivirus
Species Measles virus

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Medically Important Viruses

Or
Pathogenic Viruses
 DNA VIRUSES

DOUBLE STRANDED SINGLE STRANDED COMPLEX ds

(NON-ENVELOPED) (ENVELOPED)

ENVELOPED NON-ENVELOPED PARVOVIRIDAE POXVIRIDAE

HERPESVIRIDAE
HEPADNAVIRIDAE
CIRCULAR LINEAR

PAPILLOMAVIRIDAE ADENOVIRIDAE All families shown are

POLYOMAVIRIDAE icosahedral except for
(formerly grouped together as the poxviruses
PAPOVAVIRIDAE)

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 RNA VIRUSES

SINGLE STRANDED Positive SINGLE STRANDED DOUBLE

sense negative sense STRANDED

ENVELOPED NON-ENVELOPED ENVELOPED NON-ENVELOPED

ICOSAHEDRAL HELICAL ICOSAHEDRAL HELICAL ICOSAHEDRAL

FLAVIVIRIDAE CORONAVIRIDAE PICORNAVIRIDAE ORTHOMYXOVIRIDAE REOVIRIDAE

TOGAVIRIDAE CALICIVIRIDAE PARAMYXOVIRIDAE
RETROVIRIDAE RHABDOVIRIDAE
FILOVIRIDAE
BUNYAVIRIDAE
ARENAVIRIDAE

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 Classification of Human Viruses
"Group" Family Genome Genome size (kb) Capsid Envelope
dsDNA
Poxviridae dsDNA, linear 130 to 375 Ovoid Yes
Herpesviridae dsDNA, linear 125 to 240 Icosahedral Yes
Adenoviridae dsDNA, linear 26 to 45 Icosahedral No
Polyomaviridae dsDNA, circular 5 Icosahedral No
Papillomaviridae dsDNA, circular 7 to 8 Icosahedral No
ssDNA
Anellovirus ssDNA circular 3 to 4 Isometric No
Parvoviradae ssDNA, linear, (- or +/-) 5 Icosahedral No
Retro
Hepadnaviridae dsDNA (partial), circular 3 to 4 Icosahedral Yes
Retroviridae ssRNA (+), diploid 7 to 13 Spherical, rod or cone shaped Yes
dsRNA
Reoviridae dsRNA, segmented 19 to 32 Icosahedral No
ssRNA (-)
Rhabdoviridae ssRNA (-) 11 to 15 Helical Yes
Filoviridae ssRNA (-) 19 Helical Yes
Paramyxoviridae ssRNA (-) 10 to 15 Helical Yes
Orthomyxoviridae ssRNA (-), segmented 10 to 13.6 Helical Yes
Bunyaviridae ssRNA (-, ambi), segmented 11 to 19 Helical Yes
Arenaviridae ssRNA (-, ambi), segmented 11 Circular, nucleosomal Yes
Deltavirus ssRNA (-) circular 2 Spherical Yes
ssRNA (+)
Picornaviridae ssRNA (+) 7 to 9 Icosahedral No
Calciviridae ssRNA (+) 7 to 8 Icosahedral No
Hepevirus ssRNA (+) 7 Icosahedral No
Astroviridae ssRNA (+) 6 to 7 Isometric No
Coronaviridae ssRNA (+) 28 to 31 Helical Yes
Flaviviridae ssRNA (+) 10 to 12 Spherical Yes
Togaviridae ssRNA (+) 11 to 12 Icosahedral Yes
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 Major diseases caused by human viruses
"Group" Family Human pathogens (disease)
dsDNA
Poxviridae Variola (smallpox); Orf (pustular dermatitis); Molluscum contagiosum (pustular dermatitis)
Herpesviridae Herpes simplex 1,2 (oral, genital herpes); Varicella-zoster (chickenpox); Epstein-Barr (mononucleosis);
Cytomegalovirus (neonatal abnormalities); HHV6 (roseola); HHV8 (Kaposi's sarcoma)
Adenoviridae Adenovirus (respiratory infection, conjunctivitis)
Polyomaviridae Polyomavirus (benign kidney infection, respiratory disease, leukoencephalopathy)
Papillomaviridae Papillomavirus (warts, genital carcinoma)
ssDNA
Anellovirus Unknown
Parvoviradae B-19 (fifth disease, fetal death)
Retro
Hepadnaviridae Hepatitis B ("serum" hepatitis)
Retroviridae HIV (aids); HTLV (leukemia)
dsRNA
Reoviridae Rotavirus (infantile gastroenteritis)
ssRNA (-)
Rhabdoviridae Rabies virus (rabies)
Filoviridae Ebola virus (ebola)
Paramyxoviridae Parainfluenza virus (respiratory infection); Mumps virus (mumps);
Respiratory syncytial virus (respiratory infection); Measles virus (measles)
Orthomyxoviridae Influenza virus (influenza)
Bunyaviridae Hantaan virus (hemorrhagic fever with renal syndrome)
Arenaviridae Lassa fever virus (hemorrhagic fever)
Deltavirus Hepatitis D (fulminant acute hepatitis)
ssRNA (+)
Picornaviridae Poliovirus (polio), rhinovirus (URI), Hepatitis A ("infectious" hepatitis)
Calciviridae Norwalk (gastroenteritis)
Hepevirus Hepatitis E (acute hepatitis)
Astroviridae Astrovirus (gastroenteritis)
Coronaviridae Coronavirus (respiratory infection)
Flaviviridae Yellow fever virus (yellow fever); Hepatitis C (hepatitis)
Togaviridae Eastern Equine encephalitis virus (encephalitis); Rubella virus (rubella) 21
Virus infectious cycle
(Replication of
RNA and
DNA virus)
 3. Virus infectious cycle
Virus infectious cycle
• Viruses possess Neither a cellular structure nor organells.
• They are dependent on their host cells for energy & replication (multiplication)
• Outside of living cells, viruses are metabolically inert.
• The information required for a virus to replicate is contained in its nucleic acid (
genome)
• Following infection a virus takes over the synthesizing activities of its host cells
and Directing the host tell to transcribe and or translate its genetic information
to produce the protein and nucleic acid components required to make new
virions.
– Most DNA virus replicate and are assembled in the nucleus of the host cells.
– Whereas most RNA viruses replicate and are assembled in the cytoplasm of the host
cells.
• Mature virions are released from host cells either
– By rupture of the cell membrane as occurs with most un-enveloped (nackad) virus or
– By a process called budding in which enveloped virions are extruded from the cell
membrane.
3.2 Steps in Multiplication/Replication of a Virus
All viral multiplication sequence of events are as follows
1. Adsorption or attachment :- The virus is adsorbed at a particular
site on the host cell which is called a receptor.
2. Penetration: - Virus particles may be engulfed by animal cell by
the mechanism called viropexia. Viropexia is like phagocytosis. In
case of enveloped virus. The viral envelop may fuse with plasma
membrane and release eha nucleo-capsid in to cytoplasm.
3. Un coating: - This is a process by which the virus lose its outer
layar and capsid.
4. Bio-synthesis: - There is synthesis of viral nucleic acid and capsid
protein. Biosynthesis contain the following steps.
 Transcription of massenger RNA from viral nucleic acid.
 Translation of mRNA in to early proteins.
 Replication of viral nucleic acid.
 Synthesis of late proteins which are the components of daughter virion capsids.
 3.Multiplication of a Virus con
5. Maturation: - Assembly of daughter virions follows synthesis of
viral nucleic acid and proteins. It may take place in nucleus or
cytoplasm of the host cell. -
− Enveloped viruses gets envelop from the host cell membrane during a process
of budding.
− Non enveloped (nacked) viruses are present intracellularly as fully developed
virions.
6. Release: - Viruses release take place by lysis of infected cells or
viruses release occur without cell-lyses. Some viruses like polio
may cause cell-lyses during their release.

 Eclipse phase:- is time from stage of penetration of virus in to host

cell until appearance of mature daughter viruses. In this phase
intact viruses can not be demonstrated in host cells
 4. ANTIVIRAL AGENTS
ANTIVIRAL CHEMOTHERAPY
• Many viruses encode activities (virulence factors) that
promote the efficiency of viral replication, viral transmission,
the access and binding of the virus to target tissue, or escape
of the virus from host defense and immune resolution.
• Loss of virulence factors results in attenuation of the virus.
• Viruses also encode enzymes that are not present in un-
infected cell.
• These enzymes are critical to viral replication but unnecessary
for cellular function. It is now possible to find specific
inhibitors for viral growth.
The greatest success in antiviral chemotherapy has been achieved
by using: inhibitors of
• Nucleic acid synthesis.
• The stages of attachment of virus to host cell
• Stage of uncoating of the viral genome
• Reverse transcription of certain viral genomes
• Regulation of viral transcription
• Replication of viral nucleic acid
• Translation of viral proteins
• Assembly OR Maturation
• Release of progeny virus

→ The mechanism of action varies among anti-virals.

Antiviral agents and their targets

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Antiviral agents ….

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 5. Viral vaccines
Purpose of viral vaccines is to utilize immune response
of the host to prevent viral disease
Several remarkably effective
– Small pox eradicated

– Reducing annual incidence several viral diseases

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 How Do Vaccines Work?
• Stimulates adaptive immune response

 Natural infection prevents reoccurrence of disease

 Humoral & Cellular responses

• Vaccines prevent or modify disease. Most do NOT

prevent infection.

• Herd immunity reduces spread of disease.

 Disease agents require a certain level of transmission

to be maintained

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 Requirements of a Vaccine
To be effective a vaccine should be capable of eliciting the following ;-
• Activation of Antigen-Presenting Cells to initiate antigen
processing and producing interleukins.
• Activation of both T and B cells to give a high a high yield of
memory cells.
• Generation of Th and Tc cells to several epitopes, to overcome the
variation in the immune response in the population due to MHC
polymorphism.
• Persistence of antigen, probably on dendritic follicular cells in
lymphoid tissue, where B memory cells are recruited to form
antibody-secreting cells that will continue to produce antibody.

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 Types of viral Vaccines
1. Live whole virus vaccines

2. Killed whole virus vaccines

3. Subunit vaccines;- purified or recombinant viral antigen

4. Recombinant virus vaccines

5. DNA vaccines

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 LIVE ATTENUATED VACCINES

Ideal Condition:
• Virus alive and fully immunogenic but no virulence
• Utilizes virus mutants restricted in some steps in
pathogenesis of disease

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 Live—reduction in virulence
• The virulence of the virus is reduced by
– Administration of pathogenic or partially attenuated virus
by unusual route,
– Passage of the virus in unnatural host or host cell.
• The major vaccines used in man and animals have all been
derived by this second method.
Example  17D strain of yellow fever was
developed by passage in mice and then
in chick embryo.
 Polio viruses were passed in monkey
kidney cells
 Measles in chick embryo fibroblasts.

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 Live Vaccines
• Attenuated strains

1. Use of a related virus from another animal

2. Administration of pathogenic or partially attenuated virus

by an unnatural route

3. Passage of the virus in an "unnatural host" or host cell

Development of temperature sensitive mutants (used in

conjunction with the above mentioned methods)

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 Live Attenuated Virus Vaccines
• Advantages
– Stimulates a broad immune response
• Neutralizing antibody
• Secretory iga for mucosal tissues.
• Cell mediated immunity (ctl)
– All antigens are expressed
– Production costs are lower
• Disadvantages
• Potential for genetic instability
• Risk of reversion to greater virulence in host
– Potential for contamination
– Infection can persist or be more severe in the
immunocompromised.
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 Inactivated whole virus vaccines

• Easiest preparations to use

• Simply inactivated

• The outer virion coat should be left intact but the

replicative function should be destroyed.

• Must contain much more antigen than live vaccines

• Extreme care – no residual live virulent virus vaccine

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 Inactivated whole virus …

• Inactivation by heat or chemicals

Chemicals: formaldehyde or beta- propiolactone

• Caution: Excessive treatment can destroy

immunogenicity

• whereas insufficient treatment can leave infectious virus

capable of causing disease.

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 Live vs Dead vaccines

Feature Live Dead

 Dose low high
 No. of doses single multiple
 Need for adjuvant no yes
 Duration of immunity many years less
 Antibody response IgG IgA, IgG
 CMI good poor
 Reversion to virulence possible not possible
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 6. Virus host interaction & viral pathogenesis
6.1. Effects of viral infection on host cell

• On entry in to the body:

 The virus may replicate and remain at the primary site

 May disseminate to other tissues via the blood stream

or the mononuclear phagocyte and lymphatic system

 Or may disseminate through neurons.

• The blood stream and the lymphatic system are the

predominant means of viral transfer in the body.
 Effects of viral infection…

• The transport of virus in the blood is termed viremia.

• The virus may be either free in the plasma or may be cell

– associated in lymphocytes or macrophages.

• Replication of a virus in macrophages, the endothelial

lining of blood vessels, or the liver can cause the
infection to be amplified and initiate the development of
secondary viremia.
• In many cases, a secondary viremia precedes delivery
of the virus to the target tissue (e.g. liver, brain, skin)

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6.2. Determinants of viral disease
A. Nature of the disease and target tissue

 Portal of entry of virus

 Access of virus to target tissue

 Tissue tropism of viruses

 Permissiveness of cells for viral replication

 Viral pathogen (strain)

B. Severity of disease and Cytopatic ability of virus

• Immune status

– Competence of the immune system & prior immunity to the

virus

• Immune pathology

• Virus inoculum size

• Length of time before resolution of infection

• General health of the person

– Nutrition & other disease influencing immune status

• Genetic make up of the person & age

C. Interaction of virus with target tissue
• Access of virus to target tissue
– Stability of virus in the body
 Temperature
 Acid and bile of the GIT
– Ability to cross skin or mucous epithelial cells (e.g. cross
the GIT in to the blood stream)
– Ability to establish viremia
• Ability to spread through the RES
• Target tissue
 Specificity of viral attachment proteins.
 Tissue –specific expression of receptors
D. Cytopathologic activity of the virus

• Efficiency of viral replication in the cell

 Optimum temperature for replication

 Permissiveness of cell for replication

• Cytotoxic viral proteins

• Inhibition of cell’s macromolecular synthesis

• Accumulation of viral proteins and structures (inclusion

bodies)

• Altered cell metabolism (e.g. cell immortalization)

E. Host protective responses

• Antigen – non specific antiviral responses

 Interferon

 Natural killer cells and macrophages

• Antigen – specific immune responses

 T- Cell response

 Antibody Responses

• Viral mechanisms of escape of immune responses

 6.3. Viral pathogenesis
6.3.1. Cytopathogenesis
Three potential outcomes from a viral infection of a cell:
 Abortive infection (failed infection)
 Lytic infection (cell death)
 Persistent infection (infection without cell death)

Persistent infection include:

• Chronic(Non-Lytic or productive) infection
• Latent(Limited viral macromolecular but no virus
synthesis)infections
• Recurrent infections
• Transforming(Immortalizing)infections

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 Viral pathogenesis…..

6.3.2. Host cell permissiveness to virus

• Non-permissive cell: not allow replication of a particular
type or strain of virus
• Permissive cell: cell provides the biosynthetic machinery
to support complete replicative cycle of virus
• Semi-permissive cell: cell may be very inefficient or
support some but not all steps of virus replications

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6.4. Effect of virus on host cells
A. Direct and indirect damage
– Some viruses are able to shut down host
macromolecules synthesis and thus directly
damage host cells. The damaged cells lyse, which is
a cytopathic effect that can be detected in the
laboratory.
– Some virus infections indirectly affect the function
of tissues or organs in the host. e.g. the influenza
virus damages the respiratory epithelium and ciliary’s
activity is severely affected. This results in the
accumulation of bacteria that normally would be
eliminated by ciliary’s action.
B. Inclusion body formation
• The replication of virus in the cytoplasm or nucleus of
infected cells often results in the accumulation of viral as
well as cellular products. These accumulations, which
may be nucleic acids, proteins, and so on, can be
stained and are referred to as inclusion bodies. Some
inclusion bodies are so distinctive that their presence is
diagnostic.
• Example
Negribodies- rabies virus.
Owl’s eye-Cytomegalovirus
Cowdry type A-Herpes simplex virus
C. Cell fusion (syncytia formation)
• Enveloped viruses release specific proteins that become
incorporated in to cytoplasmic membrane of the infected cell.
These proteins act as magnets on the infected cell and attract
uninfected cells to their surface. This results in infection of the
originally un infected cell.

• Repetition of this process results in the aggregation of several

infected cells. These aggregated cells eventually fuse,
producing a giant multinucleated cell or syncytium
D. Changes in the surface antigens
• Viruses insert antigens in to the cell membrane of
infected cells.

• These antigens make the cell a target to immunological

destruction by virus – specific antibodies

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6.5. Host defense against Viral infection

6.5.1. Non-specific Immune defense

• Provide a local rapid response
• Activate the specific immune defense
• Often sufficient to control viral infection
1. Body temperature and fever
2. Interferon and other cytokines
3. Mononuclear phagocytice system
4. NK-cells

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 Host defense against Viral infection……

1. Body temperature and Fever: Limit replication &

destabilized some virus
2. Mononuclear phagocytice system:
phgocytized viral & cell debris from virus infected cells
filter many virus from the blood
Macrophage-present antigen to T-cells
3. NK-cells_kill virus infected cells

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 Host defense against Viral
infection……
4. Interferon
– The body firs active defense
– Interfere replication
– Initiate an anti-viral state in cells
– Block viral protein synthesis
– Inhibit cell growth
– Interferon alpha and beta activate NK cells
– Interferon alpha and gamma activate macrophage
– Increase MCH antigen expression
– Regulate activities of T cells

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 Host defense against Viral infection……

6.5.2. Specific host defense

6.5.2.1. Antibody mediated
- Neutralize extra cellular virus
– Block viral attachment proteins
– Destabilizes viral structure
– opsonizes viruses for phagocytosis
– promote killing of target cells by the complement
&ADDC

• Antibody resolves viral infections

• Antibody blocks viremic spread to target tissue

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6.5.2.2. Cell mediated
– Essential for controlling enveloped &non cytolitic
infection
– Recognizes viral peptides presented by MCH
molecules on cell surfaces
– CTLs(CD8) kills virus infected cells & as result
eliminate the source of new virus
– It respond to viral peptide-class I MCH protein
complex
– CD4(TH cells) important for the maturation of
antibody response
– Respond to viral peptide-class II MCH protein
complex

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 7. Epidemiology of viruses
• Infection of a population is similar to infection of a person, in
that the virus must spread through the population and is
controlled by immunization of the population. To endure
(survive), viruses must continue to infect new,
immunologically naïve, susceptible hosts.
7.1. Exposure
• People are exposed to viruses through out their lives.

• Some situations, vocations, lifestyles, and living arrangement increase the

likelihood that a person will come in contact with certain viruses.

• Many viruses are ubiquitous (found every where), as borne out by the fact that
evidence of exposure (antibodies to the virus) can be detected in most young
children (HSV –1, HHV6, varicella – zoster virus, parvovirus B19) or early adult
hood (EBV and respiratory and enteric viruses).

• Poor hygiene and crowded living, school, and job conditions promote exposure
to respiratory and enteric viruses.

• Day care centers are consistent sources of viral infections, especially viruses
spread by the respiratory and fecal-oral routes.
• Travel, summer camp, and vocations that bring people in
contact with a virus vector such as mosquitoes, put them at
particular risk for infection by arbo-viruses and other
zoonoses.

• Sexual promiscuity also promotes the spread and acquisition

of several viruses.

• Health care workers, such as physicians, dentists, nurses, and

technicians, are frequently exposed to respiratory and other
viruses but are uniquely at risk for acquiring viruses from
contaminated blood (HBV, HIV) or vesicle fluid (HSV).
7.2. Transmission of viruses

• The route of transmission depends on the source of the virus

(the tissue site of viral replication and secretion) and the ability
of the environment and the body route to the target tissue.

• Non-enveloped viruses (naked viruses) can withstand drying,

the effect of detergents, and extremes of PH and temperature.

• Non-enveloped viruses are generally transmitted by the

respiratory and fecal-oral routes and can often be acquired
from contaminated objects.
• Unlike the non-enveloped viruses, enveloped viruses
are comparatively fragile. They require an intact
envelope for infectivity. These viruses must remain wet
and are spread:

A. In respiratory droplets, blood, mucus, saliva, or semen.

B. By injection

C. By organ transplantation
• Animals can also act as vectors that spread viral disease
to other animals or humans.

• Animals can also be reservoirs.

• Viral diseases that are shared by animals or insects and

humans are called zoonoses.

• Arthropods, including mosquitoes, ticks, and sand f lies

can act as vectors for toga viruses, flavi-viruses, bunya
viruses, and reo-viruses. These viruses are often
referred to as arbo-viruses because they are

arthropod born.
• Other factors that can promote the transmission of
viruses are the potential for asymptomatic infection,
crowded living conditions, certain occupations, certain
lifestyle, day care centers, and travel.
• The persistence of a virus in a community depends on
the availability of a critical number of immunologically
naïve (sero negative), susceptible people.
• Immunization produced by natural means or by
vaccination, is the best way of reducing the number of
such susceptible people.
• The age of the person is an important factor in
determining his or her susceptibility to viral infection.
• Infants, children and the elderly are susceptible to different viruses.
• The competence of a person’s immune response and his or her
immune history determine how quickly and efficiently the infection is
resolved and can also determine the severity of symptoms.
• The geographic distribution of a virus is usually determined by
whether the requisite cofactors or vectors are present or whether
there is an immunologically naïve, susceptible population.
• Seasonal difference in the occurrence of viral disease corresponds
with behaviors that promote the spread of the virus.
• Out breaks of a viral infection often results from the introduction of a
virus (such as hepatitis A) in to a new location.
• The out breaks originate from a common source (e.g. food
preparation)
• Epidemics occur over a larger geographic area and
generally result from the introduction of a new strain of
virus in to an immunologically naïve population.

• Pandemics are worldwide epidemics, usually resulting

from the introduction of a new virus (example, HIV).

• The spread of a virus can be controlled by quarantine,

good hygiene, changes in lifestyle, elimination of the
vector, or immunization of the population.
• Quarantine is restriction of freedom of movement of
apparently well individuals who have been exposed to
infectious disease, which is imposed for the maximal
incubation period of the disease.

• The proper sanitation of contaminated items and

disinfections of the water supply are means of limiting
the spread of enteric viruses.

• The best way to limit viral spread, however, is to

immunize the population.
 References

• Principles and practice of clinical virology,5th ed.John

wiley&sons.England,2004
• Principles and practice of clinical virology,6th ed. A John
wiley&sons,Ltd.,Publication,2009
• Basic Virology. Edward K.Wagner,3rd ed.,2006
• Medical Microbiology, 5th ed., Murray, Rosenthal &
Pfaller, Mosby Inc., 2005
• Medical Microbiology, Jawtz,Melnick, & Adelberg’s,24th
Edition, vishal

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