Virology second stage

Pretest

What is the virus?

Lecture 1

1- Introduction

Viruses are the smallest known infective agents and are perhaps the simplest
form of life known ranging from about 20 nm to about 200 or 300 nm in
diameter and contain only one kind of nucleic acid RNA or DNA as their
genome, nucleic acid is encased in a protein shell which may be surrounded
by a lipid containing membrane. viruses are parasites at the genetic level and
replicating only in living cells and are inert in the extracellular environment.

Terms and definitions in virology

Capsid : the protein shell or coat protein that encloses the nucleic acid or
genome.

Capsomeres : morphologic units seen in the electron microscope on the

surface of virus particles, capsomeres represent cluster of polypeptides.

Defective virus : a virus particle that functionally deficient in some aspect

of replication.

Envelope : a lipid containing membrane that surrounded some virus

particles, virus encoded glycoproteins are exposed on the surface of the
envelope these projection are called peplomers.

The lipids in the composition of viral :

1- cholestrol. 2- phosphatidyl choline 3- phosphatidyl serine

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Nucleocapsid : the protein nucleic acid complex representing the package

from of the viral genome.

Structure units : the basic protein building blocks of the coat, structure unit
is often referred to as a protomer.

Subunit : a single folded viral polypeptide chain.

Virion : the complete virus particles or entire infectious unit is term a virion.
In some instances (e.g Papillomaviruses and Picornaviruses) virion is
identical with the nucleocapsid, In more complex virions (Herpesviruses
and Orthomyxoviruses) this includes the nucleocapsid plus a surrounding
envelope, this structure is to transfer the viral nucleic acid from on cell to
another.

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Viral Nucleic Acid

Viruses contain a single kind of nucleic acid either DNA or RNA that
encodes the genetic information necessary for replication of the virus,
genome may be single or double stranded, circular or linear, segmented or
nonsegmented, type of nucleic acid, its polarity (negative or positive) and its
size are major characteristics used for classifying viruses into families. size
of the viral DNA genome ranges from 3.2 kbp (e.g. Hepadnaviruses) to 375
kbp (e.g. Poxviruses), size of the viral RNA genome ranges from about 4 kb
(e.g. Picobirnaviruses) to 32 kb (e.g. Coronaviruses). viral nucleic acid
contains information necessary for programming the infected host cells to
synthesize virus specific macromolecules required for the production of viral
progeny.

Shape of the virus

The overall shape of the virus partical varies in different groups of viruses,
most of the animal vieuses are roughly spherical some are irregular and
pleomorphic. Poxviruses are brick shaped, Rabies virus is bullet shape,
Tobacco mosaic virus is rod shaped and Bacteriophages have a complex
morphology. viral architecture can be grouped into three types based on the
arrangement of morphologic subunits: (1) cubic (e.g. Adenoviruses), (2)
helical (e.g. Orthomyxoviruses) and (3) complex structures (e.g.
Poxviruses).

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Shape of the virus

Sizes of Viruses

Small size and the ability to pass through filters that hold back bacteria are
classic attributes of viruses however, because some bacteria may be smaller
than the largest viruses filterability is not regarded as a unique feature of
viruses. viruses are much smaller than bacteria and it was their small size
and filterability (ability to pass through filters) that led to their recognition as
a separate class of infections agents, hence they were for a time known as
filterable viruses and they were called ultramicroscopic as they were too
small to be seen under the light microscope.

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Some of the `large viruses such as Poxviruses can be seen under the light
microscope when stability stained, the virus particles seen in this manner are
known as elemantry bodies. unit of mesurment of virion size is nanometers
(nm). viruses vary widely in size, the largest among them is Poxvirus (300
nm) and is as large as the smallest bacteria (Mycoplasma) and the smallest
virus is the Parvovirus about 20 nm and are nearly as small as the largest
protein molecules such as hemocyanin.

2- General Properties of Virus

1. Viruses do not have a cellular organization.

2. They contain only one type of nucleic acid either DNA or RNA but never
both.

3. They are obligate intracellular parasites.

4. They lack the enzymes necessary for protein and nucleic acid synthesis
and are dependent for replication on the synthetic machinery of host cells.

5. They multiply by a complex process and not by binary fission.

6- They are unaffected by antibacterial antibodies.

7- Viruses may or may not have an envelope.

8- Viruses multiply only in living cells.

9- Outside of the host cells, viruses are inactive, however inside living cells
viruses show some of the characteristics of living things.

10- Viruses do not fall in the category of unicellular microorganism.

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3- Classification of Viruses

1- Type of nucleic acid : viruses are classified into two main division
depending on the type of nucleic acid they possess : Riboviruses are those
containing RNA and Deoxyriboviruses are those containing DNA.

2- Number of strands of nucleic acid : single or double stranded.

3- Polarity of the viral genome : positive or negative of viral genome.

4- The symmetry of the nucleocapsid : cubic, helical and cmplex.

5- The presence or absence of a lipid enveloped.

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Summary of the classification of DNA and RNA viruses

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Some of the Differences between Bacteria and virus

Bacteria Characteristic Viruses
bacteria are generally 1- Size viruses are generally smaller,
large, size ranges size ranges between 20 - 300
between 900-1000 nm. nm.
bacteria have a 2- Cell Wall the cell wall is absent,
lipopolysaccharide or instead a capsid (protein coat)
peptidoclycan based cell is present instead.
wall.
present in bacteria. 3- Ribosomes absent in virus.
bacteria are classified as 4- Living/Non living virus are neither living or non
living organisms. living.
relatively complex single 5- DNA and RNA contain only one type of
celled organism. nucleic acid either DNA or
RNA.
bacterial infections are 6- Infections viral infections are usually
generally localized systemic (FLU).
(pneumonia).
Most bacteria can 7- Host dependence Virus needs a host to complet
produce without a host. its reprotective cycle
bacteria binary fission a 8- Mode of virus lytic infection hijacks a
mod of asexual reproduction hosts cellular machinery and
reproduction. produced copies of itself.
visible under light 9- Under visible only under electron
microscope. Microscope microscope
antibiotics are effective 10- Treatment antiviral drugs are prescribed
for bacterial infections. for viral infections.
depends on the type of 11- Incubation depends on the type of viral
bacterial infection period infection (incubation period
(incubation period of of rabies is 20 days to 2
bacterial pneumonia is 1- months).
2 weeks).
Staphylococcus aureus, 12- Examples HIV, Hepatitis A virus,
Vibrio cholerae and etc. Rhinovirus and etc.

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Objectives

The objective of the lecture is to introduce viruses as a microorganisms

including their general characteristics, components, shape, size,
classification, comparison with bacteria and some general terms in virology.

Post test

The viral capsid is made up of :

a- lipids.

b- carbohydrate.

c- proteis.

d- nucleic acid.

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Pretest

Can viruses replicate outside living cells?

Lecture 2

Replication of DNA and RNA virus

Viruses multiply only in living cells and the host cell provides the energy,
synthetic machinery and low molecular weight precursors for the synthesis
of viral proteins and nucleic acids.

Viral Replication

The genetic information nessesary for viral replication is containd in the

viral nucleic acid but lacking biosynthesis enzymes, the virus depends on
the synthetic machinery of the host cell for replication.

The viral multiplication cycle can be divided into six sequentioal phases.

General Steps in Viral Replication Cycles

1- adsorption or attachment : virions come in contact with cells by random

collision but adsorption or attachment is specific and is by the binding of
virion surface structures known as ligands to receptors on cell surface,
receptors are components of the cell surface with which a region of the
viral surface capsid or envelope can specifically interact and initiate
infection.

In case influenza virus a surface glycoprotein (hemagglutination) binds to

sialic acid of glycoprotein receptors sites on the surface of respiratory
epithelium, in case of human immunodeficiency virus-1 (HIV-1) surface

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glycoprotein gp120 it binds to the CD4 60 kDa glycoprotein on the surface

of mature T lymphocytes.

2- penetration: after binding the virus partical is taken up inside the cell,
this is accomplished by receptor mediated endocytosis (viropexi), enveloped
viruses fuse their membranes with cellular membranse to delivir the
nucleocapsid or genome directly into the cytoplasm.

3- uncoting: this is the process of stripping the virus of its outer layers and
capsid so that the nucleic acid is released into the cell. with most viruses,
uncoating is affected by the action of lysosomal enzymes of the host cells.

4- biosynthesis: this phase includes synthesis not the viral nucleic acid and
capsid protein but also of enzymes necessary in the various stages of viral
synthesis assembly and released, in addition certain regulator proteins are
also syntgesized which serve to shut dwon the normal cellular metabolism
and direct the sequential production of viral components. in general most
DNA viruses synthesize their nucleic acid in the host cell nucleus the
exceptions are the Poxiviruses, most RNA viruses synthsize all their
components in the cytoplasm except for Orthomyxoniruses, Retroviruses
and some Paramyxoviruses, viral proteins is synthsize only in the
cytoplasm.

Steps of biosynthesis

i- transcription of messenger RNA (mRNA) from the viral nucleic acid.

ii- translation of the mRNA into early proteins, there are enzymes which
initiate and maintain synthesis of virus components.

iii- replication of viral nucleic acid.

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iv- synthesis of structural proteins which are components of virion capsids.

5- maturation: newly synthsize viral genomes and capside assemble

together to form progeny viruses, assembly of the various viral components
into virions occurs shortly after the replication of the viral nucleic acid and
may take place in either nucleus (e.g. Herpesviruses and Adenoviruses) or
cytoplasm (e.g. Picornaviruses and Poxiviruses).

6- release: viruses can be released from cell after lysis of the cell by
exocytosis or budding from the plasma membrane, viruses that exist as
naked nucleocapsid may be released by the lysis of the host cell (e.g.
Polioviruses), release of many enveloped viruses occurs after budding from
the plasma membrane without killing the cell.

The virus life cycle

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The unique feature of viral multiplication is that soon after interaction

with a host cell the infecting virion is disrupted and its infectivity is lost
this phase of the growth cycle is called the eclipse period its duration varies
depending on both the particular virus and the host cell it is followed by an
interval of rapid accumulation of infectious progeny virus particles, eclipse
period is actually one of intense synthetic activity as the cell is redirected
toward fulfilling the needs of the viral parasite.

Mechanisms

● In some cases, as soon as the viral nucleic acid enters the host cell, the
cellular metabolism is redirected toward the synthesis of new virus particles
and the cell is destroyed, in other cases the metabolic processes of the host
cell are not altered significantly although the cell synthesizes viral proteins
and nucleic acids and the cell is not killed.

● Enveloped viruses obtain their envelope by budding through a host cell

membrane in some cases the virus buds through the plasma membrane but
in other cases the envelope may be derived from internal cell membranes
such as those of the golgi body or the nucleus.

● During the replicative cycle numerous copies of viral nucleic acid and coat
proteins are produce, coat proteins assemble together to form the capsid
which encases, stabilize the viral nucleic acid against the extracellular
environment, facilitates the attachment and penetration by the virus upon
contact with new susceptible cells.

The final result of the replication of the viruses after the synthesis of viral
nucleic acid and viral proteins, the components assemble to form new
infectious virions the yield of infectious virus per cell ranges to more than
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100,000 particles and the duration of the virus replication cycle also varies
from 6 to 8 hours (e.g. Picornaviruses) to more than 40 hours (some e.g.
Herpesviruses).

Objectives

The aim of the lecture is to have general knowledge about the process of
viral replication and to identify the mechanisms that occur during the
process, with an indication of the characteristic that viruses are unique to.

Post test

Process absent in viruses is :

a- replication.

b- protein synthesis.

c- energy liberation.

d- mutation.

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Pretest

Can viruses feed on culture media as bacteria do?

Lecture 3

Cultivation and isolation of viruses

1- Cultivation of viruses

Because viruses are obligate intracellular parasites their growth

requires susceptible host cells capable of replicating them and they cannot
be grown on any inanimate culture media.

The primary purposes of viral cultivation are:

1- To isolate and identify viruses in clinical specimens.

2- To prepare viruses for vaccines.

3- To do detailed research on viral structure, multiplication cycles, genetics

and effects on host cells.

Three methods are employed for the cultivation of viruses:

1- animal inoculation (living animals). 2- embyronated eggs (chicken

embryos). 3- cell culture.

Animal inoculation

uses of animal inoculation

1- primary isolation of certain viruses

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2- for the study of pathogenesis, immune response and epidemiology of viral

diseases.

3- for the study of oncogenesis.

Animals

1- monkeys: monkeys find only limited application in virology.

2- mice: infant mice (suckling) may be inoculation by several routes

intracerebral, subcutaneous, intraperitoneal or intranasal. growth of the virus
in inoculated animals may be indicated by death, disease or visible lesions.

Embyronated eggs

The embryonated hen's egg was first used for the cultivation of viruses by
Goodpasture (1931) and the method was further developed by Burnet, the
embyryonated eggs (8-11 days old) are inoculation by several routes for the
cultivation of viruses such as chorioallantoic membrane (CAM), allantoic
cavity, amniotic cavity and yolk sac, after inoculation eggs are incubated for
2-9 days.

Chorioallantoic membrane (CAM)

Inoculation on the chorioallantoic membrane (CAM) produce visible lesions

(pocks), each infectious virus practical can form one pock, different viruses
have different pock morphology.

Allantoic cavity

Inoculation into the allantoic cavity provides a rich yield of Influenza and
some Paramyxoviruses for vaccine production.

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Amniotic sac

Inoculation into the amniotic sac is employed for the primary isolation of
the Influenza virus.

Yolk sac

yolk sac inoculation is used for the cultivation of some viruses.

Parts of Embryonated Egg

Tissue culture

Three types of tissue cultures are available :

1- Organ culture: organ cultures are useful for the isolation of some
viruses which appear to be highly specialized parasites of certin organs

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for example the tracheal ring organ culture for the isolation of coronavirus,
small bits of organs can be maintained in vitro preserving their orginal
architecture and function.

2- Explant culture: this method is now seldom employed in virology.

3- Cell cultures: this is the type of culture is routinely empoloyed for

growing viruses.

Classification of cell cultures

1- primary cell culture. 2- diploid cell strains. 3- continuous cell lines.

Growth medium

The essential constituents of the growth medium are physiologic amounts

of essential amino acids, vitamins, salts, glucose and a buffering system
generally consisting of bicarbonate in equilibrium with atmosphere
containing about 5% Carbone dioxide, this is supplemented with upto 5%
calf or fetal calf serum, antibiotics are added to prevent bacterial
contaminants and phenol red as indicator.

2- Isolation of viruses

Virus isolation it is imperative that the specimen be collected properly and

transported with least dealy to the laboratory, the reasons are that many
viruses are labile and that the samples are susceptiple to bacterial and fungal
overgrowth, viruses are best transported and stored on ice and in special
media. many viruses can be isolated as a result of their ability to form
discrete visible zones and plaques (areas where cells are killed or altered by

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the virus infection) in the host cells, to isolate viruses, we use the three
methods used to cultivation viruses.

Plaques formed by a phage in a bacterial culture

Isolating viral constituents

viruses must be broken down into their component parts by adding special
detergents e.g. sodium dodecyl sulfate to isolate the virus, these molecules
include the proteins that surround and line the outer membrane and viral
nucleic acid, to separate these molecules from each other (proteins,
enzymes and nucleic acids) we use the electrophoresis device, as the
electric field pulls the molecules through the gel so that the separation is
according to their weights.

Objectives

The objective of the lecture is how to isolate and diagnose the virus, identify
the three isolation methods and show some key details

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Post test

Which one of the following are obligate intracellular parasites :

a- bacteria.

b- slime moulds.

c- viruses.

d- blue green algae.

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Pretest

Which of the following is not affected by an antibiotics :

a- parasites.

b- fungi.

c- viruses.

b- bacteria.

Lecture 4

Antiviral chemotherapy, antiviral agent and vaccines

1- Antiviral chemotherapy

Unlike viruses bacteria and protozoans do not rely on host cellular

machinery for replication so processes specific to these organisms provide
ready targets for the development of antibacterial and antiprotozoal drugs
because viruses are obligate intracellular parasites and antiviral agents must
be capable of selectively inhibition viral functions without damaging the
host making the development of such drugs very difficult, another limitation
is that many rounds of virus replication occur during the incubation period
and the virus has spread before symptoms appear making a drug relatively
ineffective.

There is a need for antiviral drugs active against viruses for which vaccines
are not available or not highly effective because of a multiplicity of
serotypes (e.g. Rhinoviruses) or because of a constantly changing virus (e.g.
Influenza and HIV). antivirals can be used to treat established infections
when vaccines would not be effective and antivirals are needed to reduce
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Virology second stage

morbidity and economic loss caused by viral infections and to treat

increasing numbers of immunosuppressed patients who are at increased risk
of disease. the mechanisms of action vary among antivirals and can target a
viral protein enzymatic activity or block host virus protein interaction.

2- Antiviral Agents

1- Nucleoside and Nucleotide Analogs the majority of available antiviral

agents are nucleoside analogs, they inhibit nucleic acid replication by
inhibition of viral polymerases essential for nucleic acid replication.

2- Reverse Transcriptase Inhibitors they work by binding directly to the

virus encoded reverse transcriptase and inhibiting its activity.

3- Protease Inhibitors such drugs inhibit the viral protease that is required
at the late stage of the replicative cycle, protease inhibitors have been used
successfully for treatment of HIV and HCV infections.

4- Integrase Inhibitors HIV integrase inhibitors block the activity of viral

integrase and is key enzyme in HIV replication.

5- Fusion Inhibitors HIV fusion inhibitors act by disrupting the fusion of

viral envelope with the cell membrane preventing cellular infection.

6- Other types of antiviral agents such as Amantadine, Rimantadine,

Oseltamivir, Foscarnet, Acyclovir and Ganciclovir.

3- viral vaccines

The purpose of viral vaccines is to use the adaptive immune response of

the host to prevent viral disease, several vaccines have proved to be
remarkably effective at reducing the incidence of viral disease. vaccination

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is the most cost effective method of prevention of serious viral infections,

general principles immunity to viral infection is based on the development
of an immune response to specific antigens located on the surface of virus
particles or virus infected cells.

There are two types of viral vaccines

1- Killed virus vaccines

Inactivated (killed virus) vaccines are made by purifying viral preparation 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, killed virus vaccines prepared from whole virions generally
stimulate the development of circulating antibody against the coat proteins
of the virus conferring some degree of resistance to that virus strain.

Advantages of inactivated vaccines are that there is no reversion to

virulence by the vaccine virus and that vaccines can be made when no
acceptable attenuated virus is available.
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Virology second stage

Disadvantages of killed virus vaccines include relatively brief immunity

requiring boosting shots to maintain effectiveness, poor cell mediated
response, occasional hypersensitivity to subsequent infection and extreme
care is required in their manufacture to make certain that no residual live
virulent virus is present in the vaccine.

2- Attenuated live virus vaccines

Live virus vaccines utilize virus mutants that antigenically overlap with wild
type virus but are restricted in some step in the pathogenesis of disease,
attenuated live virus vaccines have Advantage of acting more like the
natural infection with regard to their effect on immunity, they multiply in the
host, tend to stimulate longer lasting antibody production, induce a good cell
mediated response and induce antibody production and resistance at the
portal of entry.

Disadvantages of attenuated live virus vaccines include a risk of reversion

to greater virulence, severe infection in immunocompromised hosts and
limited storage and shelf life in some cases.

Objectives

The lecture aimed to learn about viral vaccines and how antiviral agents
work.

Post test

Which is better, killed virus vaccines or live virus vaccines attenuated by

their stimulation of the immune system?

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Virology second stage

Pretest

When does a viral infection occur?

Lecture 5

Pathogenesis of viruses and Genetic of viruses

1- pathogenesis of viruses

To produce disease viruses must be enter a host come in contact with

susceptible cells replicate and produce injury.

Steps in viral pathogenesis

1- Entry and primary replication

Most viral infections are initiated when viruses attach and enter cells of one
of the body surfaces skin, respiratory tract, gastrointestinal tract, urogenital
tract or conjunctiva, majority of these enter their hosts through the mucosa
of the respiratory or gastrointestinal tract. some viruses can be introduced
directly into tissues or bloodstream through skin wounds, needles (e.g.
Hepatitis B and C, Human immunodeficiency virus), blood transfusions or
insect vectors (e.g. Arboviruses).

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2- Viral Spread and Cell Tropism

Some viruses such as Influenza viruses (respiratory infections) and

Noroviruses (gastrointestinal infections) produce disease at the portal of
entry and typically do not spread systematically, others can spread to distant
sites (e.g. Cytomegalovirus CMV, HIV and Rabies virus) and cause
additional disease manifestations. mechanisms of viral spread vary but the
most common route is via the bloodstream or lymphatics. some viruses
travel along neuronal axons to spread within the host (e.g. Rabies migrates
to the brain, Herpes simplex virus (HSV) travels to ganglia to produce latent
infection). presence of virus in the blood is called viremia

Viruses tend to exhibit organ and cell type specificities or viral tropism,
tropism determines the pattern of systemic illness produced during a viral
infection, as an example hepatitis B virus has a tropism for liver hepatocytes
and hepatitis is the primary disease caused by the virus. tissue and cellular
tropism by a given virus usually reflect the presence of specific cell surface
receptors for that virus.

3- Cell Injury and Clinical Illness

Destruction of virus infected cells in the target tissues and physiologic

alterations produced in the host by the tissue injury are partly responsible for
the development of disease, some tissues such as intestinal epithelium can
rapidly regenerate and withstand extensive damage better than others such as
the brain. some physiologic effects may result from nonlethal impairment of
specialized functions of cells, such as loss of hormone production. general
symptoms associated with many viral infections, such as malaise and
anorexia.

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4- Recovery from Infection

Following a viral infection the host will succumb, recover or establish a

chronic infection, recovery mechanisms include both innate and adaptive
immune responses, interferon (IFN), other cytokines, humoral and cell
mediated immunity and possibly other host defense factors are involved.

5- Virus Shedding

The last stage in pathogenesis is the shedding of infectious virus into the
environment, this is a necessary step to maintain a viral infection in
populations of hosts, shedding usually occurs from the body surfaces
involved in viral entry, during viral shedding an infected individual is
infectious to contacts. in some viral infections such as rabies humans
represent deadened infections and shedding does not occur.

2- Genetic of viruses

Viral genetics is the study of the mechanisms of heritable information in

viruses, including genome structure, replication and genetic change. viruses
obey the laws of genetics like all other living beings, several properties of
viruses such as virulence and antigenicity are under genetic control.

Mutation : changes of characteristics of daughter virus in comparison of

wild type.

-Mutation of general genes : inactivation of virus (lethal mutations).

-Mutation of other genes : changes of properties, deletion, attenuation of

properties, changes in the host cell or target tissue and resistance to
temperature…..

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Induced chemically, by radiation in nature they are caused by insufficiency

of viral polymerase, more common in RNA than in DNA.

Objectives

The objective of the lecture is how viral pathogenesis occurs from the
beginning of the entry of the viral type into the living body to its spread
outside the body and to address some basic information about the genetics of
viruses.

Post test

The method of entry of all types of viruses into the living body is the same?

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Pretest

Why is infection considered seasonal for some types of influenza viruses?

Lecture 6

Influenza viruses

Respiratory illnesses are responsible for more than half of all acute illnesses
each year in the united states, Orthomyxoviridae (e.g. Influenza viruses) are
a major determinant of morbidity and mortality caused by respiratory
disease and influenza has been responsible for millions of deaths worldwide.

Mutability, high frequency of genetic reassortment and resultant antigenic

changes in the viral surface glycoproteins make influenza viruses formidable
challenges for control efforts. Influenza type A is antigenically highly
variable and is responsible for most cases of epidemic influenza, Influenza
type B may exhibit antigenic changes (lesser degree) and sometimes causes
epidemics and Influenza type C is antigenically stable and causes only mild
illness in immunocompetent individuals. Influenza A strains are also known
for aquatic birds, chickens, ducks, pigs, horses and seals.

Structure and Composition

Influenza virus particles are usually spherical and about (80–120 nm) in
diameter, the single stranded, negative sense RNA genomes of influenza A
and B viruses occur as eight separate segments, influenza C viruses contain
seven segments of RNA. influenza virus particles contain nine different
structural proteins. the nucleoprotein (NP) associates with the viral RNA to
form a ribonucleoprotein (RNP) structure 9 nm in diameter, three large

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proteins (PB1, PB2 and PA) are bound to the viral RNP and are responsible
for RNA transcription and replication.

Two virus encoded glycoproteins, hemagglutinin (HA) and neuraminidase

(NA) are inserted into the envelope and are exposed as spikes about 10 nm
long on the surface of the particle, these two surface glycoproteins
determine antigenic variation of influenza viruses and host immunity. HA
represents about 25% of viral protein and the NA about 5%. Influenza
viruses are hardy in vitro and may be stored at 0–4°C for weeks without loss
of viability. lipid solvents, protein denaturants, formaldehyde and irradiation
destroy infectivity.

Genetic reassortment

because of the segmented nature of the genome, when a cell is coinfected by

two different viruses of a given type mixtures of parental gene segments

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may be assembled into progeny virions, this phenomenon called genetic

reassortment may result in sudden changes in viral surface antigens a
property that explains the epidemiologic features of influenza and poses
significant problems for vaccine development.

Classification

Genus Influenza virus A contains human and animal strains of influenza

type A, Influenza virus B contains human strains of type B and Influenza
virus C contains influenza type C viruses of humans and swine.

Influenza virus infections in human

Many cells in the respiratory tract are infected and eventually killed,
Influenza infections cause cellular destruction of the superficial mucosa of
the respiratory tract but do not affect the basal layer of epithelium, complete
reparation of cellular damage probably takes up to 1 month, viral damage to
the respiratory tract epithelium lowers its resistance to secondary bacterial
pathogens especially Staphylococci and Streptococci. the fever and systemic
symptoms associated with influenza reflect the action of cytokines in
addition viral NA lowers the viscosity of the mucous film in the respiratory
tract laying bare the cellular surface receptors and promoting the spread of
virus to lower portions of the tract within a short time.

Transmission of Influenzaviruses Influenza virus spreads from person to

person by airborne droplets or contact with contaminated hands or surfaces.

Incubation period from exposure to virus and the onset of illness varies
from 1 day to 4 days depending on the size of the viral dose and the immune
status of the host, viral shedding starts the day preceding onset of symptoms

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and peaks within 24 hours and remains elevated for 1–2 days and then
declines over the next 5 days.

Interferon is detectable in respiratory secretions about 1 day after viral

shedding begins and it is believed that the innate immunity response
contributes to host recovery from infection, specific antibody and cell-
mediated responses cannot be detected for another 1–2 weeks.

Clinical Findings

Influenza attacks mainly the upper respiratory tract and it poses a serious
risk for elderly adults, very young children and people with underlying
medical conditions such as lung, kidney, heart problems, diabetes, cancer or
immunosuppression.

Influenza Virus Replication

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Objectives

The objective of the lecture is to introduce the influenza virus, its general
characteristics, structure, shape and how it multiplies inside a living cell.

Post test

A substance by the host in response to viral infection but protecting it from

further viral infection is called :

a- phytotoxin.

b- antibody.

c- interferon.

d- hormone.

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Pretest

Which system Paramyxoviruses infect in human body?

Lecture 7

Paramyxoviruses and Rubella viruse

1- Paramyxoviruses

The Paramyxoviruses include the most important agents of respiratory

infections of infants and young children (e.g. Respiratory Syncytial Virus
RSV and Parainfluenzaviruses) as well as the causative agents of two of the
most common contagious diseases of childhood e.g. mumps and measles
that disseminated throughout the body and produce disease.

World Health Organization estimates that acute respiratory infections and

pneumonia are responsible every year worldwide for the deaths of 4 million
children younger than 5 years, Paramyxoviruses are the major respiratory
pathogens in this age group, all members of Paramyxoviridae initiate
infection via the respiratory tract whereas replication of the respiratory
pathogens is limited to the respiratory epithelia.

Important Properties of Paramyxoviruses

Virion: Spherical or pleomorphic, 150 nm or more in diameter and helical

nucleocapsid 13 or 18 nm.

Composition: RNA (1%), protein (73%), lipid (20%) and carbohydrate

(6%).

Genome: Single stranded RNA, linear, nonsegmented, negative sense and

~15 kb.
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Proteins: 6–8 structural proteins.

Envelope: Contains 3 viral glycoprotein and very fragile.

Replication: Cytoplasm, particles bud from plasma membrane.

Outstanding characteristics: Antigenically stable, Particles are labile yet

highly infectious.

Prevention and Treatment

Contact isolation precautions are necessary to manage nosocomial outbreaks

of parainfluenza, include restriction of visitors, isolation of infected patients,
and gowning and handwashing by medical personnel. the antiviral drug
ribavirin has been used with some benefit in treatment of
immunocompromised patients with lower respiratory tract disease and no
vaccine is available.

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Virology second stage

Epidemiology

Parainfluenza viruses are a major cause of lower respiratory tract disease in

young children are widely distributed geographically. type 3 is most
prevalent with about two thirds of infants infected during the first year of life
and virtually all have antibodies to type 3 by age 2 years, Infections with
types 1 and 2 occur at a lower rate, reaching prevalences of about 75% and
60% respectively by 5 years of age.

Transmission of Parainfluenzaviruses are transmitted by direct person to

person contact or by large droplet aerosols. Infections can occur through
both nose and eyes.

Pretest

What is rubella virus?

2- Rubella (German Measles)

Rubella (German measles) is an acute febrile illness characterized by a rash

and lymphadenopathy that affects children and young adults, it is the mildest
of common viral exanthemas, infection during early pregnancy may result
in serious abnormalities of the fetus including congenital malformations and
mental retardation, the consequences of rubella in utero are referred to as
congenital rubella syndrome, Rubella virus a member of the Togaviridae
family is the sole member of the genus Rubivirus, Rubella is not transmitted
by arthropods.

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Virology second stage

Immunity

Rubella antibodies appear in the serum of patients as the rash fades and the
antibody titer rises rapidly over the next 1–3 weeks, much of the initial
antibody consists of IgM antibodies which generally do not persist beyond 6
weeks after the illness. IgM rubella antibodies found in a single serum
sample obtained 2 weeks after the rash give evidence of recent rubella
infection and IgG rubella antibodies usually persist for life. one attack of the
disease confers lifelong immunity because only one antigenic type of the
virus exists.

Clinical findings

Rubella usually begins with malaise, low grade fever and a morbilliform
rash appearing on the same day, rash starts on the face and extends over the
trunk and extremities and rarely lasts more than 3 days and transient

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Virology second stage

arthralgia and arthritis are commonly seen in adults especially women, rare
complications include thrombocytopenic purpura and encephalitis, the
disease is difficult to diagnose clinically because the rash caused by other
viruses (e.g. Enteroviruses) is similar.

Objectives

The aim of the lecture is to introduce the general characteristics of the

paramyxoviruses and the rubella virus.

Post test

Does the German measles virus belong to the paramyxovirus family?

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Virology second stage

Pretest

Which system picornaviruses infect in human body?

Lecture 8

Picornaviruses (Enterovirus and Rhinovirus groups)

Picornaviridae represent a very large virus family with respect to the

number of members but one of the smallest in terms of virion size and
genetic complexity, they include two major groups of human pathogens :
enteroviruses and rhinoviruses.

Many picornaviruses cause diseases in humans ranging from severe

paralysis to meningitis, myocarditis, respiratory illnesses, undifferentiated
febrile illness and conjunctivitis. etiology is difficult to establish because
different viruses may produce the same syndrome, same picornavirus may
cause more than a single syndrome and some clinical symptoms cannot be
distinguished from those caused by other types of viruses, the most serious
disease caused by any enterovirus is poliomyelitis.

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Virology second stage

Enteroviruses are transient inhabitants of the human alimentary tract and

may be isolated from the throat or lower intestine, Rhinoviruses are
associated with the respiratory tract and isolated chiefly from the nose and
throat, less common picornaviruses associated with human illness include
hepatitis A virus, parechovirus, cardiovirus and Aichi virus.

Polioviruses

poliomyelitis is an acute infectious disease that in its serious form affects the
central nervous system (CNS), the destruction of motor neurons in the spinal
cord results in flaccid paralysis. most Poliovirus infections are subclinical
and does not multiply in muscle. Poliovirus particles are enteroviruses they

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are inactivated when heated at 55°C for 30 minutes and Polioviruses are not
affected by ether or sodium deoxycholate.

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Virology second stage

Rhinoviruses are the common cold viruses they are the most commonly
recovered agents from people with mild upper respiratory illnesses, they are
usually isolated from nasopharyngeal secretions but may also be found in
throat and oral secretions. these viruses as well as Adenoviruses,
Enteroviruses and Influenza viruses cause upper respiratory tract
infections including the common cold syndrome, Rhinoviruses are also
responsible for about half of asthma exacerbations.

Comperae between INF and COLD

FLU Signs and symotoms COLD

Abrupt Symptom onset Gradual

Usual Fever Rare

Usual , ofen sever General aches and Slight

pains

Fairly common Chills Uncommon

Can last up to 2-3 week Fatigue and weakness Quite mild

Sometimes Sneezing Common

Sometimes Stuffy nose Common

Sometimes Sore throat Common

Common, can become Chest discomfort and Mild to moderate,

sever cough haching cough

Common Headache Rare

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Clinical Findings

The average adult has one or two attacks each year, usual symptoms in
adults include sneezing, nasal obstruction, nasal discharge and sore throat
and other symptoms may include headache, mild cough, malaise and a chilly
sensation, there is little or no fever and the nasal and nasopharyngeal mucosa
become red and swollen. secondary bacterial infection may produce acute
otitis media, sinusitis, bronchitis or pneumonitis especially in children.

The incubation period is brief from 2 to 4 days and the acute illness usually
lasts for 7 days although cough may persist for 2–3 weeks.

Objectives

The objective of the lecture is to introduce the general definition of

picornaviruses and some of the diseases they cause.

Post test

Of the following which disease is caused by virus?

a- malaria.

b- T.B.

c- polio.

d- leprosy.

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Virology second stage

Pretest

What do you know about herpes viruses?

Lecture 9

Herpesviruses

Herpesvirus family contains several important human viral pathogens.

Clinically, herpesviruses exhibit a wide spectrum of diseases, some have an
extensive host cell range and others have a narrow host cell range. the
outstanding property of herpesviruses is their ability to establish lifelong
persistent infections in their hosts and to undergo periodic reactivation,
their frequent reactivation in elderly and immunosuppressed patients causes
serious health complications, curiously, the reactivated infection may be
clinically quite different from the disease caused by the primary infection.

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Important Properties of Herpesviruses

Virion: Spherical, 150–200 nm in diameter and cubic.

Genome: Double stranded DNA, linear and 125–240 kbp.

Proteins: More than 35 proteins in virion.

Envelope: Contains viral glycoproteins, Fc receptors.

Replication: Nucleus, bud from nuclear membrane.

Outstanding characteristics:

Establish latent infections

Persist indefinitely in infected hosts

Frequently reactivated in immunosuppressed hosts

Some cause cancer

Overview of Herpesvirus Diseases (some)

A wide variety of diseases are associated with infection by herpesviruses and

primary infection and reactivated disease by a given virus may involve
different cell types and present different clinical pictures. HSV-1 and HSV-2
infect epithelial cells and establish latent infections in neurons, type 1 is
associated with oropharyngeal lesions and type 2 infects the genital mucosa
both viruses can also cause neurologic disease.

VZV causes chickenpox (varicella) the virus causes herpes zoster (shingles),
adults who are infected for the first time with varicella-zoster virus can
develop serious viral pneumonia. CMV replicates in epithelial cells of the

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Virology second stage

respiratory tract, salivary glands and kidneys and persists in lymphocytes,

CMV is an important cause of congenital defects, neonatal hearing loss and
mental retardation.

Some of the Differences picornaviruses and herpesviruses

Picornaviruses Characteristic Herpesviruses

Cubic 1- Shape of Virion Spherical
28–30 nm 2- Dimeter of virion 150–200 nm
single stranded RNA 3- Genome double stranded DNA
four viral proteins 4- Proteins more than 35 proteins
None 5- Envelope Contain
Cytoplasm 6- Replication Nucleus
None 7- Latent infection establish latent
infections
None 8- Cancer some cause cancer

Objectives

The aim of the lecture is to introduce the general characteristics of herpes

viruses and the types to which they belong, comparing them with picorna
viruses.

Post test

What is the characteristic of herpes viruses?

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Virology second stage

Pretest

What is the oncogenic viruses?

Lecture 10

Oncogenic viruses or Human Cancer Viruses

Viruses are etiologic factors in the development of several types of human

tumors including two of great significance worldwide cervical cancer and
liver cancer, at least 15–20% of all human tumors worldwide have a viral
cause, viruses that have been strongly associated with human cancers are
HumanPapillomaViruses (HPVs) (genital tumors), Human
Immunodeficiency Virus (HIV), Epstein-Barr virus (EBV) (nasopharyngeal
carcinoma) and Hepatitis B and C virus (hepatocelleular carcinoma).

General fetures of viral carcinogensis

1. Viruses can cause cancer in animals and humans.

2. Tumor viruses frequently establish persistent infections in natural hosts.

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Virology second stage

3. Host factors are important determinants of virus induced tumorigenesis.

4. Viruses are seldom complete carcinogens.

5. Virus infections are more common than virus related tumor formation.

6. Long latent periods usually elapse between initial virus infection and
tumor appearance.

7. Viral strains may differ in oncogenic potential.

8. Viruses may be either direct- or indirect acting carcinogenic agents.

9. Oncogenic viruses modulate growth control pathways in cells.

10. Animal models may reveal mechanisms of viral carcinogenesis.

11. Viral markers are usually present in tumor cells.

12. One virus may be associated with more than one type of tumor.

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Multistep Carcinogenesis

Carcinogenesis is a multistep process that is multiple genetic changes must

occur to convert a normal cell into a malignant one, carcinogenesis can be
divided into four steps : tumor initiation, tumor promotion, malignant
conversion and tumor progression and tumors usually develop slowly over a
long period of time and number of mutations underlying this process is
estimated to range from five to eight.

Observation suggest that activation of multiple cellular oncogenes and

inactivation of tumor suppressor genes are involving in the evolution of
tumors whether or not a virus is involved.

It appears that a tumor virus usually acts as a cofactor and providing only
some of the steps required to generate malignant cells. viruses are necessary
but not sufficient for development of tumors with a viral etiology.

Important Properties of Papillomaviruses

Virion: cubic, 55 nm in diameter.

Composition: DNA (10%) and protein (90%).

Genome: double stranded DNA, circular and 8 kbp.

Proteins: two structural proteins.

Envelope: none.

Replication: nucleus.

Carcinogenesis : cause of human cancer especially cervical cancer.

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Objectives

The lecture aimed at general definition of human cancer viruses from

general characteristics and a summary of the occurrence of the
carcinogenesis process.

Post test

Are cancerous diseases caused by viruses transmitted?

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Pretest

Which organ infects by hepatitis viruses?

Lecture 11

Hepatitis Viruses

Viral hepatitis is a systemic disease primarily involving the liver most cases
of acute viral hepatitis in children and adults are caused by one of the
following five agents: Hepatitis A virus (HAV) the etiologic agent of viral
hepatitis type A (infectious hepatitis), Hepatitis B virus (HBV) which is
associated with viral hepatitis B (serum hepatitis), Hepatitis C virus (HCV)
the agent of hepatitis C (common cause of posttransfusion hepatitis),
Hepatitis D (HDV) a defective virus dependent on coinfection with HBV
and Hepatitis E virus (HEV) the agent of enterically transmitted hepatitis.

Symptoms of a viral liver can include:

Hepatitis viruses produce acute inflammation of the liver resulting in a

clinical illness characterized Jaundice (a change in the color of the skin and
the whites of the eyes to a yellow color), feeling sick, abdominal pain, lack
of appetite, nausea, vomiting, diarrhea, slight rise in temperature and
headache. regardless of the virus type, identical histopathologic lesions are
observed in the liver during acute disease.

Pathology

Hepatitis is a general term meaning inflammation of the liver

microscopically, there is spotty parenchymal cells degeneration with
necrosis of hepatocytes and a diffuse lobular inflammatory and disruption of

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liver cell cords and accompanied by reticuloendothelial (Kupffer) cell

hyperplasia, the damaged hepatic tissue is usually restored in 8–12 weeks.

Viral hepatitis

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Different of Hepatitis Viruses

Virus Hepatitis Hepatitis Hepatitis Hepatitis Hepatitis

A B C D E
1- Family Picornaviri Hepadnaviridae Flaviviridae Unclassified Hepeviridae
dae
2- Genus Hepatovirus Orthohepadnavirus Hepacivirus Deltavirus Hepevirus

3- Virion 27 nm, 42 nm, 60 nm, 35 nm, 30–32 nm,

cubic Spherical spherical spherical cubic
4- Envelope No Yes Yes Yes No

5- Genome ssRNA dsDNA ssRNA ssRNA ssRNA

6- Genome 7.5 3.2 9.4 1.7 7.2

size (kb)
7- Stability Heat and Acid sensitive Ether Acid Heat stable
acid sensitive, sensitive
Stable acid
sensitive
8- Chronic Never Often Often Often Never

disease
9- Oncogenic No Yes Yes Unknown No

10-Incubation 15-45 day 45-160 day 15-150 day 30-60 day 16-60 day

period

Objectives

The lecture aimed to identify the types of hepatitis viruses.

Post test

What is the name of the viral family to which hepatitis viruses belong?
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Virology second stage

Pretest

What is the rabies virus?

Lecture 12

Rabies viruses and other neurotropic viruses

Rabies viruses

Many different viruses can invade the central nervous system and cause
disease, Rabies is an acute infection of the central nervous system that is
almost always fatal and the virus is usually transmitted to humans from the
bite of a rabid animal, although the number of human cases is small rabies is
a major public health problem because it is widespread among animal
reservoirs.

Structure

Rabies virus is a rhabdovirus with morphologic and biochemical properties

in common with vesicular stomatitis virus of cattle and several animal, plant,
and insect viruses. Rhabdoviruses are rod or bullet shaped particles
measuring 75 × 180 nm, the particles are surrounded by a membranous
envelope with protruding spikes 10 nm long, peplomers are composed of
trimers of the viral glycoprotein. inside the envelope is a ribonucleocapsid,
genome is single stranded, negative sense RNA, 12 kb and molecular weight
4.6 × 106 million.

Classification

The viruses are classified in the family Rhabdoviridae, Rabies viruses

belong to the genus lyssavirus.

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Infection rhabdoviruses are very widely distributed in nature, infecting

vertebrates, invertebrates, and plants. many of the animal rhabdoviruses
infect insects but rabies virus does not.

Reactions to physical and chemical agents

Rabies virus survives storage at 4°C for weeks and at −70°C for years and it
is inactivated by CO2, so on dry ice it must be stored in glass sealed vials.

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Rabies virus is killed rapidly by exposure to ultraviolet radiation or

sunlight, by heat (1 hour at 50°C) by lipid solvents (ether, 0.1% sodium
deoxycholate) by trypsin by detergents and by extremes of pH.

Clinical Findings

Rabies is primarily a disease of lower animals and is spread to humans by

bites of rabid animals or by contact with saliva from rabid animals, the
disease is an acute, fulminant, fatal encephalitis and the incubation period in
humans is typically 1–3 months but may be as short as 1 week or more than
a year and it is usually shorter in children than in adults.

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The clinical spectrum can be divided into three phases: a short prodromal
phase, an acute neurologic phase and coma, prodrome lasting 2–10 days
may show any of the following nonspecific symptoms: malaise, anorexia,
headache, photophobia, nausea, vomiting, sore throat and fever and usually
there is an abnormal sensation around the wound site.

During the acute neurologic phase which lasts 2–7 days, patients show signs
of nervous system dysfunction such as nervousness, apprehension,
hallucinations and bizarre behavior including : increased salivation and
perspiration. a large fraction of patients will exhibit hydrophobia (fear of
water) or aerophobia (fear when feeling a breeze). the act of swallowing
precipitates a painful spasm of the throat muscles this phase is followed by
convulsive seizures or coma and death. the usual incubation period in dogs
ranges from 3 to 8 weeks but it may be as short as 10 days. clinically the
disease in dogs is divided into the same three phases as human rabies.

Important Properties of Rhabdoviruses

Virion: Bullet shaped, 75 nm in diameter × 180 nm in length.

Composition: RNA (4%), protein (67%), lipid (26%) and carbohydrate

(3%).

Genome: Single stranded RNA, linear, nonsegmented, negative sense,

molecular weight 4.6 million, and size 12 kb.

Proteins: Five major proteins.

Envelope: Present.

Replication: Cytoplasm, virions bud from plasma membrane.

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Other neurotropic viruses

Overview

A neurotropic virus is a virus that is capable of infecting nerve tissue.

Examples

Neurotropic viruses that cause infection include Japanese Encephalitis,

polio, mumps, measles and rabies as well as diseases caused by members of
the family Herpesviridae such as herpes simplex, varicella zoster, Epstein
Barr and cytomegalovirus.

Terminology

A neurotropic virus is said to be neuroinvasive e.g. Herpes Simplex Virus

if it is capable of accessing or entering the nervous system and
neurovirulent e.g. Rabies virus if it is capable of causing disease within the
nervous system. Both terms are often applied to central nervous system
infections.

Objectives

The lecture aims to learn about the characteristics of the rabies virus and
symptoms of the disease and to identify other viruses that affect the nervous
system.

Post test

Is the rabies virus transmitted from one person to another?

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Virology second stage

Pretest

What do you know about arbovirus?

Lecture 13

Arboviruses and viral haemorrhagic viruses

Arboviruses

The arthropod borne viruses (arboviruses) represent ecologic groupings of

viruses with complex transmission cycles involving arthropods, these viruses
have diverse physical and chemical properties and are classified in several
virus families, the major arbovirus diseases worldwide are yellow fever,
dengue and Japanese B encephalitis.

Classification

Arboviruses are classified among Bunyaviridae, Flaviviridae, Reoviridae

and Togaviridae families.

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Transmission of arboviruses by bloodsucking arthropods from one

vertebrate host to another.

Human arboviruses infection

Diseases produced by arboviruses may be divided into three clinical

syndromes : (1) fevers of an undifferentiated type with or without a
maculopapular rash and usually benign, (2) encephalitis (inflammation of
the brain), often with a high case-fatality rate and (3) hemorrhagic fevers
also frequently severe and fatal and some arboviruses may be associated
with more than one syndrome e.g. dengue.

viral haemorrhagic viruses

Viral hemorrhagic fevers (VHFs) are a group of diseases that are caused by
several distinct families of viruses, the term “viral hemorrhagic fever”
refers to a condition that affects many organ systems of the body and
damages the overall cardiovascular system and reduces the body’s ability to

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function on its own. symptoms of this type of condition can vary but often
include bleeding or hemorrhaging, some VHFs cause relatively mild illness
while others can cause severe life threatening disease and most VHFs have
no known cure or vaccine.

Although VHFs are caused by several families of viruses, these viruses

share some common characteristics:

1- They are RNA viruses meaning viruses that have ribonucleic acid (RNA)
as their genetic material.

2- They are covered or enveloped in a lipoprotein outer layer making it

easier to destroy these viruses with physical (heat, sunlight and gamma rays)
and chemical (bleach, detergents and solvents) methods.

3- They naturally exist in animal or insect populations referred to as host

populations.

4- They spread to people when a person encounters an infected animal or

insect host and after the initial spread into the human population and some
VHF viruses can continue to spread from person to person.

5- Outbreaks of VHFs in people can be difficult to prevent since they

cannot be easily predicted.

Transmition

Person to person transmission of some VHFs can occur, VHF viruses can
spread to people when they come in contact with infected animals or insects.
for many VHFs person to person transmission can then continue often

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through direct contact or in healthcare facilities without adequate infection

control procedures.

Signs and symptoms of VHFs

include (by definition) fever and bleeding : flushing of the face and chest,
small red or purple spots (petechiae), swelling, hypotension, circulatory
shock, malaise, muscle pain, headache, vomiting and diarrhea occur
frequently, the severity of symptoms varies with the type of virus.

Objectives

The aim of the lecture is to identify viruses that are transmitted by

arthropods and the syndromes that cause them, as well as to identify viruses
that cause hemorrhagic fever, the symptoms they cause, the method of
diagnosis and others.

Post test

Arthropod borne viruses are

a- ribo virus.

b- reo virus.

c- arbo virus.

d- none of these.

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Virology second stage

Pretest

What are the largest types of viruses below in terms of size?

Lecture 14

Adeno , pox and parvo viruses

Adenoviruses

Adenoviruses can replicate and produce disease in the respiratory,

gastrointestinal, urinary tracts and in eye, many adenovirus infections are
subclinical and virus may persist in the host for months and about one third
of the 57 known human serotypes are responsible for most cases of human
adenovirus disease, a few types serve as models for cancer induction in
animals.

Important Properties of Adenoviruses

Virion: cubic, 70–90 nm in diameter.

Composition: DNA (13%) and protein (87%).

Genome: Double stranded DNA, linear and 26–45 kbp.

Proteins: Important antigens.

Envelope: None.

Replication: Nucleus.

Poxviruses

Poxviruses are the largest and most complex of viruses infecting humans and
the family encompasses a large group of agents that are similar

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Virology second stage

morphologically and share a common nucleoprotein antigen, Infections with

most poxviruses are characterized by a rash.

Parvoviruses

Parvoviruses are the smallest DNA animal viruses, Parvovirus B19 is

pathogenic for humans and has a tropism for erythroid progenitor cells.

Classification

There are two subfamilies of Parvoviridae: the Parvovirinae, which infect

vertebrates and Densovirinae which infect insects.

Compere between poxviruses and parvoviruses

Poxviruses. Charectrastc Parvoviruses

Complex. 1- Virion symmetry Cubic.
300–400 nm in length × 2- Virion diameter 18–26 nm.
230 nm.
130–375 kbp. 4- Size of genome 5.6 kb.
DNA (20%), protein 5- Composition DNA (3%), protein
(80%). (90%), lipid (5%).
Double stranded DNA. 6- Genome Single stranded DNA
contain more than 100 7- Proteins One major (VP2) and
polypeptides. one minor (VP1).
Present. 8- Envelop None.
Cytoplasm. 9- Replication Nucleus.
Large and complex. 10- Size Very simple.
smallpox virus. 11- Example B19.

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Virology second stage

Objectives

The aim of the lecture is to introduce the general definition of adenovirus,

pox, and parvovirus, with a comparison between pox and parvoviruses.

Post test

The above viruses, whichever is smaller in diameter?

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Pretest

What is the name of the virus that causes AIDS?

Lecture 15

Retroviruses and ADIS

Retroviruses

There are RNA viruses that belong to family Retroviridae (Re = Revers, tr =
transcriptase) members of this family possess the characteristic biochemical
feature is the presence of RNA dependent DNA polymerase (revers
transcriptase) within the virus. Retroviruses are spherical, enveloped viruses,
80–110 nm in diameter, whose genome contains two copies of linear,
positive sense and single stranded RNA.

Each monomer RNA is 7–11 kb in size and particles contain a helical

nucleocapsid within an cubic capsid and replication is unique, the virion
contains a reverse transcriptase enzyme that produces a DNA copy of the
RNA genome this DNA becomes circularized and integrated into host
chromosomal DNA and the virus is then replicated from the integrated
“provirus” DNA copy and virion assembly occurs by budding on plasma
membranes. Hosts remain chronically infected.

AIDS

Human Immunodeficiency Virus (HIV) types derived from primate

lentiviruses are the etiologic agents of Acquired Immune Deficiency
Syndrome (AIDS), illness was first described in 1981 and HIV-1 was

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isolated by the end of 1983 since then AIDS has become a worldwide
epidemic.

The family Retroviridae is classified into three subfamilies

subfamily Genus Virus Disease

Oncovirinae Retrovirus HTLV-1 and Adult T cell
HTLV-2 leukemia/lymphoma
Lntivirinae Lentivirua HIV-1 and ADIS
HIV-2
Spumavirinae Spumavirus Human foamy Nil
virus

Millions are now infected worldwide once infected individuals remain

infected for life. within a decade if left untreated the vast majority of HIV
infected individuals develop fatal opportunistic infections as a result of HIV
induced deficiencies in the immune system. AIDS is one of the most
important public health problems worldwide at the start of the 21st century.

Routes of transmission

Virus is present in the blood, semen, cervical and vaginal secretions and
these sources are important in transmission, HIV is spread only by three
modes

1- sexual contact with infected persons (heterosexual or homosexual)

efficiency anal intercourse 1% and vaginal intercourse 0.1%.

2- by blood and blood products, efficiency >90%.

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3- from infected mother to babies (intrapartum, perinatal and postnatal)

efficiency 13-40%.

structure of HIV

1- Envelope glycoprotein spike (gp120). 2- Transmembrane pedicle

glycoprotein (gp41). 3- Outer icosahedral shell of nucleocapsid (p18). 4-
Cone shaped core of nucleocapsid (p24). 5- Inner core. 6- Viral proteins
associated with RNA. 7- Viral RNA. 8- Reverse transcriptase. 9- Envelope
lipid bilayer.

Clinical Findings

Symptoms of acute HIV infection are nonspecific and include fatigue, rash,
headache, nausea, and night sweats, AIDS is characterized by pronounced
suppression of the immune system and development of a wide variety of
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severe opportunistic infections or unusual neoplasms. the more serious

symptoms in adults are often preceded by a prodrome that can include
fatigue, malaise, weight loss, fever, shortness of breath, chronic diarrhea,
white patches on the tongue and lymphadenopathy. the interval between
primary infection with HIV and the first appearance of clinical disease is
usually long in adults averaging about 8–10 years.

Objectives

The aim of the lecture is to learn about retroviruses and also about the more
dangerous viruses that belong to this family.

Post test

Why is the HIV considered a dangerous virus?

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Refrences

1- Jawetz, Melnick & Adelberg's.(2016).medical microbiology.McGraw-

Hill,27th, new york:851.

2- Surinder Kumar.(2016).essentialsa of microbiology.JAYPEE,1th, new

delhi:627.

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