In 1898, Friedrich Loeffler and Paul Frosch found evidence that the cause of foot-and-mouth disease in livestock was an infectious particle smaller than any bacteria. This was the first clue to the nature of viruses, genetic entities that lie somewhere - PowerPoint PPT Presentation

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In 1898, Friedrich Loeffler and Paul Frosch found evidence that the cause of foot-and-mouth disease in livestock was an infectious particle smaller than any bacteria. This was the first clue to the nature of viruses, genetic entities that lie somewhere

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Some viruses may remain dormant inside host cells for long periods, causing no obvious change in their host cells (a stage known as the lysogenic phase). – PowerPoint PPT presentation

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Title: In 1898, Friedrich Loeffler and Paul Frosch found evidence that the cause of foot-and-mouth disease in livestock was an infectious particle smaller than any bacteria. This was the first clue to the nature of viruses, genetic entities that lie somewhere


1
Introduction to the Viruses
In 1898, Friedrich Loeffler and Paul Frosch
found evidence that the cause of foot-and-mouth
disease in livestock was an infectious particle
smaller than any bacteria. This was the first
clue to the nature of viruses, genetic entities
that lie somewhere in the grey area between
living and non-living states. Viruses depend on
the host cells that they infect to reproduce.
When found outside of host cells, viruses exist
as a protein coat or capsid, sometimes enclosed
within a membrane. The capsid encloses either DNA
or RNA which codes for the virus elements. While
in this form outside the cell, the virus is
metabollically inert examples of such forms are
pictured below.
When it comes into contact with a host cell, a
virus can insert its genetic material into its
host, literally taking over the host's functions.
An infected cell produces more viral protein and
genetic material instead of its usual products.
Some viruses may remain dormant inside host cells
for long periods, causing no obvious change in
their host cells (a stage known as the lysogenic
phase). But when a dormant virus is stimulated,
it enters the lytic phase new viruses are
formed, self-assemble, and burst out of the host
cell, killing the cell and going on to infect
other cells. The diagram below at right shows a
virus that attacks bacteria, known as the lambda
bacteriophage, which measures roughly 200
nanometers.
2
The origin of viruses is not known. Two theories
of viral origin1- Viruses may be derived from
DNA or RNA or from both nucleic acid components
of host cells that became able to replicate
autonomously and evolve independently.2-
Viruses may be degenerate forms of intracellular
parasites.
Evolutionary Origin of Viruses
Classification of VIRUSES
Viruses are separated into major groupings called
families on the basis of morphology, genome
structure, and replication. Virus families have
the suffix viridae-. Within each family,
subdivisions, called genera, are usually based on
physicochemical or serologic properties. Genus
names carry the suffix virus-. Subfamilies
virinae. In 1995, the international committee on
taxonomy of viruses had organized more than 4000
animal and plant viruses into 71 families, 11
subfamilies, and 164 genera, with hundreds of
viruses still unassigned. Currently 24 families
contain viruses that infect humans and animals.
According to the type of nucleic acid viruses
are classified into DNA and RNA viruses.
3
Poxvirus Adenovirus

4
DNA Viruses
A- Parvoviruses B- Polyomaviuses Formerly
part of Papovaviridae family before it splits
into 2 families. C- Papillomaviruses - Formerly
part of Papovaviridae family before it splits
into 2 families. D- Adenoviruses E-
Herpesviruses F- Poxviruses G- Hepadnaviruses
RNA Viruses
A- Picornaviruses
H- Reoviruses
O- Bornaviruses B- Flaviviruses
I-
Arboviruses P- Filoviruses C
Togaviruses
J- Arenaviruses
Q- Other viruses D- Coronaviruses
K- Bunyaviruses
R- Viroids E- Caliciviruses
L-
Orthomyxoviruses S- Prions F-
Retroviruses
M- Paramyxoviruses G- Astrovirses

N- Rhabdoviruses
5
Virus Structure
Icosahedral symmetry
Complex symmetry
Helical symmetry
6
Types of Symmetry
1- Icosahedral ( Cubic ) Symmetry 2- Helical
Symmetry 3- Complex Structure
Virus Structure
  • Capsid protein shell that encloses the nucleic
    acid. It is built of structure units.
  • STRUCTURE UNITS are the smallest functional
    equivalent building units of the capsid.
  • CAPSOMERS are morphological units seen on the
    surface of particles and represent clusters of
    structure units.
  • The capsid together with its enclosed nucleic
    acid is called the NUCLEOCAPSID.
  • The nucleocapsid may be invested in an ENVELOPE
    which may contain material of host cell as well
    as viral origin.
  • The VIRION is the complete infective virus
    particle

7

Cultivation of Viruses
Because viruses are unable to reproduce
independently of living cells, viruses cannot be
cultured in the same way as bacteria and
eucaryotic microbes. B) In the early years
animal viruses were cultivated in suitable host
animals or in embryonated eggs.
More recently, the animal viruses were able to
grown in cell culture. 1) Host cells are grown in
a petri dish or other container. A monolayer of
cells form2) The viruses are spread in the cells
and allowed to settle and attach3) A layer of
agar is overlayed on the cells.4) As the virus
replicates, cells lyse or become misshapened.
This results in plaques.

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Reaction of Viruses to Physical and Chemical
Agents
1- Heat and Cold. 2- Stabilization of Viruses
by Salts. 3- pH. 4- Radiation. 5- Photodynamic
Inactivation. 6- Ether Susceptibility. 7-
Detergents. 8- Formaldehyde. 9- Antibiotics and
Other Antibacterial Agents.
10
Replication of Viruses
Papova Virus Replication
General Steps in Viral Replication Cycle A-
Attachment B- Penetration C- Uncoating D-
Early transcription E- Early Translation F-
Nucleic acid synthesis G- Late transcription and
translation H- Assembly and release

11
Influnza Virus Replication

12

Reovirus Replication

13
Coronavirus
Influenzavirus
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15
Pathogenesis and Control of Viral Diseases
More than 300 viruses are known to infect humans
and to cause as many as 50 different
syndromes. Steps in Viral Pathogenesis A- Viral
entry and primary replication. B- Viral Spread
and Cell Tropism. C- Cell Injury and Clinical
Illness. D- Recovery From Infection. E- Virus
Shedding. Host Immune Response 1- Both humeral
and cellular immunity are involved in control of
viral infection. 2- Mononuclear cells and
lymphocytes are involved in viral infection. 3-
The capsid serves as the targetfor the immune
response. 4- Cytotoxic T lymphocytes lyse virus
infected cells. 5- Secretory IgA antibody is
important against viral infections of the
respiratory or gastrointestinal tract. 6- Among
the nonimmune responses is the induction of
interferone.
16
Adverse Effect of Certain Viruseson the Host
Immune Response
1- Some viruses infect and damage cells of the
immune system(AIDS). 2- Development of
pathologic changes and clinical illness. 3-
Immunopathologic disorder due to vaccine
immunization. 4- Development of
autoantibodies. Viruses have a variety of ways
that serve to suppress or evade the host immune
response and thus avoid eradication 1-
Oftentimes the viral proteins involved in
modulating the host response are not essential
for the growth of the virus. 2- Some viruses
infect cells of the immune system and abrogate
their function(AIDS). 3- They may infect neurons
that express little or no class 1
MHC(herpesviruses). 4- Form proteins that
inhibit MHC function(adenoviruses). 5- Viruses
may mutate and change the antigenic sites on
virion proteins(influenza virus). 6- Regulate
the level of viral surface proteins(herpesvirus).
17
Viral Persistance Infections
Viral infections are usually self-limiting.
Sometimes, however, the virus persists for long
periods of time in the host. Long-term
virus-host interaction may take several forms 1-
Chronic infections. 2- Latent infections. 3-
Inapparent or subclinical infections. Acute
Viral Respiratory Infections. Viral Infections of
the Gastrointestinal Tract. Viral skin
Infections Viral Infections of the CNS Congenital
Viral Infections. Rubella, CMV, Herpes simplex,
Varicella-zoster, HBV, Enterovirus, HIV,
Parvovirus B19
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Prevention and Treatment of Viral Infections
As bacteria and protozoa do not relay on host
cellular machinery for replication, so processes
specific to these organisms provide ready targets
for the development of antibacterial and
antiprotozoal drugs. However, because viruses
are obligate intracellular parasites, antiviral
drugs must be capable of selectively inhibiting
viral functions without damaging the host, making
the development of such drugs very difficult.
Furthermore an ideal drug would reduce disease
symptoms without modifying the viral infection so
much as to prevent an immune response in the
host. There is a need for antiviral drugs active
against viruses for which vaccines are not
available or not highly effective. A- Nucleoside
analogs. B- Nucleotide analogs. C-
Nonnucleoside Reverse transcriptase
inhibitors. D- Protease inhibitors
Saquinavir. E- Other types Amentadine,
Rimantadine, Foscarent, Methisazone. F-
Interferons Properties Synthesis
Antiviral activity and other biologic effects.
Clinical studies.
21
Viral Vaccines
General Properties Killed Virus
Vaccines Advantages Disadvantages Attenuated
Live-Virus Vaccines Advantages Disadvantage Future
Prospects
22
Simplified diagram of the Bacteriophage p22
virus. Original measures 995 pixels across
23
  • above) Ebola virus docks with cell membrane at
    middle left. Viral RNA (yellow) is released into
    the cytoplasm where it directs the production of
    new viral proteins and genetic material. New
    viral genomes are rapidly coated in protein to
    create cores. These viral cores stack up in the
    cell and migrate to the cell surface.
    Transmembrane proteins (purple) are produced
    which are ferried to the cell surface. Cores push
    their way through the cell membrane becoming
    enveloped in cell membrane and collecting their
    transmembrane proteins (spikes) as they do so.
    Examples of coiled virions are shown in the
    background.

24
Simplified diagram of the Bacteriophage Lambda
showing combined lytic and lysogenic processes.
25
Generalised scheme showing the ways that viruses
can enter animal cells. Some viruses can use more
than one strategy. Other means are also employed.
26

SARS virion
27
At left, a phage has attached to the LPS layer of
the bacterial cell wall. At right, the phage tail
has contracted and the phage DNA (red rope like
structure) is shown entering the cell.


Bacteriophage T4 virus attacking a bacterial cell

28
Ways of Entrance of Viruses to Animal Cells
  • . NAKED VIRUS - TRANSLOCATION particle crosses
    cell membrane intact (cf Principles of Molecular
    Virolgy, 3rd Edition, Alan J. Cann, Academic
    Press p 117)
  • 2. NAKED VIRUS - GENOME INJECTION virus attaches
    to cell surface and releases its genome which
    penetrates the cytoplasm via a pore that has been
    created in the plasma membrane. ( Bacteriophages,
    which attack bacterial cells, also inject their
    genomes and may use molecular "syringes" to do
    so, please see our diagram of T4 phages
    injecting. )
  • 3. NAKED VIRUS - ENDOCYTOSIS virus attaches to
    cell surface receptor molecules and sinks into a
    clathrin coated pit. The pit invaginates and
    finally closes off creating a clathrin coated
    vesicle (drawn as a cage like sphere) and so the
    contained virus particle is drawn into the
    cytoplasm. The clathrin molecular cage soon
    dissociates into component triskelions (the
    propeller like objects) which leave a vesicle.
    The resulting uncoated vesicle transports the
    contained virion to an endosome. At some stage
    thereafter, the viral components are released.
    The virus shown in this example is an Adenovirus.
  • 4. ENVELOPED VIRUS - ENDOCYTOSIS MEMBRANE
    FUSION virus enters cell by receptor mediated
    endocytosis. The cell membrane merges (fuses)
    with the endosome membrane and so the virus
    components are released. The virus shown here is
    an influenza virus, please see our Influenza
    virus life cycle illustration .
  • 5. ENVELOPED VIRUS - MEMBRANE FUSION virus
    enters the cell when its outer membrane fuses
    with the plasma membrane at the cell surface. The
    viral contents are then spilled into the
    cytoplasm of the cell. This example is HIV, which
    is unusual in having a conical core (most viral
    cores tend to be more spherical). Please see our
    HIV illustrations.

29
  • HIV attacks a macrophage (top middle) and a
    Helper T Cell (lower left). New virus particles
    then bud from the macrophage. A B-lymphocyte
    (bottom right) gives rise to Plasma Cells
    (reddish cells on right) that produce antibodies
    (Y shaped molecules in red) that bind to HIV. A
    killer cell (bottom middle) will attack virus
    infected cells. The interaction of HIV and the
    immune system is very complex and varies over
    time. This image is available for licensing
    worldwide. The
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