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Block 6 Week 4 Colt > Viral Pathogenesis - AuCoin > Flashcards

Viral Pathogenesis - AuCoin Flashcards

1
Q

What are the four cellular responses to viral infection?

A
  1. no effect
  2. cytopathology
  3. hyperplasia
  4. cancer
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2
Q

Can you have infection without symptoms?

A

yes

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3
Q

When the cell response is inclusion body formation, cell transformation, or cell dysfunction, what is the host response?

A

mild to severe disease

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4
Q

what are inclusion bodies?

A

nuclear or cytoplasmic aggregates of viral proteins that are stainable

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5
Q

T/F: most viral infections are symptomatic

A

false; most are subclinical

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6
Q

T/F: the same disease may be caused by a variety of viruses

A

true

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7
Q

T/F: the same virus may cause a variety of diseases

A

true

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8
Q

T/F: viral morphology has a correlation to disease symptoms

A

false

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9
Q

pathology is determined by host and viral factors and is influenced by patient (blank)

A

genetics

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10
Q

a virus is more (blank) if it commonly causes more severe symptoms in a patient

A

virulent

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11
Q

What are important factors to consider when looking at the steps of viral pathogenesis for making a vaccine?

A
  1. cellular recpeptor for viral entry into host
  2. route of infection–respiratory/GI/blood; what Abs are made at 1ry site of rep
  3. How is it transmitted
  4. Is there immune mediated cell damage
  5. Is the virus completely cleared or does it persist and does it SHED
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12
Q

why, if both measles and rhinovirus enter via the lungs, that rhinovirus has a short incubation while measles long?

A

rhinovirus will replicate in the lungs and cuase symptoms there, while measles may have to hitch a ride on a macrophage to get to the parotid gland to cause infection

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13
Q

What is the most common route of spread through the host?

A

blood or lymphatics

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14
Q

what is the presence of virus in the blood called?

A

viremia

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15
Q

Viruses may be free in the blood or associated with a specific (blank)

A

cell type

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16
Q

T/F: viruses may spread via nerves

A

true (like HSV and rabies)

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17
Q

What is the difference between primary and secondary viremia?

A

1ry viremia is the virus in the blood immediately after infection on its way to target tissues.

2ndry viremia is the virus reentering the blood after replicating in its target organs

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18
Q

What determines the pattern of systemic illness caused by a virus?

A

tropism, what tissues it infects

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19
Q

The relation between cell surface receptors and viral (blank) determines tropism

A

VAPs

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20
Q

T/F: the coded function of the cell surface receptors that bind VAPs is to solely bind to VAPs

A

FALSE, they just happen to have affinity for the VAPs

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21
Q

A lack of what would keep a virus from replicating even if it did infect a cell?

A

a lack of cellular transcription factors

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22
Q

what is the major immune response elicited with viral infection?

A

IFN production

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23
Q

What two types of cells are activated to respond to the site of viral infection?

A

mononuclear cells and lymphocytes

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24
Q

What do CTLs recognize that allow killing of virally infected cells?

A

viral polypeptides displayed on the cell surface

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25
Neutralizing Abs directed against what two viral structures prevents viral infection?
capsid or glycoproteins
26
Secretory Ig(blank) protects against infection of viruses via the respiratory or GI tracts giving MUCOSAL IMMUNITY
IgA
27
How do IFNs prevent viral infection?
they interfere with viral rep via activation of NK cells and macrophages, increase recognition of infection by up-regulating Ag presentation to T cells and increase the ability of uninfected cells to resist new infection.
28
What systemic symptoms are associated with IFNs?
aching muscles and fever
29
How soon does IFN production begin post infection?
hours
30
IFNs are part of the (innate/adaptive) response to viral infection
innate
31
What is another name for IFNg?
IFN type II
32
IFNg is essential for defense against what types of infections?
viral, some bacterial, and some protozoal infections
33
IFNg activates (blank) cells and induces (blank) expression
macrophages; MHC
34
Dendritic cells secrete (blank)times more IFN than a similarly induced fibroblast
1000x
35
a cell must be (blank) for a viral infection to occur
permissive
36
Are ssRNA or dsDNA viruses stronger inducers of IFN synth?
ssRNA
37
T/F: bacterial endotoxin and dsRNA can induce IFN synth
true
38
when does Ab appear in response to viral infection
days after
39
IFNs play an important role in (specific/nonspecific) defense
nonspecific
40
At what day does IFN titer peak?
day 5
41
At what day does Ab titer begin to rise?
day 10
42
T/F: IFN protects the virally infected cell that produced the IFN in the first place
false
43
T/F: IFN itself is an antiviral agent
false
44
What happens once IFN binds to a cell?
activates transcription factors that translocate into the nucleus to mediate IFN-inducible GENES
45
What are the IFN-inducible antiviral proteins?
protein Kinase R (PKR) and Rnase L
46
What is the function of PKR?
dsRNA dependent protein kinase that phosphorylates and INACTIVATES eIF-2 to PREVENT CELL AND PROTEIN SYNTH
47
What is the function of Rnase L?
destroys ALL RNA in the cell, both viral and host
48
What two ways can viruses block IFN activity?
they can block IFN expression or IFN induced signal transduction
49
virally encoded immunomodulatory proteins inhiibit (blank) function
MHC
50
T/F: viruses may inhibit general cytokine activity
true
51
Viruses mutate and change antigenic proteins to (blank)
evade the immune system
52
T/F: most viral infections are self-limiting
true
53
(blank) infections give no overt sign of their presence
subclinical
54
A replicating virus that is continuously detectable at low levels a is (blank) infection
chronic or persistent
55
What does it mean when an infection is latent?
virus is in a hidden form and no new virus is being made
56
Intermittent flare ups of clinical disease happen in (blank) patients with a chronic infection
immunocompromised
57
HSV 1 primarily infects the mouth while HSV2 infects the (blank)
genitals
58
Why do generalized skin rashes develop as a result of viral infections?
the virus spreads to the skin from the blood stream following rep at a different site
59
Does polio first replicate at the sight of infection or at its target location?
site of infection
60
How does a virus gain access to the CNS?
replication within cerebral endothelial cells
61
What are the two ways that viruses can gain access to the CNS?
rep in cerebral endothelial cells or via neuronal transport with initial uptake at sensory nerve endings
62
pathologic reaction may include CNS cell necrosis, inflammation, and phagocytosis by (blank cells)`
glial cells
63
What cells, when infected, will loosen the tight junctions between the cerebral endothelial cells?
glial cells
64
What is the most common route of viral infection?
infection of the respiratory tract via inhalation of aerosolized droplets
65
What are the host defenses against respiratory tract infections?
mucus, ciliary action, lymphoid cells , alveolar macrophages and secretory IgA
66
Do all viruses that enter in the lung as a primary site remain in the lung?>
No, some travel to develop other symptoms, like chicken pox
67
How are GI viruses spread?
contaminated food or fecal oral route
68
What types of viruses normally cause GI infections and why?
NAKED CAPSID; they are exposed to harsh elements like acid, bile salts, and proteolytic enzymes
69
rota virus and Norwalk virus both cause (blank)
GE
70
Is the incubation period of Gi viruses short or long?
short
71
Do maternal viral infections result in fetal viremia?
NO
72
T/F: Maternal-fetal viremia is a serious danger to the fetus
true
73
What two viruses are resonsible for congenital defects?
Rubella and HCMV
74
Deafness, eye abnormalities, and congenital heart disease are defects caused by (blank) virus
Rubella
75
What is the LEADING cause of infectious deafness?
HCMV
76
What virus causes deafness, learning disabilities, and mental retardation?
HCMV
77
T/F: antiviral agents work by inhibiting cellular responses to viral infection
false; they inhibit viral functions within the cell but not the cellular functions themselves
78
What are the stages of infection that are targets for antivirals?
``` attachment of virus to host cells uncoating of the viral genome viral nucleic acid synthesis translation of viral proteins release of progeny virus ```
79
What are the four general classes of antivirals?
1. Nucleoside analog 2. Reverse transcriptase inhibitor 3. Protease inhibitor 4. Fusion inhibitor
80
How do nucleoside analogs work?
Incorporate a terminal nucleoside in the viral Pol
81
How do RT-inhibitors work?
bind to RT to disrupt enzyme catalytic site
82
How do protease inhibitors work?
inhibits viral proteiase that is required at the late stage of HIV rep cycle
83
How do fusion inhibitors work?
Prevent viral and cell membrane fusion in ENTRY of HIV into cells
84
What is the most cost effective method of preventing serious viral infections
IMMUNIZATION
85
What are the targets of viral vaccines?
viral glycoproteins
86
T/F: viral immunity is also conferred via Abs to viral core proteins and non-structural proteins (like riboproteins)
FALSE
87
Viruses that infect the mucosa require what Ig class?
IgA; influenza
88
Viruses that have a viremic spread are controlled with what Ig class?
IgG; polio, hepatitis A/B, varicella
89
Cell mediated immunity is used against systemic infections to control the (blank)
latent state; herpesvirus
90
Multiple viral (blanks) can complicate the dev of a vaccine
serotypes; rhinovirus OR rapidly mutating viruses (HIV)
91
Attenuated live vaccines antigenically overlap with (blank) viruses
wild-type
92
How do you make an attenuated virus?
cell passage in animals or cell culture
93
After being vaccinated, where do you want the vaccine to induce an Ab response and resistance?
at the portal of entry
94
Do live viruses or killed viruses give longer immunity?
live viruses
95
Do live or killed viruses give more effective protection?
live
96
what types of Ig are produced by killed viruses?
IgG
97
What types of Ig are produced by live viruses?
IgG and IgA
98
Do killed viruses produce mucosal immunity?
NO, no IgA!!
99
Compare cell mediated immunity in killed vs live viruses>?
``` killed= poor live= good ```
100
Are heat killed or live viruses stable at room temp?
heat killed
101
T/F: live virus vaccines can be given in combos
true
102
T/F: antibody response to each component of these vaccines is comparable with antibody response to the individual vaccines administered separately
ture

Block 6 Week 4 Colt (10 decks)

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