Download - Virology
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Viruses are very small particles which
infect humans, animals, plants and even
bacteria.
Obligate intracellular parasites.
Viruses range in size from 20-400nm.Are viruses living organisms?
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NO! They can only replicate in living cells ,
employ host cell’s replicative and metabolic
pathways.
Outside cells they are essentially inert
macromolecules (Protein & NA).
Obligate intracellular
parasites
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EssentiEssentialal
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Core of genetic material(nucleic acid):
Single or double strands DNA or RNA, linear or
circular, one piece or segmented.
Protein coat or capsid:
Composed of a large number of subunits
(capsomeres).
Protects viral genes from inactivation by
adverse environmental factors, help
attachment to specific receptors on host cells.
Core + capsid = nucleocapsid
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Envelope:
Lipid or lipoprotein bilayer, not present in all
virus species, derived at least partially from
host cell membrane , contain viral
glycoprotein
• Structural
• Functional
Enzymes:
Found only in very few number of viruses.
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Virion Virion
• Complete virus particle : nucleic acid +
protein coat, which may be surrounded by an
envelope.
• It is the form in which the virus moves between
cells or hosts.
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Viral Structure - Viral Structure - OverviewOverview
Fig 1. Schematic overview of the structure of animal viruses
** does not exist in all viruses
Nucleic acid
CapsidNucleocapsid
Envelope protein
Membrane proteinViral envelope**
Spike protein
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Continue
The nucleocapsid which may have
Icosahedral: (Cubic) Has 20 faces, each an
equilateral triangle (e.g. adenoviruses).
Helical: Protein binds around DNA/RNA in a
helical fashion (e.g. Influenza virus).
Complex: no specific symmetry
(e.g. Bacteriophage , Poxviruses)
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Icosahedral Helical Complex
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The host cell act as a factory
providing substrates, energy, and
machinery for synthesis of coat
proteins , nucleic acid genomes.
Recognition and attachment to the
target cell:
It depends on legends “ Surface protein
” of the virus and receptors in the host
cell.
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HIV binds to CD4 receptors in cells of
immune system.
EBV binds to CD21 receptors on B cells.
Poliovirus attach only to cells in CNS and
GIT.
Attachment step initiate irreversible
structural changes in the virion.
Attachment step is temperature dependent.
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Penetration or engulfment:
• Non enveloped “Naked” viruses penetrate
by
Receptor mediated endocytosis.
Translocation of the virion across the host cell
membrane.
• Enveloped viruses penetrate cells through
Fusion of viral envelope with host cell membrane.
May or may not involve receptor mediated
endocytosis.
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Uncoating:
Enveloped viruses are usually uncoated upon
fusion to the cell membrane.
The virus then delivered to the replication
site.
• DNA viruses replicates in the nucleus
except poxvirus.
• RNA viruses replicates in the cytoplasm
except retroviruses (HIV).
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Expression of viral genomes and
synthesis of viral components:
It is the most important step in virus
replication.
It depends on the formation of functional
mRNA capable of binding to the ribosome
and being translated into proteins.
DNA viruses that replicates in the nucleus
utilize the cell’s DNA dependent RNA
polymerase.
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While poxvirus which replicates in the
cytoplasm must encode for such enzyme.
RNA viruses must encodes for enzymes
which transcript the RNA.
Protein synthesis takes place in two stages:
Early stage: synthesis of proteins that
inhibit the cell metabolism and enzymes
(polymerases) necessary for nucleic acid
replication.
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Late stage: synthesis of protein capsids.
Replication differs according to the type of
the nucleic acid core.
Assembly:
Association of cores and coats.
Usually starts as soon as necessary pieces
are synthesized.
It looks like a box of capsomeres enclosing
the genome.
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Release:
Naked viruses are released after lyses of the
cell while enveloped viruses are released
usually by budding.
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Time course of Time course of replicationreplication
The time interval after penetration and
before assembly is called eclipse cycle.
During the eclipse cycle infective virion
couldn’t be isolated.
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Structure: DNA or RNA (most satisfactory for
microbiologists).
Morphology: icosahedral, helical or complex,
also enveloped or non, and others, picorna virus
(small), togavirus (cloak), coronavirus (crown),
rhabdovirus (rod).
Disease: hepatitis virus, encephalitis virus,
influenza virus (most satisfactory for medicine).
Tissue (tropism): adenovirus (glands),
enterovirus (intestine) or myxovirus (mucous).
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Viruses grow only in living cells which may be:
I) Tissue culture: I) Tissue culture:
Animal or human tissue culture pieces treated
with trypsin to separate the cell.
They are grown in presence of growth medium
containing serum.
A monolayer or sheet of cells is formed on the
flat surface of the container (glass or plastic
bottle or tube).
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There are three types of tissue cultures:
a) Primary cell lines: fragments of tissue e.g.
monkey kidney. They can only divide for 4-6
subcultures, then degenerate.
b) human diploid cell lines: Usually fibroblasts
from human embryo tissue. They grow rapidly
and can be subcultured 50 times.
c) Continuous cell lines: are derived from tumor
cells and can be subcultured indefinitely e.g. Hella
cells derived from the carcinoma of the cervix.
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II) Chick or duck embryo:II) Chick or duck embryo:
The virus is allowed to grow in one of the
following cavities within the fertilized egg.
a) Embryo e.g. yellow fever virus.
b) Allantoic or Amniotic cavity: e.g. influenza virus.
c)Chorioallantoic membrane: e.g. pox and herpes
viruses.
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III) Intact animal: III) Intact animal:
The white suckling mouse is widely used for
encephalitis viruses, calves are used for pox
virus.
Cultivation in animals has the disadvantage of
easy transmission of infection.
Rarely used now.
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1. Cytopathogenic or cytopathic effect (CPE):
Characteristic changes due to permanent or
temporary cell damage as cell death
(poliovirus), cluster formation (adenovirus),
giant cell formation (measles and mumps
viruses) or cell transformation (tumor viruses).
2. Inclusion bodies:
Observed by light microscope.
They are aggregates or just sites of replication
of the virus.
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e.g.
Cytoplasmic Negri bodies in brain cells of
rabies infected animal, cytoplasmic Guarnieri's
bodies of poxvirus.
Nuclear bodies of adenovirus.
Nuclear and cytoplasmic bodies in case of
cytomegalovirus.
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3. Haemadsorption:
Viruses which contain haemagglutinin spikes
e.g. influenza virus are able to form clumps of
RBCs if added to the tissue culture.
4. Interference:
Host cells infected with a virus may acquire
resistance to infection by a second virus, of the
same type or another one (it is not common to
all viruses e.g. not found between mumps,
measles and rubella).
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Some viruses do not produce CPE, however, their
growth can be proved by their ability to interfere with
another CPE producing virus e.g. rubella and ECHO
(Enteric Cytopathic Human Orphan) virus.
5. Fluorescent antibody staining.
6. Detection of viral antigens by serology.
7. Acid production:
Normal cells produce acids, thus:
• Normal tissues + Phenol red Yellow (acid color).
• Infected tissues + Phenol red Red (alkaline color).
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A. Local infections:
1. Skin: e.g. warts caused by papillomavirus.
2. Respiratory tract infections affecting the
mucous membranes e.g. influenza and
common cold.
3. Alimentary tract e.g. more than 60% of
diarrhea in infants is caused by rotavirus.
Local infections are characterized by short
incubation period and short lasting
immunity.
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B. Systemic infection:
The virus passes through lymphatics, blood,
tissues or nerves, reaching the target tissue
(tropism), e.g. hepatitis, measles,
poliomyelitis.
Administration of neutralizing antibodies
before the viraemic phase could prevent the
development of the disease.
Systemic infections are characterized by long
incubation period and long lasting immunity.
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C. Persistent infection: Due to escape of the virus from the host
defense mechanism. It is either1. Latent infection: the virus remain hidden
most of the time with intermittent reactivation and development of the disease e.g. herpes simplex and adeno infections. The virus is not detected during latency.
2. Chronic infection: the virus usually has long incubation period and is always shedding i.e. can be detected all the time, during symptoms and in absence of symptoms, e.g. hepatitis B.
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3. Slow infection: are viruses with long
incubation period and slow multiplication
e.g. subacute sclerosing panencephalitis
caused by a variant of measles virus.
4. Congenital or teratogenic infection:
many viruses penetrate the placenta during
pregnancy causing congenital defect in the
embryo, e.g. rubella, cytomegalo, hepatitis
viruses and HIV.
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5. Oncogenicity (tumor causing): resulting in transformation of infected cells.
Viral genes become integrated into host cell chromosome e.g. of DNA viruses (herpes simplex type 2 virus, Epestein Barr virus, hepatitis B&C viruses and papovirus) e.g. of RNA viruses is the retrovirus group {human T lymphotropic viruses 1&2 (HTLV 1&2)} c.f. HIV formerly known as HTLV 3 which is non oncogenic.
With RNA tumor viruses, viral RNA acts as a template for synthesis of viral DNA- through the action of reverse transcriptase. The DNA copy of the viral RNA is integrated into the host cell chromosome.
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