Microbiology Department FK Umsu

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MICROBIOLOGY DEPARTMENT FK UMSU

Viruses only exist to make more


viruses.

The structure of viruses allows


them to succeed in their main
mission  reproduction
LYTIC CYCLE
Once attached to a host cell, the virus injects its nucleic acid
into cell and take over the operation to produce multiple
copies of the virus. As the host cells filled with newly
assembled virus, it burst.
LYSOGENIC CYCLE
Some virus may enter host and remain hidden for years and
doesn’t seem to affect cell function. At some point, it can
become active and take over the cell, then destroy the host
cells.
Transcripti Assembly
ATTACHM Penetration Uncoating on and and
ENT
Translation Release
Adsorption
 Highly specific, the surface of
the virion contains structures
that interact receptors on the
surface of the host cell. It
defines and limits the host
species and type of cell that can
be infected by a particular
virus. Damage to the binding
sites on the virion or blocking
by specific antibodies
(neutralization) can render
virions non-infectious.
Receptors are involved
in adsorption
Spikes and phage tails may carry attachment protein
PENETRATION
The process whereby
the virion enters the
cell;
as a result of direct
fusion of the viral
envelope with the
plasma membrane of
the cell or
endocytosis.
Uncoating
The protein coat of the virion
dissociates and the viral genome is
released into the cytoplasm.
Transcription and
Translation
Transcription and translation of viral
mRNA and synthesis of the structural
"late" proteins which are needed to make
new virions.
 DNA viruses are mostly ds while RNA viruses are
ss.
 RNA mutation rate is higher than DNA (because
host DNA polymerase has refining activity)
 DNA replication takes place in the nucleus while
RNA replication takes place in cytoplasm.
 DNA viruses are stable while RNA viruses
areunstable.
 DNA viruses injected their viral genetic code into
the host DNA for duplication and decoding. RNA
viruses skip DNA for duplication and decoding.
Assembly
The proteins self-assemble
and a genome enters each
new capsid. This takes place
either in the nucleus or in the
cytoplasm of the cell, or
sometimes, just beneath the
cell surface.
Release
Release of new infectious
virions is the final stage of
replication. This may occur
either by budding from
plasma membrane (for
enveloped viruses), or else
by disintegration (lysis) of
the infected cell (for non-
enveloped viruses). Some
viruses use the secretory
pathway to exit the cell.
 Viruses that infects only bacterias
 A major factor that
control which cell type a
virus can infect
 presence of certain
receptor on the cell
surface to which the
virus must attach in order
to gain entry into cell
 Horizontal (from one host to another between two individuals)
 Vertical (from
mother to
fetus)
 Sometimes there are needs of isolation
 Most important are mucosa
of respiratory and
gastrointestinal tract.
 Intact epidermis presents a
barriero viruses (but maybe
overcome through
microtrauma or mechanical
inoculation – bloodsucking
arthropoda)
Localized
Disseminated (eg: axonal)
Generalized viremia /
Lymphatics
Generalized infection

Viruses usually
replicate at portal of
entry andthen
disseminated via the
lymphatic or blood
stream.
Example: polioviruses,
measles
Time from exposure to an organism to the
onset of clinical disease
 may vary from 1 days to years
Implantation of
virus at portal
of entry

Sites of
shedding Local
viruses to replication
environtment

Spread to
target organs
Accessibility of virus to tissue
Cell susceptibility to virus multiplication
Virus susceptibility to host defenses
DIRECT CELL DAMAGE: INDIRECT CELL DAMAGE:
 Diversion of the cell’s energy  Integration of viral genome
 Shutoff of the cell  Induction of mutatons inthe
maromolecular synthesis host genome
 Competition of viral mRNA  Inflammation
for cellular ribosomes  Host immune response
 Inhibition of the interferon
defense mechanism
Organ damage caused by viruses is
mainly DEGENERATIVE nature.
Inflammatory reactions are secondary
process.
Infections may go unnoticed if cell
destructions is insignificant  silent /
subclinical infection
Due to
destroyed
infected cells
Exacerbation of
infection
Complex
Immunological
formed with
process
viral component
Heal/subdue
infection
Normal cells Transformed cells
Non specific  innate immunity.
Recognizes acromolecules expressed
by microbial pathogens (PAMP).
Specific (humoral and cellular)
specific virus-induced defense
mechanism and must be activated by
antigen presented.
 Different signal
different pathway
Most viral infections are self-limiting,
resulting in either clearance of the pathogen or
death of the host. However, a subset
of viruses can establish
permanent infection and persist indefinitely
within the host.
Take an example of a virus, WHAT DO WE NEED TO KNOW?
 Michael T Madigan_ Kelly S Bender_ Daniel Hezekiah Buckley_ W Matthew Sattley_
David Allan Stahl-Brock Biology of Microorganisms-Pearson (2019)
 Tortora G.J., Funke B.R., Case C.L.-Microbiology_ An introduction-Pearson (2013)

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