2. .
a cellular intruder
Virus properties
• It can only be seen with an electron microscope (except for the
smallpox virus) • It contains nucleic acid (genome) of only one type (DNA or RNA) •
It does not have any special metabolic activity, but rather depends on the host cell to
manufacture its own DNA and proteins. Their envelopes (in the enveloped
species) are derived from the envelopes of host
forced
• The smallest infectious agent is 10 nm - 300 nm • Its presence inside
living cells is necessary for its transcription
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3. Comparison of viruses and cells
many
cells
None or few
Yes (most cells)
proteins
cell membrane in all cells
missing
present in eukaryotes
Replication by binary fission
the
missing
present
mitochondria;
few
enveloped in some viruses
many
Adjective
viruses
lipoprotein membrane
enzymes
ribosomes;
DNA or RNA, not both DNA pattern
DNA and RNA together
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4. virus structure
RNA or DNA Genome: Core ÿ double-stranded ds or
single-stranded ss, linear or circular . It is the infectious
part responsible for the replication of the virus and the transmission of its antigenic
characteristics and characteristics. ÿ Capsid: a protein. It consists of subunits (called
capsular particles). Antigenic protects the genome, gives the virus its shape and
contributes to fixing it on the
intruded cell. ÿ Envelope : lipoproteins, derived from the cytoplasmic or nuclear
membrane of the host cell It has antigenic glycoprotein spikes that contribute to its
adhesion to the host cell It is not found in all viruses (only enveloped viruses) It
makes the virus
more sensitive to heat and disinfectants ÿ Surface proteins: (capsule proteins + coat
glycoproteins) are the main antigens against which the immune reaction is formed
In the body + Determines the selectivity
ÿ Enzymes that help in reproduction
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5. Virus shapes Determined
by the method of regularity and spatial
alignment of the capsules 1- Cubic symmetry: Symmetry Cubical:
crystalline icosahedron form - the most
coherent and rigid - adenoviruses. •-2 Symmetry Helical: elongated in the
form of a bent or spiral
strip. Influenza virus •-3 Symmetry Complex: complex oval like smallpox and
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6. Replication Virus
Reproduce by copying or multiplying: dependent on the host cell to provide it with energy and to manufacture
its nucleic acid and viral proteins through the following
stages: 1- Attachment: via surface capsular proteins or envelope spines -
specific receptors. 2- Penetration and removal of viral
envelopes: Uncoating & Penetration 3- Eclipse: Period of eclipse: a period of loss
of infectious ability and the inside of the cell is not seen.
4- Synthesis of viral components within the cell : Synthesis Viral Intracellular manufacture of copies of
viral acid and viral proteins (early) and then structural (late). 5- Assembly and assembly
in the nucleus or cytoplasm of the host cell . - Either by bursting the host cell
and liberating the viruses from it (non-enveloped viruses) -
Or by budding: Pudding acquires its lipid protein envelope from the nuclear or cytoplasmic
membrane
for the added cell
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8. Viral growth curve
• Latent Period: The time between the onset of infection and the appearance of the virus
The virus continues to accumulate
• Ranging from minutes (phages) ÿ hours (human viruses) • Eclipse
period: virus disappears but DNA
outside the cell
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9. Classification of viruses
Viruses
• Chemical and morphological criteria
are used • The two viral components used in classification are:
ÿ DNA (its molecular weight and structure) ÿ
Capsula (its size, regularity and encapsulation)
Many criteria were used such as sensitivity to ester, type of infected tissues
or clinical syndromes caused by them (intestinal viruses, neurogenic ...)
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10. Atypical virus-like agents
3. Viroids: a single cyclic RNA without a protein coat or . It multiplies and causes
plant diseases, and no human disease has been known to happen to
it. . Prions: raw protein granules without nucleic acid. Slow diseases (Creutzfeldt
- Jacob), resistant to radiation, heat and acids , inactivated by hypochlorite, NaOH
and autoclave.
4
envelope
1
. Defective viruses: nucleic acid + protein, but they cannot replicate without a
helper virus because of a mutation or deletion of part of their genetic material (all
viruses, during their replication, produce more defective viruses than infective
ones, 1/100 are assumed to have a role in healing, as they affect the growth of
infective viruses).
2. Pseudovirions: contain the host DNA within the capsule
instead of the virus DNA. due to host cell DNA
fragmentation . Crude but
.
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12. Pathogensis of Viral Infection • First :
Infected cell 4 main effects of viral infection: 1.
Bodies Inclusion : proteins or viral
granules in the nucleus or
cytoplasm ÿ Diagnostic importance (Negry bodies in the dog virus) 2.
Death : Inhibition of macromolecule synthesis Inhibition of
host cell proteins synthesis and then inhibition of RNA, DNA
synthesis as a secondary
effect 3 Cell fusion and formation of giant cells: characteristic of
herpesviruses and paramyxoviruses due to the
implantation of viral proteins in the
cell membrane . No morphological or
5
4
.
.
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13. Pathogenic mechanisms of viral infections
Pathogensis of viral infection
• Second: The Patient Infected: The pathogenicity of
the infected patient includes : 1. Transmission
and entry of the virus 2.
Replication and damage to
cells of other organs 3. Spread of the virus to cells
and 4. The immune response as a defense and a
contributor to disease 5. Recovery or the persistence of the virus in
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14. Pathogenicity - transmission
• 5- Placenta: from mother to fetus (German measles and
CMV) • 6-
Organ transfer: transplantation of a graft from a donor carrying CMV virus
– Entry of viruses into the body: • 1-
Respiratory tract: through respiratory droplets or direct contact – remains local (cold) or spreads to become
systemic (mumps virus) • 2- Digestive
tract: viruses that tolerate heartburn and bile salts (coated are damaged by these factors) • 3- Urogenital
tract : local infections (herpes simplex virus type 2) or systemic
Generalized (hepatitis B and AIDS)
• 4- Skin: localized (human papillomavirus that causes warts) or circulating and
causing systemic diseases (hepatitis D, C, B and AIDS) ÿ
or surgical contaminants
to arrive
Arthropodsbite via via
skin penetrate
and cutting
tools, syringes, penetrating needles , and /or infected
legs of bitten animals
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15. Target organs and tissues in viral infections The
virus spreads
in the body through the lymph, blood, rarely the nerves, then it
goes to the target organs, the most
important of which are: 1- Skin: Human
papillomavirus. CAM: It is reached by the bloody route or through t
-2
3- Liver: Hepatitis
viruses. 4- Blood:
HIV. 5- Other tissues: salivary glands: mumps v
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16. Host defenses in viral infections
• Non-specific defenses: 1-
Interferons: glycoproteins produced by cells after exposure to stimuli, including viruses ÿ ÿ:
produced by leukocytes ÿ ÿ:
produced by fibroblasts
gamma ÿ: produced by
lymphocytes - appear within 48 hours (faster than antibodies) - their effect is nonspecific - they do not
affect
Except after the virus enters the cells - Prevents the translation of viral mRNA ÿ
disables the synthesis of viral proteins - Human interferon prepared by genetic engineering methods is use
2- Phagocytosis : macrophages in the reticuloendothelial system and alveolar
macrophages 3- Fever: disruption of the viral envelopes and decreases virus
replication 4- Mucociliary cleaning: smoking increases the frequency of respiratory
viral infections 5- Factors that modify host
defenses : ÿ Age: the two extremes of age
are the most ÿ Ingestion of
corticosteroidsaffect
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17. Host defenses in viral infections
• Specific defenses : • First:
active immunity • Cellular immunity:
very important • Mononuclear and
lymphocytic infiltration is characteristic of viral infection • It dissolves
viruses or produces cytokines and interferons • Toxic T cells
attack viral antigens within the cell membrane ÿ cell death • cause systemic symptoms. •
Some viral infections may
inhibit cellular immunity: negative tuberculin test after measles infection. • Humoral immunity: protects
against a second infection by forming modified antibodies that prevent the virus from attaching to
receptors. Or it prevents shedding of the coat, thus inhibiting replication and
facilitating phagocytosis • Complement antigen-antigen complexes may activate, causing tissue
damage (chronic hepatitis B) • IgA is important in viruses that enter the respiratory and alimentary route / IgG -
be in
blood. • Second: Passive
immunity - with human serum
containing antibodies - is s
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18. Clinical forms of viral infections:
• Incubation period: from entry of the virus until symptoms
appear, short or
long. • Precursors: general symptoms,
not specific ones. • Viral infection: accidental or asymptomatic,
acute or chronic, local or sy
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19. Clinical forms of viral infections:
Incubation for months or years without
symptoms such as HIV or prion-causing infections (koro disease and clinical
insanity).
-4
Slow virus infections
Latent
viral: infection
-5
:
:
:
clinical -1
Persistent without or with
symptoms) Herpes simplex virus (viral production
stops but virus reactivation intermitten
under
-3
2- Infections that are
not visible
at the site
of
infection
Persistent
chronic viral infection
: Like hepatitis B. (Production of the virus
Local or systemic
incubation, short: at the site of virus entry without viremia . It leaves short-
term immunity. The essential role of IgA. Cold viruses after entry spread blood or
lymph. long incubation. long term. It is
useful to give
gamma globulin to the patient's contacts
immunity
Systemic: infection
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20. Diagnosis of viral infections
• Direct detection of the virus: -
Seeing it with a
microscope - or cultivating it on
private farms - or detecting one of its antigens or
its DNA. • Indirect
detection: - Detection
of antibodies through serological tests
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21. Diagnosis
• Direct detection :
1- Light microscopy: large viruses such as smallpox or
sighting (Negri bodies in X infected with
rabies virus) - Tzanck smear (H.
torticollis in herpes virus) 2- Electron microscopy :
after staining with special dyes 3- Immunoelectron microscopy: by adding
specific
antibodies 4- Immunofluorescence microscope : fluorescein
- tagged antibodies 5- Immunoassays : enzymatic ELISA
or radiological RIA 6- DNA hybridization:
DNA probes 7- Polymerase chain reaction (PCR): the most
specific and sensitive 8- Virus isolation Implantation of viruses on tissue
cultures, chicken egg embryos, or laboratory an
entries
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22. Methods of cultivating viruses First : Tissue cultures:
human or animal tissue that detects virus
replication through: 1- Detection of cellular
pathological effects: CPE
(cell death - becomes round and gathers like clusters - forming bulky cells) 2-
Formation Plaque
3- Formation of bodies of inclusion or
inclusion: inside the nuclei or inside the cytoplasm
6- Staining with antibodies and fluorescence: Staining Antibody
Fluorescent: Detection Of Viral Antigens 7-8 Neutralization
viral: Second: Fertilized eggs or chicken
embryos Third: Whole animals:
white mice, rabbits and guinea pig.
4- Transformation of cells into malignant cells:
Transformation in the form of veins 5- Haemadsorption: agglutinati
Rosettes
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23. Diagnosis
Dermatological tests
• Indirect detection : •
Serological diagnosis: elevation of virus antibodies 4-fold or more at intervals
of 2-3 weeks . • IgM
detection: indicates acute infection or recent infection. In the newborn, it
indicates an infection acquired inside the uterus because it does
not cross the placenta • Among the serological tests used: virus modification
test - complement fixation - scintillation or immunofluorescence - ELISA -
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24. Treatment of viral infections Difficult
due to the presence of the virus inside the cells and the difficulty of selectively
affecting the virus without affecting the host cells.
• 1- Antiviral drugs: target enzymes or affect the stages of viral replication -
Nucleoside
homologs : Acyclovir (Herophrenia) - Ganciclovir (CMV) - Ribavirin (Hepatitis C) -
Nucleotide
homologues: cidofovir ( Herophrenia) - RT
inhibitors : Treatment of the AIDS virus - Protease inhibitors :
terminate the action of the enzyme required to replicate the
virus -
Amantadine and Ramantadine: Synthetic - prevent penetration of the
virus (influenza A virus)
• 2- Interferons : Recombinant human interferon-ÿ (prepared by genetic engineering me
B,C viral
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25. Prevention of viral infections - active immunity
•
the murdered
naked DNA
It is given to pregnant women and immunocompromised. (Risk of
reactivation) Hepatitis B
-2
live weakened:
-5
against
-1
=
viral antigens
Genetic engineering
preparedsynthetic
vaccines- 3 - viral -
4 peptides
of
constituent antibodies
virus
The use of
antibodies
immune response and incitement
•
•
•
•
:
•
:
• Viral vaccines: complete
virus units that have lost their infectious ability - they are given safely to
pregnant women and those with weak immunity - they leave short-term immunity and need
supportive doses - they do not induce local
immunity at the place of entry. Weakened by repeated cultivation
in an animal host or tissue culture: Induce long-term humoral immunity - Induce good
cellular immunity - Induce local immunity at
the place of its entry. • Its half-life is limited, it is damaged by heat, and it is not left at room temperat
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26. Prevention of viral infections - passive immunity
• Passive immunization: Serums containing specific antibodies to
viruses - useful for rapid prevention after exposure to a dangerous
virus - rabies or hepatitis B. Rapid but short-term.
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