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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
Q

Neutralizing Abs directed against what two viral structures prevents viral infection?

A

capsid or glycoproteins

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26
Q

Secretory Ig(blank) protects against infection of viruses via the respiratory or GI tracts giving MUCOSAL IMMUNITY

A

IgA

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27
Q

How do IFNs prevent viral infection?

A

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.

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28
Q

What systemic symptoms are associated with IFNs?

A

aching muscles and fever

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29
Q

How soon does IFN production begin post infection?

A

hours

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30
Q

IFNs are part of the (innate/adaptive) response to viral infection

A

innate

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31
Q

What is another name for IFNg?

A

IFN type II

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32
Q

IFNg is essential for defense against what types of infections?

A

viral, some bacterial, and some protozoal infections

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33
Q

IFNg activates (blank) cells and induces (blank) expression

A

macrophages; MHC

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34
Q

Dendritic cells secrete (blank)times more IFN than a similarly induced fibroblast

A

1000x

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35
Q

a cell must be (blank) for a viral infection to occur

A

permissive

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36
Q

Are ssRNA or dsDNA viruses stronger inducers of IFN synth?

A

ssRNA

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37
Q

T/F: bacterial endotoxin and dsRNA can induce IFN synth

A

true

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38
Q

when does Ab appear in response to viral infection

A

days after

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39
Q

IFNs play an important role in (specific/nonspecific) defense

A

nonspecific

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40
Q

At what day does IFN titer peak?

A

day 5

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41
Q

At what day does Ab titer begin to rise?

A

day 10

42
Q

T/F: IFN protects the virally infected cell that produced the IFN in the first place

A

false

43
Q

T/F: IFN itself is an antiviral agent

A

false

44
Q

What happens once IFN binds to a cell?

A

activates transcription factors that translocate into the nucleus to mediate IFN-inducible GENES

45
Q

What are the IFN-inducible antiviral proteins?

A

protein Kinase R (PKR) and Rnase L

46
Q

What is the function of PKR?

A

dsRNA dependent protein kinase that phosphorylates and INACTIVATES eIF-2 to PREVENT CELL AND PROTEIN SYNTH

47
Q

What is the function of Rnase L?

A

destroys ALL RNA in the cell, both viral and host

48
Q

What two ways can viruses block IFN activity?

A

they can block IFN expression or IFN induced signal transduction

49
Q

virally encoded immunomodulatory proteins inhiibit (blank) function

A

MHC

50
Q

T/F: viruses may inhibit general cytokine activity

A

true

51
Q

Viruses mutate and change antigenic proteins to (blank)

A

evade the immune system

52
Q

T/F: most viral infections are self-limiting

A

true

53
Q

(blank) infections give no overt sign of their presence

A

subclinical

54
Q

A replicating virus that is continuously detectable at low levels a is (blank) infection

A

chronic or persistent

55
Q

What does it mean when an infection is latent?

A

virus is in a hidden form and no new virus is being made

56
Q

Intermittent flare ups of clinical disease happen in (blank) patients with a chronic infection

A

immunocompromised

57
Q

HSV 1 primarily infects the mouth while HSV2 infects the (blank)

A

genitals

58
Q

Why do generalized skin rashes develop as a result of viral infections?

A

the virus spreads to the skin from the blood stream following rep at a different site

59
Q

Does polio first replicate at the sight of infection or at its target location?

A

site of infection

60
Q

How does a virus gain access to the CNS?

A

replication within cerebral endothelial cells

61
Q

What are the two ways that viruses can gain access to the CNS?

A

rep in cerebral endothelial cells or via neuronal transport with initial uptake at sensory nerve endings

62
Q

pathologic reaction may include CNS cell necrosis, inflammation, and phagocytosis by (blank cells)`

A

glial cells

63
Q

What cells, when infected, will loosen the tight junctions between the cerebral endothelial cells?

A

glial cells

64
Q

What is the most common route of viral infection?

A

infection of the respiratory tract via inhalation of aerosolized droplets

65
Q

What are the host defenses against respiratory tract infections?

A

mucus, ciliary action, lymphoid cells , alveolar macrophages and secretory IgA

66
Q

Do all viruses that enter in the lung as a primary site remain in the lung?>

A

No, some travel to develop other symptoms, like chicken pox

67
Q

How are GI viruses spread?

A

contaminated food or fecal oral route

68
Q

What types of viruses normally cause GI infections and why?

A

NAKED CAPSID; they are exposed to harsh elements like acid, bile salts, and proteolytic enzymes

69
Q

rota virus and Norwalk virus both cause (blank)

A

GE

70
Q

Is the incubation period of Gi viruses short or long?

A

short

71
Q

Do maternal viral infections result in fetal viremia?

A

NO

72
Q

T/F: Maternal-fetal viremia is a serious danger to the fetus

A

true

73
Q

What two viruses are resonsible for congenital defects?

A

Rubella and HCMV

74
Q

Deafness, eye abnormalities, and congenital heart disease are defects caused by (blank) virus

A

Rubella

75
Q

What is the LEADING cause of infectious deafness?

A

HCMV

76
Q

What virus causes deafness, learning disabilities, and mental retardation?

A

HCMV

77
Q

T/F: antiviral agents work by inhibiting cellular responses to viral infection

A

false; they inhibit viral functions within the cell but not the cellular functions themselves

78
Q

What are the stages of infection that are targets for antivirals?

A 
attachment of virus to host cells
uncoating of the viral genome 
viral nucleic acid synthesis
translation of viral proteins
release of progeny virus
79
Q

What are the four general classes of antivirals?

A
  1. Nucleoside analog
  2. Reverse transcriptase inhibitor
  3. Protease inhibitor
  4. Fusion inhibitor
80
Q

How do nucleoside analogs work?

A

Incorporate a terminal nucleoside in the viral Pol

81
Q

How do RT-inhibitors work?

A

bind to RT to disrupt enzyme catalytic site

82
Q

How do protease inhibitors work?

A

inhibits viral proteiase that is required at the late stage of HIV rep cycle

83
Q

How do fusion inhibitors work?

A

Prevent viral and cell membrane fusion in ENTRY of HIV into cells

84
Q

What is the most cost effective method of preventing serious viral infections

A

IMMUNIZATION

85
Q

What are the targets of viral vaccines?

A

viral glycoproteins

86
Q

T/F: viral immunity is also conferred via Abs to viral core proteins and non-structural proteins (like riboproteins)

A

FALSE

87
Q

Viruses that infect the mucosa require what Ig class?

A

IgA; influenza

88
Q

Viruses that have a viremic spread are controlled with what Ig class?

A

IgG; polio, hepatitis A/B, varicella

89
Q

Cell mediated immunity is used against systemic infections to control the (blank)

A

latent state; herpesvirus

90
Q

Multiple viral (blanks) can complicate the dev of a vaccine

A

serotypes; rhinovirus OR rapidly mutating viruses (HIV)

91
Q

Attenuated live vaccines antigenically overlap with (blank) viruses

A

wild-type

92
Q

How do you make an attenuated virus?

A

cell passage in animals or cell culture

93
Q

After being vaccinated, where do you want the vaccine to induce an Ab response and resistance?

A

at the portal of entry

94
Q

Do live viruses or killed viruses give longer immunity?

A

live viruses

95
Q

Do live or killed viruses give more effective protection?

A

live

96
Q

what types of Ig are produced by killed viruses?

A

IgG

97
Q

What types of Ig are produced by live viruses?

A

IgG and IgA

98
Q

Do killed viruses produce mucosal immunity?

A

NO, no IgA!!

99
Q

Compare cell mediated immunity in killed vs live viruses>?

A 
killed= poor
live= good
100
Q

Are heat killed or live viruses stable at room temp?

A

heat killed

101
Q

T/F: live virus vaccines can be given in combos

A

true

102
Q

T/F: antibody response to each component of these vaccines is comparable with antibody response to the individual vaccines administered separately

A

ture

Block 6 Week 4 Colt (10 decks)

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