Virus-Cell Interactions and Infections
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1
cellular
tropism
of
viruses
is
determined
by the
presence
of
appropriate
cellular
receptors
and
frequently,
cell-type
specific
transmission factor.
Viruses
typically
encode
genes
that
modulate
host-cell
function
for
their
own
benefit
and of
course
the
host
has
elaborate
innate
defense
to
restrict
viral
functions.
Thus
the
viral
and cellular
factor
that
influence
the
outcome
of
infection
are
often
in
delicate
balance
and
easily
shifted
one
way
or
the
other.
Virus
infection
causes
a
wide
variety
of
potentiality
victorious
changes
in
the
many
different kinds
of
cells
that
occur
in
the
animal
host.
The
disruption
of
cellular
function,
the
induction
of cell
death
or
transformation
or
the
activation
of
an
inappropriate
immune
response
are
all potentiality
manifested
as
disease
by
the
infected
host.
Many
virus-cell
interactions
are
transient
and
asynchronous,
involving
intermediate
steps
on
the pathway,
each
featuring
dynamic
interactions
between
different
viral
and
cellular
components.
V
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T
Y
P
E
S
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F
V
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C
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L
L
I
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T
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R
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C
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N
Viral
infection
may
be
Cytocidal
or
non
cytocydal
and
productive
or
non-productive
that
is,
not all
infection
leads
to
cell
death
or
the
production
and
release
of
new
versions.
However
criticalchanges
can
occur
in
virus
infected
cells
regardless
of
whether
the
infection
is
productive
or
not.
Some
of
the
most
important
of
all
nonproductive
virus
cell
interactions
are
those
associated
with
persistent
infections
or
latent
infections.
The
term
persistent
infection
simply
describes
an infection
that
lasts
a
long
time.
The
term
latent
infection
describes
an
infection
that
"exists
but
is not
exhibited,"
i.e.,
an
infection
in
which
infectious
virions
is
not
formed.
In
either
case,
the
virus or
its
genome
is
maintained
indefinitely
in
the
cell,
either
by
the
integration
of
the
viral
nucleic acid
into
the
host
cell
DNA
or
by
carriage
of
the
viral
nucleic
acid
in
the
form
of
an
episome.
In these
instances,
the
cell
survives,
indeed
may
divide
repeatedly.
In
some
instances
such
cells
never
release
virions,
in
others
the
infection
may
become
productive
when
induced
by
an appropriate
stimulus.
Persistent
or
latent
infections
may
also
be
associated
with
cell
transformation.
The
various
types
of
interaction
that
can
occur
between
virus
and
cell
are summarized.
FIGURE:
VIRUS-CELLINTERACTION
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T
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V
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Figure:
Unstained
confluent
monolayers
of
the
three
main
types
of
cultured
cells
as
they
appear
by
low
power
light
microscopy
through
the
wall
of
the
glass
or
plastic
flask
in
which
they
form
a
monolayer.
(A)
Primary
monkey
kidney
epithelial
cells
obtained
directly
by
the
dissociation
of
cells
from
a
kidney;
this
produces
a
mixed
population
of
mainly
epithelial
cells.
(B)
Diploid
cell
line
of
fetal
fibroblasts.
(C)
Continuous
line
of
malignant
epithelial
cells.
C
Y
T
O
C
I
D
A
L
C
H
A
N
G
E
S
I
N
V
I
R
U
S
-
I
N
F
E
C
T
E
D
C
E
L
L
S
Cytopathic
viruses
kill
the
cells
in
which
they
replicate.
When
a
monolayer
of
cultured
cells
is inoculated
with
a
cytopathic
virus,
the
first
round
of
infection
yields
progeny
virus
that
spreads through
the
medium
to
infect
adjacent
as
well
as
distant
cells
eventually
all
cells
in
the
culture may
become
infected.
The
resulting
cell
damage
is
known
as
a
cytopathic
effect
(CPE).
Cytopathic
effect
can
usually
be
observed
by
low-power
light
microscopy
of
unstained
cell cultures.
M
e
c
h
a
n
i
s
m
s
o
f
C
e
l
l
D
a
m
a
g
e
So
many
pathophysiologic
changes
occur
in
cells
infected
with
cytopathic
viruses
that
the
death of
the
cell
usually
cannot
be
attributed
to
any
particular
event;
rather,
cell
death
may
be
the
final result
of
the
cumulative
action
of
many
insults.
I
n
h
i
b
i
t
i
o
n
o
f
H
o
s
t
C
e
l
l
N
u
c
l
e
i
c
A
c
i
d
S
y
n
t
h
e
s
i
s
Inhibition
of
host
cell
DNA
synthesis
is
common
in
viral
infections.
It
is
an
inevitable consequence
of
viral
inhibition
of
host
cell
protein
synthesis
and
its
effect
on
the
machinery
of DNA
replication,
but
some
viruses
employ
more
specific
mechanisms.
For
example,
poxviruses produce
a
DNAse
that
degrades
cellular
DNA,
and
herpes
viruses
specifically
displace
the synthesis
of
host
cell
DNA
with
their
own
synthetic
processes.
I
n
h
i
b
i
t
i
o
n
o
f
H
o
s
t
C
e
l
l
R
N
A
T
r
a
n
s
c
r
i
p
t
i
o
n
Many different classes of viruses including poxviruses, rhabdoviruses, reoviruses,
paramyxoviruses,
and
picornaviruses,
inhibit
host
cell
RNA
transcription.
In
some
instances,
this inhibition
may
be
the
indirect
consequence
of
viral
effects
on
host
cell
protein
synthesis,
which decreases
the
availability
of
transcription
factors
required
for
RNA
polymerase
activity.
In
other instances,
viruses
encode
specific
transcription
factors
for
the
purpose
of
regulating
the
expression
of
their
own
genes
and,
in
some
instances;
these
factors
modulate
the
expression
of
cellular
genes as
well.
For
example,
herpesviruses
encode
proteins
that
bind
directly
to
specific
viral
DNA sequences,
thereby
regulating
the
transcription
of
viral
genes.
Figure:
Cytopathic
effects
produced
by
different
viruses.
The
cell
monolayers
are
shown
as
they
would
normally
be
viewed
in
the
laboratory,
unfixed
and
unstained.
(A)
Typical
cytopathology
of
an
enterovirus:
rapid
rounding
of
cells,
progressing
to
complete
cell
lysis.
(B)
Typical
cytopathology
of
a
herpesvirus:
focal
areas
of
swollen
rounded
cells.
(C)
Typical
cytopathology
of
a
paramyxovirus:
focal
clusters
of
cells
are
fused
to
form
syncytia.
(D)
Hemadsorption:
erythrocytes
adsorb
to
infected
cells
that
have
incorporated
hemagglutinin
into
the
plasma
membrane
.
I
n
h
i
b
i
t
i
o
n
o
f
P
r
o
c
e
s
s
i
n
g
o
f
H
o
s
t
C
e
l
l
m
R
N
A
s
Many
viruses,
including
vesicular
stomatitis
viruses,
influenza
viruses,
and
herpesviruses, interfere
with
the
splicing
of
cellular
primary
mRNA
transcripts
that
are
needed
to
form
mature mRNAs.
In
some
instances,
spliceosomes
are
formed,
but
subsequent
catalytic
steps
are
inhibited.
For
example,
a
protein
synthesized
in
herpesvirus-
infected
cells
suppresses
RNA
splicing
and leads
to
reduced
amounts
of
cellular
mRNAs
and
the
accumulation
of
primarymRNA
transcripts.
I
n
h
i
b
i
t
i
o
n
o
f
H
o
s
t
C
e
l
l
P
r
o
t
e
i
n
S
y
n
t
h
e
s
i
s
The
shutdown
of
host
cell
protein
synthesis,
while
viral
protein
synthesis
continues,
is
a characteristic
of
many
virus
infections.
This
shutdown
is
particularly
rapid
and
profound
in picornavirus
infections,
but
it
is
also
pronounced
in
togavirus,
influenzavirus,
rhabdovirus, poxvirus,
and
herpesvirus
infections.
With
some
other
viruses,
the
shutdown
occurs
late
in
the course
of
infection
and
is
more
gradual,
whereas
with
noncytocidal
viruses,
such
as
pestiviruses, arenaviruses,
and
retroviruses,
there
is
no
shutdown
and
no
cell
death.
The
mechanisms underlying
the
shutdown
of
host
cell
protein
synthesis
are
varied:
some
are
as
mentioned
earlier, whereas
others
include
(1)
the
production
of
viral
enzymes
that
degrade
cellular
mRNAs,
(2)
the
production
of
factors
that
bind
to
ribosomes
and
inhibit
cellular
mRNA
translation,
and
(3)
the alteration
of
the
intracellular
ionic
environment
favoring
the
translation
of
viral
mRNAs
over cellular
mRNAs.
Most
importantly,
some
viral
mRNAs
simply
out
compete
cellular
mRNAs
for cellular
translation
machinery
by
mass
action;
i.e.,
the
large
excess
of
viral
mRNA
outcompetes cellular
mRNA
for
host
ribosomes.
Viral
proteins
may
also
inhibit
the
processing
and
transport
of cellular
proteins
from
the
endoplasmic
reticulum,
and
this
inhibition
may
lead
to
their degradation.
This
effect
is
seen
in
lentivirus
and
adenovirus
infections.
C
y
t
o
p
a
t
h
i
c
E
f
f
e
c
t
s
o
f
T
o
x
i
c
V
i
r
a
l
P
r
o
t
e
i
n
s
Large
amounts
of
various
viral
components
may
accumulate
in
the
cell
late
in
infection.
Most
cell
damage
has
been
recognized
as
the
supervening
of viral
replication
events
on
cellular
events.
Some exceptions
for
example,
the
toxicity
of
adenovirus
penton
and
fiber
proteins
seems
direct and
independent
of
adenovirus
replication.
C
y
t
o
p
a
t
h
i
c
C
h
a
n
g
e
s
I
n
v
o
l
v
i
n
g
C
e
l
l
M
e
m
b
r
a
n
e
s
Cellular
membranes
participate
in
many
phases
of
viral
replication,
from
viral
attachment
and entry,
to
the
formation
of
replication
complexes,
to
virion
assembly.
Viruses
may
alter
plasma
membrane
permeability,
affect
ion
exchange
and
membrane
potential,
induce
the
synthesis
of
new intracellular
membranes,
and
induce
the
rearrangement
of
previously
existing
membranes.
A generalized
increase
in
membrane
permeability,
detected
by
entry
into
cells
of
normally
excluded macromolecules
or
escapes
of
intracellular
molecules,
occurs
early
during
picornavirus, alphavirus,
reovirus,
rhabdovirus,
and
adenovirus
infections.
Most
importantly,
enveloped
viruses also
direct
the
insertion
of
their
surface
glycoproteins,
including
fusion
proteins,
into
host
cell membranes
as
part
of
their
budding
process,
often
leading
to
membrane
fusion
and
syncytium formation.
C
e
l
l
M
e
m
b
r
a
n
e
F
u
s
i
o
n
a
n
d
S
y
n
c
y
t
i
u
m
F
o
r
m
a
t
i
o
n
A
conspicuous
feature
of
infection
of
cell
monolayers
by
lentiviruses,
paramyxoviruses, morbilliviruses,
pneumoviruses,
some
herpesviruses,
and
some
other
viruses
is
the
production
of
syncytia
which
result
from
the
fusion
of
an
infected
cell
with neighboring
infected
or
uninfected
cells.
Such
syncytia
may
represent
an
important
mechanism
of
viral
spread
in
tissues. Cell membrane
fusion
is
mediated
by
viral
fusion
proteins
or
fusion
domains.
N
O
N
-
C
Y
T
O
C
I
D
A
L
C
H
A
N
G
E
S
I
N
V
I
R
U
S
-
I
N
F
E
C
T
E
D
C
E
L
L
S
Non-Cytocidal
viruses
usually
don’t
kill
cell
in
which
they
will
replicate.
On
the
contrary,
they often
cause
persistent
infection,
in
which
infected
cell
produce
and
release
virions
but
overall cellular
metabolism
is
little
affected.
In
many
instances
the
infected
cells
even
continue
grow
and divided.
E
f
f
e
c
t
o
f
N
o
n
-
C
y
t
o
c
i
d
a
l
V
i
r
a
l
I
n
f
e
c
t
i
o
n
o
n
F
u
n
c
t
i
o
n
o
f
S
p
e
c
i
a
l
i
z
e
d
C
e
l
l
Some
viruses
such
as
pestiviruss,
arenaviruses
and
retroviruses
that
do
not
shut
down
host
cell DNA,
RNA
or
protein
synthesis
or
do
not
killed
their
host
cell
produce
important pathophysiologic
changes
in
their
host
by
affecting
crucial
functions
that
are
neither
associated with
the
integrity
of
the
cells
or
their
basic
housekeeping
functions.
I
n
c
l
u
s
i
o
n
B
o
d
i
e
s
A
characteristic
morphological
change
in
cells
infected
by
certain
virus
is
the
formation
of Inclusion
Bodies,
which
may
be
recognized
by
light
microscopy
following
fixation
and
staining.
Depending
on
the
virus
Inclusion
Bodies
may
be
intranuclear
or
intracytoplasmic,
single
or multiple,
large
or
small,
round
or
irregular
shape
and
acidophilic
or
basophilic.
P
o
l
a
r
i
t
y
o
f
V
i
r
a
l
I
n
f
e
c
t
i
o
n
In
the
course
of
their
replication
viruses
belonging
to
several
families
of
enveloped
virus
insert their
glycoprotein
into
plasma
membrane
of
their
host
cell,this
insertion
is
not
a
random
matter.
For
example
in
reservoir
host
species
rabies
virus
is
shed
from
the
apical
surface
of
salivary
gland epithelial
cells
where
it
enters
the
saliva
and
is
transmitted
by
bite.
However,
lentiviruses
bud from
basolateral
plasma
membranes
and
pass
directly
from
cell
to
cell
or
become
disseminated through
tissue
spaces
and
the
bloodstream.
U
l
t
r
a
s
t
r
u
c
t
u
r
a
l
C
h
a
n
g
e
s
i
n
V
i
r
u
s
-
I
n
f
e
c
t
e
d
C
e
l
l
s
Early
changes
in
cell
structure often
are
dominated
by
proliferation
of
various
cell
membranes:
for
example,
herpesviruses
cause increased
synthesis,
even
reduplication,
of
nuclear
membranes;
flaviviruses
cause
proliferation
of the
endoplasmic
reticulum;
picornaviruses
and
caliciviruses
cause
a
distinctive
proliferation
of vesicles
in
the
cytoplasm;
and
many
retroviruses
cause
peculiar
fusions
of
cytoplasmic
membranes.
Other
ultrastructural
changes
that
are
prominent
in
many
viral
infections
include disruption
of
cytoskeletal
elements,
mitochondrial
damage,
and
changes
in
the
density
of
the cytosol.
Late
in
the
course
of
infection,
many
cytolytic
viruses
cause
nuclear,
organelle,
and cytoplasmic
rarefaction
and/or
condensation,
with
terminal
loss
of
host
cell
membrane
integrity.
Viral infections exhibit diverse cellular tropism based on receptor interactions, impacting cell function through modulation and potential host defense responses. Infections can lead to various outcomes, from cell death to persistent or latent states, with nuanced effects on cellular behavior. Different virus-cell interactions highlight the complexity and consequences of viral infections on host cells.
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Page|1 VIRUS VIRUS- -CELL CELLINTERACTION INTERACTION cellular tropism of viruses is determined by the presence of appropriate cellular receptors and frequently, cell-type specific transmission factor. Viruses typically encode genes that modulate host-cell function for their own benefit and of course the host has elaborate innate defense to restrict viral functions. Thus the viral and cellular factor that influence the outcome of infection are often in delicate balance and easily shifted one way or the other. Virus infection causes a wide variety of potentiality victorious changes in the many different kinds of cells that occur in the animal host. The disruption of cellular function, the induction of cell death or transformation or the activation of an inappropriate immune response are all potentiality manifested as disease by the infected host. Many virus-cell interactions are transient and asynchronous, involving intermediate steps on the pathway, each featuring dynamic interactions between different viral and cellular components.
Page|2 TYPES TYPESOF Viral infection may be Cytocidal or non cytocydal and productive or non-productive that is, not all infection leads to cell death or the production and release of new versions. However criticalchanges can occur in virus infected cells regardless of whether the infection is productive or not. Some of the most important of all nonproductive virus cell interactions are those associated with persistentinfections or latentinfections. The term persistent infection simply describes an infection that lasts a long time. The term latent infection describes an infection that "exists but is not exhibited," i.e., an infection in which infectious virions is not formed. In either case, the virus or its genome is maintained indefinitely in the cell, either by the integration of the viral nucleic acid into the host cell DNA or by carriage of the viral nucleic acid in the form of an episome. In these instances, the cell survives, indeed may divide repeatedly. In some instances such cells never release virions, in others the infection may become productive when induced by an appropriate stimulus. Persistent or latent infections may also be associated with cell transformation. The various types of interaction that can occur between virus and cell are summarized. OFVIRUS VIRUS- -CELL CELLINTERACTION INTERACTION FIGURE: VIRUS-CELLINTERACTION
Page|3 Types Typesof ofVirus Virus- -Cell CellInteraction Interaction TYPE OF INFECTION PRODUCTION OF INFECTIOUS VIRIONS EFFECTS ON CELL EXAMPLES Cytocidal Morphologic changes in Cells (cytopathic effects); Inhibition of protein, RNA and DNAsynthesis; Cell death Alphaherpesviruses, enteroviruses, Reoviruses Yes No cytopathic effect; Little metabolic disturbance; cells Continue to divide; may Be loss of the special Functions of some Differentiated cells Pestiviruses, Persistent, productive Arenaviruses, rabies virus, most Retroviruses Yes Persistent, nonproductive Canine distemper Virus in brain Polyomavirus, Adenoviruses No,but virus may Be Induced Usually nil Alteration in cell morphology; cells can be Passaged indefinitely; May produce tumors When transplanted to Experimental animals No, oncogenic Murine, avian leukosis, and DNA viruses Transformation sarcoma Viruses Yes, oncogenic retroviruses
Page|4 Figure: Unstained confluent monolayers of the three main types of cultured cells as they appear by low power light microscopy through the wall of the glass or plastic flask in which they form a monolayer. (A) Primary monkey kidney epithelial cells obtained directly by the dissociation of cells from a kidney; this produces a mixed population of mainly epithelial cells. (B) Diploid cell line of fetal fibroblasts. (C) Continuous line of malignant epithelial cells. CYTOCIDAL CYTOCIDALCHANGES CHANGESIN INVIRUS VIRUS- -INFECTED INFECTEDCELLS CELLS Cytopathic viruses kill the cells in which they replicate. When a monolayer of cultured cells is inoculated with a cytopathic virus, the first round of infection yields progeny virus that spreads through the medium to infect adjacent as well as distant cells eventually all cells in the culture may become infected. The resulting cell damage is known as a cytopathiceffect (CPE). Cytopathic effect can usually be observed by low-power light microscopy of unstained cell cultures. Mechanisms Mechanismsof So many pathophysiologic changes occur in cells infected with cytopathic viruses that the death of the cell usually cannot be attributed to any particular event; rather, cell death may be the final result of the cumulative action of many insults. ofCell CellDamage Damage
Inhibition Inhibitionof ofHost HostCell CellNucleic NucleicAcid AcidSynthesis Synthesis Inhibition of host cell DNA synthesis is common in viral infections. It is an inevitable consequence of viral inhibition of host cell protein synthesis and its effect on the machinery of DNA replication, but some viruses employ more specific mechanisms. For example, poxviruses produce a DNAse that degrades cellular DNA, and herpes viruses specifically displace the synthesis of host cell DNA with their own synthetic processes. Inhibition Inhibitionof ofHost HostCell CellRNA RNATranscription Transcription Many different classes of viruses including poxviruses, rhabdoviruses, reoviruses, paramyxoviruses, and picornaviruses, inhibit host cell RNA transcription. In some instances, this inhibition may be the indirect consequence of viral effects on host cell protein synthesis, which decreases the availability of transcription factors required for RNA polymerase activity. In other instances, viruses encode specific transcription factors for the purpose of regulating the expression of their own genes and, in some instances; these factors modulate the expression of cellular genes as well. For example, herpesviruses encode proteins that bind directly to specific viral DNA sequences, thereby regulating the transcription of viral genes. Figure: Cytopathic effects produced by different viruses. The cell monolayers are shown as they would normally be viewed in the laboratory, unfixed and unstained. (A) Typical cytopathology of an enterovirus: rapid rounding of cells, progressing to complete cell lysis. (B) Typical cytopathology of a herpesvirus: focal areas of swollen rounded cells. (C) Typical cytopathology of a paramyxovirus: focal clusters of cells are fused to form syncytia. (D) Hemadsorption: erythrocytes adsorb to infected cells that have incorporated hemagglutinin into the plasma membrane.
Inhibition Inhibitionof Many viruses, including vesicular stomatitis viruses, influenza viruses, and herpesviruses, interfere with the splicing of cellular primary mRNA transcripts that are needed to form mature mRNAs. In some instances, spliceosomes are formed, but subsequent catalytic steps are inhibited. For example, a protein synthesized in herpesvirus- infected cells suppresses RNA splicing and leads to reduced amounts of cellular mRNAs and the accumulation of primarymRNA transcripts. ofProcessing Processingof ofHost HostCell CellmRNAs mRNAs Inhibition Inhibitionof ofHost HostCell CellProtein ProteinSynthesis Synthesis The shutdown of host cell protein synthesis, while viral protein synthesis continues, is a characteristic of many virus infections. This shutdown is particularly rapid and profound in picornavirus infections, but it is also pronounced in togavirus, influenzavirus, rhabdovirus, poxvirus, and herpesvirus infections. With some other viruses, the shutdown occurs late in the course of infection and is more gradual, whereas with noncytocidal viruses, such as pestiviruses, arenaviruses, and retroviruses, there is no shutdown and no cell death. The mechanisms underlying the shutdown of host cell protein synthesis are varied: some are as mentioned earlier, whereas others include (1) the production of viral enzymes that degrade cellular mRNAs, (2) the production of factors that bind to ribosomes and inhibit cellular mRNA translation, and (3) the alteration of the intracellular ionic environment favoring the translation of viral mRNAs over cellular mRNAs. Most importantly, some viral mRNAs simply out compete cellular mRNAs for cellular translation machinery by mass action; i.e., the large excess of viral mRNA outcompetes cellular mRNA for host ribosomes. Viral proteins may also inhibit the processing and transport of cellular proteins from the endoplasmic reticulum, and this inhibition may lead to their degradation. This effect is seen in lentivirus and adenovirus infections. Cytopathic CytopathicEffects Effectsof ofToxic ToxicViral ViralProteins Proteins Large amounts of various viral components may accumulate in the cell late in infection. Most cell damage has been recognized as the supervening of viral replication events on cellular events. Some exceptions for example, the toxicity of adenovirus penton and fiber proteins seems direct and independent of adenovirus replication. Cytopathic CytopathicChanges ChangesInvolving InvolvingCell CellMembranes Membranes Cellular membranes participate in many phases of viral replication, from viral attachment and entry, to the formation of replication complexes, to virion assembly. Viruses may alter plasma
membrane permeability, affect ion exchange and membrane potential, induce the synthesis of new intracellular membranes, and induce the rearrangement of previously existing membranes. A generalized increase in membrane permeability, detected by entry into cells of normally excluded macromolecules or escapes of intracellular molecules, occurs early during picornavirus, alphavirus, reovirus, rhabdovirus, and adenovirus infections. Most importantly, enveloped viruses also direct the insertion of their surface glycoproteins, including fusion proteins, into host cell membranes as part of their budding process, often leading to membrane fusion and syncytium formation. Cell CellMembrane MembraneFusion Fusionand andSyncytium SyncytiumFormation Formation A conspicuous feature of infection of cell monolayers by lentiviruses, paramyxoviruses, morbilliviruses, pneumoviruses, some herpesviruses, and some other viruses is the production of syncytia which result from the fusion of an infected cell with neighboring infected or uninfected cells. Such syncytia may represent an important mechanism of viral spread in tissues. Cell membrane fusion is mediated by viral fusion proteins or fusion domains. NON NON- -CYTOCIDAL CYTOCIDALCHANGES CHANGESIN INVIRUS VIRUS- -INFECTED INFECTEDCELLS CELLS Non-Cytocidal viruses usually don t kill cell in which they will replicate. On the contrary, they often cause persistent infection, in which infected cell produce and release virions but overall cellular metabolism is little affected. In many instances the infected cells even continue grow and divided. Effect Effectof ofNon Non- -Cytocidal CytocidalViral ViralInfection Infectionon onFunction Functionof ofSpecialized SpecializedCell Cell Some viruses such as pestiviruss, arenaviruses and retroviruses that do not shut down host cell DNA, RNA or protein synthesis or do not killed their host cell produce important pathophysiologic changes in their host by affecting crucial functions that are neither associated with the integrity of the cells or their basic housekeeping functions.
Inclusion InclusionBodies Bodies A characteristic morphological change in cells infected by certain virus is the formation of Inclusion Bodies, which may be recognized by light microscopy following fixation and staining. Depending on the virus Inclusion Bodies may be intranuclear or intracytoplasmic, single or multiple, large or small, round or irregular shape and acidophilic or basophilic. Polarity Polarityof ofViral ViralInfection Infection In the course of their replication viruses belonging to several families of enveloped virus insert their glycoprotein into plasma membrane of their host cell,this insertion is not a random matter. For example in reservoir host species rabies virus is shed from the apical surface of salivary gland epithelial cells where it enters the saliva and is transmitted by bite. However, lentiviruses bud from basolateral plasma membranes and pass directly from cell to cell or become disseminated through tissue spaces and the bloodstream. Ultrastructural UltrastructuralChanges Changesin inVirus Virus- -Infected InfectedCells Cells Early changes in cell structure often are dominated by proliferation of various cell membranes: for example, herpesviruses cause increased synthesis, even reduplication, of nuclear membranes; flaviviruses cause proliferation of the endoplasmic reticulum; picornaviruses and caliciviruses cause a distinctive proliferation of vesicles in the cytoplasm; and many retroviruses cause peculiar fusions of cytoplasmic membranes. Other ultrastructural changes that are prominent in many viral infections include disruption of cytoskeletal elements, mitochondrial damage, and changes in the density of the cytosol. Late in the course of infection, many cytolytic viruses cause nuclear, organelle, and cytoplasmic rarefaction and/or condensation, with terminal loss of host cell membrane integrity.
