Pathogenesis and control of vira disease Flashcards
1
Q
What are the 4 cellular responses to infection?
A
no effect, cytopathology, hyperplasia, cancer
2
Q
(blank) are nuclear or cytoplasmic aggregates of stainable substances, usually viral proteins
A
inclusion bodies
3
Q
Many viral infections are (blank)
A
subclinical
4
Q
T or F
the same disease may be produced by a variety of viruses
A
T
5
Q
T or F
the same disease may produce a variety of diseases
A
T
6
Q
T or F
the disease produced bears no relationship to viral morphology
A
T
7
Q
pathology is determined by what 3 factors?
A
viral factors
host factors
family genetics
8
Q
What is the study of origin and development of disease?
A
pathogenesis
9
Q
(blank) are events during infection that results in disease manifestation in the host
A
disease pathogenesis
10
Q
A strain of virus is more (blank) than another strain if it commonly produces a more severe disease
A
virulent
11
Q
What are the steps of viral pathogenesis?
A
viral entry into the host primary site of viral replication viral spread cellular injury host immune response viral clearance or persistent infection viral shedding
12
Q
Is this a characteristic of local or systemic viral infections:
site of pathology is at portal of entry?
A
local
13
Q
Is this a characteristic of local or systemic viral infections:
site of pathology is at distant site?
A
systemic
14
Q
Is this a characteristic of local or systemic viral infections:
incubation period is relatively long?
A
systemic
15
Q
Is this a characteristic of local or systemic viral infections:
incubation period is relatively short?
A
local
16
Q
Is this a characteristic of local or systemic viral infections:
viremia is absent
A
local
17
Q
Is this a characteristic of local or systemic viral infections:
viremia is present
A
distant
18
Q
Is this a characteristic of local or systemic viral infections:
duration of immunity is variable (may be short)
A
local
19
Q
Is this a characteristic of local or systemic viral infections: Duration of immunity is usually lifelong.
A
distant
20
Q
Is this a characteristic of local or systemic viral infections:
role of secretory IgA in resistance is usually NOT important
A
distant
21
Q
Is this a characteristic of local or systemic viral infections: role of secretory IgA in resistance is usually important
A
local
22
Q
What are the ways that viruses attach and enter cells?
A
skin
respiratory tract
GI tract
urogenital tract
23
Q
after primary site of entry, the virus may spread within the host. What is the most common route?
A
blood or lymphatics
24
Q
What do you call presence of virus in the blood?
A
viremia
25
T or F
| viruses may be free in the blood?
T
| They may be free in the blood or associated with a specific cell type
26
What 2 viruses have neuronal spread?
HSV
| rabies virus
27
viruses tend to exhibit organ and cell specificities, this is called (blank)
tropism
28
What does tropism determine?
the pattern of system illness produced
29
tissue and cell tropism relates to the presence of cell surface receptors that the viral (blank) bind to initiate entry
VAP (glycoproteins)
30
Why might a virus not produce viral proteins in a host cell?
due to lack of cellular transcription factor
31
the outcome of viral infections reflects the interplay between (blank and blank)
viral and host factors
32
The induction of (blank) is among the major immune response
interferons
33
(blank and blank) are activated and respond to sites of viral infection
mononuclear cells
| lymphocytes
34
Virus infected cells may be lysed by (blank) resulting from recognition of viral polypeptides on the cell surface
CTLs
35
(blank) directed against capsid or glycoproteins blocks the viral infection of cells.
neutralizing antibody
36
(blank) protects against infection by viruses through the respiratory or GI tracts (mucosal immunity)
secretory IgA antibody
37
What are IFNs?
host encoded proteins that are part of the cytokine family that inhibit viral replication
38
How soon do you get production of interferons (IFNs)?
within hours of viral replication
39
Interferons are essential to the (blank) antiviral immune response
innate
40
(blank) is critical for immunity against viral, some bacterial and protozoal infections
IFN gamma or type II interferon
41
(blank) is an important activator of macrophages and induces (bank) molecule expression
IFN gamma
| MHC
42
(blank) secrete 1000 times more IFN than a similiarly induced fibroblast.
dendritic cells
43
cells must be (blank) to produce IFNs
induced
44
Infection with virus is a strong (blank) of IFNs
inducer
45
Single stranded RNA viruses is a (weaker/stronger) inducer of INF than DNA viruses
stronger
46
Can you induce IFNs via double stranded RNA an bacterial endotoxins?
yes
47
When are IFNs detectable and then what happens once they are?
soon after viral infection
| viral production decreases
48
(blank) does not appear in response to viral infection until days following infection.
antibody
49
therefore IFNs play a primary role in the (blank) defense of the host against viral infections
nonspecific
50
Does IFN protect the virus infected cell that produce it?
no
51
Is IFN the antiviral agent?
no. it induces the synthesis of other proteins that inhibit viral replication
52
How does IFN work?
it binds IFN receptor, which activates transcription factors that translocate into the nucleus to mediate IFN-inducible genes
53
What are 2 IFN-inducible enzymes produced when a virus infects a cell?
protein kinase R (PKR)
| Rnase L
54
What is a dsRNA-dependent protein kinase which phosphorylates and inactivates cellular initiation factor eIF-2 preventing cellular and viral proteins?
proken kinase R (PKR)
55
What is an interferon-induced ribonuclease which, upon activation, destroys all RNA in the cell (both cellular and viral)?
Rnase L
56
Some viruses infect and damage cells of the immune system.. give an example
HIV infects T lymphocytes and destroy their ability to function
57
Viruses may encode (blank) proteins that inhibit MHC function (adenoviruses, herpesviruses)
immunomodulatory proteins
58
What does poxvirus and measles virus inhibit?
cytokine activity
59
Viruses may mutate and change antigenic sites of (blank)
virion proteins (influenza, HIV)
60
Infections are acute when a virus first infects a host, most infections are (blank)
self-limiting
61
(blank) infections are those that give no overt sign of their presence
subclinical
62
(blank) infections occur when replicating viruses can be continuously detected at low levels
chronic/persistent
63
(blank) infections are those in which the virus persists in a hidden form, no new virus is produced.
latent
64
There will be (blank) flare ups of clinical disease when a virus can be detected. You are then (blank)
intermittent
| immunocompromised
65
How does the latent herpesvirus infection work?
get primary infection, viral transit up peripheral nerve,
THEN fever, sunlight, menstruation (HSV1) or x-irradiation will cause latent virus in DRG to become active and you get recurrence
66
Some viruses enter skin through abrasion. Which viruses do this?
poxviruses, papillomaviruses, herpes simplex viruses
67
Some viruses are introduced by the bite of arthropod vectors. What virus does this?
arboviruses
68
Some viruses are injected during blood transfusions or contaminated needles. What viruses do this?
Hep B
| HIV
69
Why do generalized skin rashes occur with viral infections?
they develop because virus spreads to the skin via the bloodstream following replication at some other site.
70
Explain poliomyelitis infection
- poliovirus multiplies at primary site of infection prior to systemic spread
- in poliomyelitis the virus enters by the alimentary tract (multiplies in these tissues)
- then will spread to CNS
71
How do you prevent the spread of poliomyelitis to the CNS?
by antibodies from vaccination
72
Viruses can gain access to the brain by the (blank) or (blank)
bloodstream
| peripheral nerve fibers (neuronal spread)
73
How can you get viruses to the brain through the bloodstream?
via viral replication in endothelia cells of cerebral vessels
74
(blank) can be taken up at sensory nerve endings.
virions
75
(blank) travels in axons to the dorsal root ganglion
herpesvirus
76
Many viruses that infect the CNS can cause (blank) or (blank)
encephalitis
| meningitis
77
Viral CNS infections can cause pathological reactions that include what?
CNS cell necrosis
inflammation
phagocytosis by glial cells
78
Most common viral route of infection is via the (blank) in aerosolized droplets or saliva
respiratory tract
79
What are the host defenses in the respiratory tract that viruses overcome?
mucus, ciliary action, lymphoid cells, alveolar macrophages and secretory IgA
80
Many respiratory infections remain localized to the lung, however some spread to develop characteristic symptoms. What viruses do this?
chickenpox
measles
rubella
81
How do you get GI viral infections?
fecal oral route, through poorly cooked or contaminated food
82
The viruses that infect the GI tract have to deal with very harsh environments (acid, bile salts (detergents), proteolytic enzymes). Because of this, are enveloped or naked viruses more prevalent in the GI tract?
naked
83
(blank) is short term disease ranging from mild, watery diarrhea to severe febrile illness (vomiting, diarrhea, and prostration)
acute gastroenteritis
84
(blank) and (blank) viruses are major causes of gastroenteritis.
rotaviruses
| norwalk
85
Most maternal viral infections do not result in (blank) and (blank)
viremia
| fetal involvement
86
If a virus crosses the placenta and infection occurs in utero, what will happen?
the fetus will be in serious danger
87
(blank) and (blank) are presently the primary agents responsible for congenital defects in newborns.
rubella
| cytomegalovirus
88
What are the symptoms of congenital rubella syndrome?
deafness
eye abnormalities
congenital heart disease
89
What is the leading cause of deafness, learning disabilities, and mental retardation in children?
congenital HCMV
90
What is antiviral chemotherapy?
agents that are capable of inhibiting viral and not cellular function
91
When do you use antivirals?
when vaccines aren't available
92
What are the most amenable stages of infection to target?
- attachment of virus to host cells
- uncoating of the viral genome
- viral nucleic acid synthesis
- translation of viral proteins
- release of progeny virus
93
What does this:
| inhibits viral polymerase by incorporating a terminal nucleoside
nucleoside analog
94
What does this:
| binds to reverse transcriptase to disrupt enzymes catalytic site
reverse transcriptase inhibitor
95
What does this:
| inhibits the viral protease that is required at the late stage of the HIV replicative cycle
protease inhibitor
96
What does this:
| blocks viral and cellular membrane fusion step involved in entry of HIV into cells
fusion inhibitor
97
viral (blank) utilize the immune response of the host to prevent viral disease
vaccines
98
What is the most cost effective method of prevention of serious viral infections?
vaccinations
99
What are common targets for vaccines?
surface viral glycoproteins
100
(blank) is important in resistance to infection by viruses that replicate in mucosal membranes (influenza)
mucosal immunity (IgA)
101
Viruses that have a viremic mode of spread need to be controlled with (blank)
serum antibodies (IgGs)
102
(blank) is involved against systemic infections (control latent state)
cell-mediated immunity
103
(blank) can complicate the development of an effective vaccine.
multiple viral serotypes (rhinoviruses)
104
(blank) are challenging to produce an effective vaccine (HIV)
rapidly mutating virus
105
What is a killed-virus vaccine?
virus is propagated then inactivated with minimal damage to the viral structural proteins
106
How do killed-virus vaccines work?
stimulate development of circulating antibody against viral membrane proteins. A boost usually needs to be administered
107
Parental administration of killed vaccine may not be ideal to protect (blank) or (blank) virus. Why?
respiratory or GI
| IgG ad IgM are induced rather than IgA
108
Cell mediated immunity to killed viruses is usually generally (blank)
poor
109
What are attenuated live virus vaccines?
utilize virus mutants that antigenically overlap with wild-type virus
110
How do you make an attenuated virus?
by serial passages in animals or cell cultures
111
How do attenuated viruses work?
act like the natural infection, they replicate in the host and induce good antibody and cell mediated immunity. They induce antibody response and resistance at the portal of entry
112
do you need multiple or single doses for killed vaccines?
multiple for killed
| single for live
113
Which is better a killed vaccine or a live vaccine? why?
live because it has longer better immunity.
114
What is the proper use of present vaccines?
-Must be administered in proper dosage
-Live virus vaccines to multiple viruses can be given in combination with out reduction in immunity.
(trivalent live polio vaccine or MMR are very effective vaccines)
115
T or F
antibody response to each component of these vaccines is comparable with antibody response to the individual vaccines administered separately
T
116
A variety of foreign proteins may stimulate immune responses after the (bank) and (blank) system
innate and intrinsic
117
Humoral response begins with interaction of a specific receptor on precursor (blank) with antigen
B lymphocytes
118
Binding of antigen promotes (blank) into antibody secreting cells (plasma cells).
differentiation
119
Naïve T cells are activated in lymph nodes following (Blank) binding of viral peptides displayed on dendritic cells.
TCR
120
(blank) is expressed on all cells except RBCs
MHC 1
121
(blank) is expressed mainly on APCs (dendritic cells, macrophages, B cells)
MHC II
122
What do TH cells do?
Help B cells differentiate into plasma cells
| Help T cells differentiate into CTL that can kill infected cells
