Pathogenicity Flashcards
1
Q
episodic interruptions of the well
being of a normally healthy host (referring to the
A
lytic cycle
2
Q
However, another type of bacterial virus could ensue in
the host population - a persistent infection … called the
A
lysogenic cycle
3
Q
it is only upon the
introduction of a
virus into a __
population that
widespread disease
and host morbidity
occurs.
A
novel
4
Q
- process by which viruses cause disease; study of
effects of viral infection on the host.
A
pathogenesis
5
Q
sum total of the virus-encoded functions that
contribute to virus propagation in the infected cell, host organism,
and population
A
pathogenicity
6
Q
describes the genetic ability of members of a given specific virus population
(which can be considered to be genetically more or less equivalent) to cause a
disease and spread through a population.
A
pathogenicity
7
Q
- Thus, a major factor in the pathogenicity of a given virus is its
A
genotype
8
Q
Genetically, ___contains a large number of mutations in the spike
protein, including 30 amino acid substitutions, three short deletions and one
insertion, compared with the ancestral SARS-CoV-2.
A
omicron
9
Q
combination of expression of the viral genes controlling
pathogenicity, physiological response of the infected individual and response
of the population to the presence of the virus propagating in it – determines
severity
A
virulence
10
Q
used as a quantitative or relative measure of the pathogenicity of the
infecting virus—i.e. a virus is either pathogenic or nonpathogenic, but its
virulence is stated in relative terms (“virus A is more virulent than virus
B” or “virus strain A is more virulent in animal species Y than species Z”).
A
virulence
10
Q
individuals who have never
been exposed to any form of the virus leading to an
immune response
A
immunologically naive individuals
11
Q
a virus that can cause no disease at all due to reasons such as accumulation of
mutations in pathogenic genes
A
avirulent strain
12
Q
may be developed as complete or partial against the most virulent type
A
immunity
13
Q
study of human infectious disease caused by viruses and other pathogens (epizoology
in animals).
A
epidemiology
14
Q
study of animal infectious disease
A
epizoology
15
Q
dynamic, effective physiological responses to infectious disease have evolved in the organism
A
virus host interaction
16
Q
___respond by exploiting their naturally occurring genetic variation to
accumulate and select mutations to become wholly or partially resistant to these
responses.
A
viruses
17
Q
There is good circumstantial evidence that the specific
origin of this pis the result of an ancestral
species being infected with an immunosuppressive protoretrovirus.
A
placental mammals
18
Q
lay their eggs in caterpillars.
A
parasitic wasps
19
Q
When infected with a ___, virus
become maintained as a persistent genetic
passenger in the ovaries and egg cells of the
wasps.
A
polydnavirus
20
Q
Wasps uninfected with __have their
larvae often destroyed by caterpillar host
immune defense at the earliest stages of the
wasp’s embryonic development.
A
polydnavirus
21
Q
viruses can only infect free __
A
algae
22
Q
cannot infect the same algae when the algae
exist semi-symbiotically with a species of
paramecium
A
viruses
23
Q
viruses cannot infect the same algae when the algae
exist semi-symbiotically with a species of
___
A
paramecium
24
* it is a good guess that existence of the __is a
strong selective pressure toward establishing or
stabilizing the symbiotic relationship.
virus
25
infection of a cell with a single virus particle results in the
synthesis of more than one (often by a factor of several
powers of 10) infectious virus - a
productive infection
26
actual number of infectious viruses produced in an infected
cell is called the
burst size
27
Evade host’s natural protective and cleansing mechanisms; at
the cellular level, the virus takes over necessary host-cell
functions for its own replication processes
what step in infection process
entry into host and primary virus replication
28
Evade immediate host defenses (innate immune and
inflammatory responses) and natural barriers to spread
what step in infection process
Local or general spread in the host (defined
by cell and tissue tropism), with secondary
virus replication
29
Exit host body at site and at concentration needed to ensure
infection of the next host
what stage of viral infection
shedding from host
30
Adaptive immune responses mediate clearance, although
clearance is not always complete; viruses may persist and
contribute to long-term shedding or chronic disease
what stage of viral infection
clearance from host
31
infection is present but replication cycle is not completed
non-productive infections
32
virus genome in cell is integrated in the genome or multiple copies of circular DNA (non productive infections)
latent infections
33
non productive infection where genome does not persist in cells
for mutants, or those with defective genes
abortive
34
outcomes of infection
state of coexistence between cell and infecting virus
disease
35
cell infections have 4 outcomes
abortive infection
latent infection
productive infectoin
programmed cell death
36
also known as silent infection
latent infection
37
persistent infections include
HIV
38
Morphologic changes in cells (cytopathic
effects); inhibition of protein, RNA, and
DNA synthesis; cell death
what infection
cytocidal
39
No cytopathic effect; little metabolic
disturbance; cells continue to divide;
may be loss of the special functions of
some differentiated cells
what infection
persistent, productive
40
does cytocidal infection produce virions?
yes
41
example of cytocidal infection viruses
Alphaherpesviruses,
enteroviruses, reoviruses
42
example of persistent, productive infection
Pestiviruses,
arenaviruses, rabies
virus, most retroviruses
43
does persistent, productive viruses produce virions?
yes
44
No effect or loss of specialized functions
persistent, nonproductive
45
does persistent, nonproductive produce infectious virions?
no, but virus may be induced by trauma
46
example of persistent non productive virions
Papillomavirus in the skin
47
Alteration in cell morphology; cells can
be passaged indefinitely; may produce
tumors when transplanted to
experimental animals
what kind of infection
transformation
48
do transformation infections produce virions? (oncogenic DNA viruses)
no,
49
example of transformation virus
(oncogenic DNA viruses)
Polyomavirus,
adenoviruses
50
example of transformatio ninfection (oncogenic retroviruses)
Murine, avian leukosis
and sarcoma viruses
51
do oncogenic retroviruses (Transformation infection) produce infectious virions>
yes
52
characterized by loss of cell functions
that are essential to survival.
cytopathic infections
53
are
final outcomes of cytopathic infections (3)
cell degeneration
necrosis
virus-induced apoptosis
54
meaning “cell death”
cytocydal
55
meaning “cell
lysis” or “rupture”
cytolytic
56
required for release of nonenveloped viral progeny
cell lysis
57
progeny of enveloped viruses can be released by ___
from viable cells
budding
58
Cyto-pathological effects of the diseases caused
by viruses result from the interplay of several
factors:
toxic effects of viral gene products
rxn of host to infected cells expressing viral genes
modifications of host gene expression by structural or functional interactions
destruction of cells
59
virus can have multiple results
cell fusion
lysis
transformation
latent infection
persistent infection
60
- follow after cytoskeletal
disruption.
cell rounding
61
can occur by protein syn inhibition, genotoxic
effects etc.
necrosis
62
is a programmed cell death - result in
morphologic changes distinct from necrosis or
lysis (i.e. forms of nonprogrammed cell death),
and is a form of host defense.
apoptosis
63
may be seen following
infection with enveloped viruses.
synctia formation
64
a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells or by division of nuclei.
synctyia
65
Displaced host cell DNA from the nuclear matrix result in
chromatin margination along the nuclear membrane as aggregates of viral nucleic acid
and protein accumulate i.e canine distemper
type of inclusion bodies
intranuclear inclusion
66
typical of viruses replicating to high levels in the cytoplasm, again
reflecting aggregates of viral genomes engaged in transcription and replication. i.e typical
of infections caused by poxviruses, paramyxoviruses, rhabdoviruses, and reoviruses
what inclusion bodies
cytoplasmic inclusions
67
causes changes in cell shape (e.g.
rounding) that are characteristic of many
viral Infections.
disruption of cell cytoskeleton
68
Damage to specific filament systems: for
example, canine distemper virus,
vesicular stomatitis viruses, vaccinia
virus, and herpesviruses cause
a ___of actin-containing
microfilaments, and enteroviruses
induce extensive damage to
microtubules
depolymerization
69
* with ___viruses, there is no dramatic inhibition of host-cell protein synthesis, and no
cell death.
noncytocidal
70
Inhibition of both host-cell DNA replication and mRNA transcription is a consequence of DNA
virus infection when cellular machinery is redirected to ___templates.
viral templates
71
cumulative effect of inhibition of host-cell protein synthesis and depletion of nucleotide pools can
be the loss of cellular ___, resulting in a sequence of degeneration and necrosis.
homeostasis
72
Following virus infection,
breakage, fragmentation,
rearrangement and/or
changes in the number of
chromosomes may occur leading to
cancer
73
which is essentially a mechanism of cell suicide that the host
activates as a last resort to eliminate viral factories before progeny virus production is
complete.
programmed cell death
74
program cell death can be activated thru
intrinsic pathway
extrinsic pathway
75
The mitochondrial pathway is activated as a result of increased
permeability of mitochondrial membranes subsequent to cell injury, such as that associated with a viral
infection.
what activation of programmed cell death
intrinsic (mitochondrial) pathway
76
activated by engagement of specific cellmembrane receptors, which are members of the tissue necrosis factor (TNF) receptor family (TNF, Fas,
and others).
what activation of programmed cell death
extrinsic (death receptor patway)
77
enzymes that mediate death of the cell
(the so-called executioner phase)
caspase
78
altered plasma membrane ___affect ion
exchange and membrane potential; induce the
synthesis of new intracellular membranes; or the
rearrangement of previously existing ones
permeability
79
* viral proteins inserted into the cell membrane in
preparation for viral assembly (budding) may
contact a neighboring uninfected cell, mediate
attachment to and ___with the membranes of
that neighboring cell.
fusion
80
suggested as a means by which viruses spread in
tissues: ___bridges may allow subviral entities,
such as viral nucleocapsids and nucleic acids, to
spread while avoiding host defenses
fusion
81
viral membrane ___serves as a receptor
for ligands on the surface of erythrocytes.
glycoprotein
82
may bind to infected cells that
express these viral envelope proteins on their
surface (hemadsorption) or cell free viruses may
cross-link erythrocytes to form aggregates
(hemagglutination), indicating the presence of
virus infection.
erythrocytes
83
Erythrocytes may bind to infected cells that
express these viral envelope proteins on their
surface in a process called
hemadsorption
84
or cell free viruses may
cross-link erythrocytes to form aggregates in a process called
hemagglutination
85
The interaction of virus with the cell membrane and/or
subsequent events, may change the physiological parameters of infected cells,
including
movement of ions, formation of secondary messengers, and activation
cascades leading to altered cellular activities
86
* Usually do not kill the cells in which replication occurs.
noncytophatic viruses
87
nocause persistent infection during which infected cells produce and release virions but cellular
metabolism that is essential to maintaining homeostasis is either not affected or is minimally
affected.
non-cytopathic effects
88
terminally differentiated cells such as __, once destroyed, are not replaced, and
persistently infected differentiated cells may lose their capacity to carry out specialized
functions.
neurons
89
refers to the preference of the virus’s host of replication in distinct
kinds of cells in an organ
virus tropism
90
3 factors affecting viral pathogenesis
virus tropism
virus factors
host factors
91
determined through the capability of viral surface proteins to bind or fuse to
the surface receptors of targeted cells to initiate an infection
virus tropism
92
HIV-1 requires target cells to express co-receptors ___ and __
CCR5 or CXCR4 along with CD4 receptor
93
is dependent on host transcription factors which are
expressed only within the glial cell.
JC virus gene expression
94
JC virus
human polyomavirus 2
95
viral genetics that encode viral factors can determine the
degree of pathogenesis triggered by viral infections
virus factors
96
* for a virus to spread and cause disease to the body, it must to encode
specific virus genes within its genome, which allow it to beat the
preventive physical barriers and to modulate the immune system’s ability
to block replication of the virus.
what factor affecting viral pathogenesis
virus factosr
97
viral infections have demonstrated various manifestations that
range from asymptomatic to asymptomatic, or even critical illness, because on
the host’s factors.
what viral pathogenicity factor
host factor
98
genetic factors include
age
immunocompetence
genetics
99
are more serious diseases in adults,
mumps
polio
epstein-barr virus
100
virus more serious in infants
rotavirus
101
- consequence of the dysregulated growth of cells derived from a few or a
single, genetically altered progenitor cell(s).
neoplasms
102
onsidered to originate from an oligoclonal or monoclonal outgrowth of a single cell
regardless of the composition of several cell types.
neoplasms
103
genetic changes responsible for ___may be caused by naturally occurring
mutations, chemical or physical agents or infectious agents including viruses, but all
involve certain common cellular pathways.
neoplasia
104
m is a new growth (syn. tumor) which can be benign or malignant;
neoplasm
105
is the process that leads to the formation of neoplasms (syn. carcinogenesis);
neoplasia
106
is the study of neoplasia and neoplasms;
oncology
107
is a growth produced by abnormal cell proliferation that remains localized and does
not invade adjacent tissue;
benign neoplasm
108
is locally invasive and may also be spread to other parts of the body
(metastasis).
malignant neoplasm
109
are cancers of epithelial cell origin
carcinomas
110
are cancers that arise from cells of mesenchymal origin
sarcomas
111
Solid neoplasms of lymphocytes are designated (3)
lymphosarcoma
malignant lymphoma
lymphoma
112
are cancers of hemopoietic origin characterized by circulation of cancerous cells.
leukemias
113
result of nonlethal genetic injury, as may be acquired by chemical or
physical damage, or from viral infections
neoplasm
114
neoplasms results from the clonal expansion of cells that have suffered genetic
damage, typically in one of four types of normal regulatory genes (4)
protooncogenes
tumor supression genes
apoptosis regulation genes
DNA repair mediation genes
115
which are cellular genes that regulate growth and differentiation;
proto oncogenes
116
that inhibit growth, typically by regulating the cell cycle;
tumor supressor genes
117
nvolves a multistep progression resulting from the cumulative effects of
multiple mutations.
carcinogenesis
118
* normal cellular genes that encode proteins that function in normal cellular growth and
differentiation
protooncogenes
119
protooncogenes include genes of (5)
* 1) growth factors;
* (2) growth factor receptors;
* (3) intracellular signal transducers;
* (4) nuclear transcription factors;
* (5) cell cycle control proteins.
120
- derived by mutation of normal cellular proto-oncogene counterparts
oncogenes
121
expression of oncogenes results in production of oncoproteins that mediate
autonomous (unregulated) growth of neoplastic cells.
oncogenes
122
Viruses are classified as ___viruses if part of the viral genome is present in tumors,
with expression within the tumor of some viral genes
tumor
123
characteristics of neoplasm (4)
(1) self-sufficient, proliferate without external stimuli; e.g. result of unregulated oncogene activation;
(2) insensitive to normal regulatory signals that would limit their growth, such as transforming
growth factor and the cyclin-dependent kinases that normally regulate orderly progression of cells
through the various phases of the cell cycle;
(3) resistant to apoptosis because of either the activation of antiapoptotic molecules or the inhibition
of mediators of apoptosis such as p53;
(4) limitless potential for replication
124
immortal cells include
HeLa
125
self-sufficient, proliferate without external stimuli of Neoplasm can be due to
unregulated oncogene activation
126
neoplasms occur due to insensitive to normal regulatory signals that would limit their growth, such as ___ ___
transforming growth factor
127
resistant to apoptosis because of either the activation of antiapoptotic molecules or the inhibition
of mediators of apoptosis such as
p53
128
Cancers also may have the ability to invade and spread to distant tissues in a process called
metastasis
129
neoplasms
typically promote the proliferation of new __ ___s that support their growth.
blood vessels
