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Block 6 Week 4 > Pathogenesis and control of vira disease > Flashcards

Pathogenesis and control of vira disease Flashcards

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1
Q

What are the 4 cellular responses to infection?

A

no effect, cytopathology, hyperplasia, cancer

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2
Q

(blank) are nuclear or cytoplasmic aggregates of stainable substances, usually viral proteins

A

inclusion bodies

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3
Q

Many viral infections are (blank)

A

subclinical

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4
Q

T or F

the same disease may be produced by a variety of viruses

A

T

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5
Q

T or F

the same disease may produce a variety of diseases

A

T

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6
Q

T or F

the disease produced bears no relationship to viral morphology

A

T

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7
Q

pathology is determined by what 3 factors?

A

viral factors
host factors
family genetics

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8
Q

What is the study of origin and development of disease?

A

pathogenesis

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9
Q

(blank) are events during infection that results in disease manifestation in the host

A

disease pathogenesis

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10
Q

A strain of virus is more (blank) than another strain if it commonly produces a more severe disease

A

virulent

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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
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12
Q

Is this a characteristic of local or systemic viral infections:
site of pathology is at portal of entry?

A

local

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13
Q

Is this a characteristic of local or systemic viral infections:
site of pathology is at distant site?

A

systemic

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14
Q

Is this a characteristic of local or systemic viral infections:
incubation period is relatively long?

A

systemic

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15
Q

Is this a characteristic of local or systemic viral infections:
incubation period is relatively short?

A

local

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16
Q

Is this a characteristic of local or systemic viral infections:
viremia is absent

A

local

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17
Q

Is this a characteristic of local or systemic viral infections:
viremia is present

A

distant

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18
Q

Is this a characteristic of local or systemic viral infections:
duration of immunity is variable (may be short)

A

local

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19
Q

Is this a characteristic of local or systemic viral infections: Duration of immunity is usually lifelong.

A

distant

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20
Q

Is this a characteristic of local or systemic viral infections:
role of secretory IgA in resistance is usually NOT important

A

distant

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21
Q

Is this a characteristic of local or systemic viral infections: role of secretory IgA in resistance is usually important

A

local

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22
Q

What are the ways that viruses attach and enter cells?

A

skin
respiratory tract
GI tract
urogenital tract

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23
Q

after primary site of entry, the virus may spread within the host. What is the most common route?

A

blood or lymphatics

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24
Q

What do you call presence of virus in the blood?

A

viremia

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25
Q

T or F

viruses may be free in the blood?

A

T

They may be free in the blood or associated with a specific cell type

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26
Q

What 2 viruses have neuronal spread?

A

HSV

rabies virus

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27
Q

viruses tend to exhibit organ and cell specificities, this is called (blank)

A

tropism

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28
Q

What does tropism determine?

A

the pattern of system illness produced

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29
Q

tissue and cell tropism relates to the presence of cell surface receptors that the viral (blank) bind to initiate entry

A

VAP (glycoproteins)

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30
Q

Why might a virus not produce viral proteins in a host cell?

A

due to lack of cellular transcription factor

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31
Q

the outcome of viral infections reflects the interplay between (blank and blank)

A

viral and host factors

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32
Q

The induction of (blank) is among the major immune response

A

interferons

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33
Q

(blank and blank) are activated and respond to sites of viral infection

A

mononuclear cells

lymphocytes

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34
Q

Virus infected cells may be lysed by (blank) resulting from recognition of viral polypeptides on the cell surface

A

CTLs

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35
Q

(blank) directed against capsid or glycoproteins blocks the viral infection of cells.

A

neutralizing antibody

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36
Q

(blank) protects against infection by viruses through the respiratory or GI tracts (mucosal immunity)

A

secretory IgA antibody

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37
Q

What are IFNs?

A

host encoded proteins that are part of the cytokine family that inhibit viral replication

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38
Q

How soon do you get production of interferons (IFNs)?

A

within hours of viral replication

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39
Q

Interferons are essential to the (blank) antiviral immune response

A

innate

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40
Q

(blank) is critical for immunity against viral, some bacterial and protozoal infections

A

IFN gamma or type II interferon

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41
Q

(blank) is an important activator of macrophages and induces (bank) molecule expression

A

IFN gamma

MHC

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42
Q

(blank) secrete 1000 times more IFN than a similiarly induced fibroblast.

A

dendritic cells

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43
Q

cells must be (blank) to produce IFNs

A

induced

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44
Q

Infection with virus is a strong (blank) of IFNs

A

inducer

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45
Q

Single stranded RNA viruses is a (weaker/stronger) inducer of INF than DNA viruses

A

stronger

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46
Q

Can you induce IFNs via double stranded RNA an bacterial endotoxins?

A

yes

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47
Q

When are IFNs detectable and then what happens once they are?

A

soon after viral infection

viral production decreases

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48
Q

(blank) does not appear in response to viral infection until days following infection.

A

antibody

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49
Q

therefore IFNs play a primary role in the (blank) defense of the host against viral infections

A

nonspecific

50
Q

Does IFN protect the virus infected cell that produce it?

A

no

51
Q

Is IFN the antiviral agent?

A

no. it induces the synthesis of other proteins that inhibit viral replication

52
Q

How does IFN work?

A

it binds IFN receptor, which activates transcription factors that translocate into the nucleus to mediate IFN-inducible genes

53
Q

What are 2 IFN-inducible enzymes produced when a virus infects a cell?

A

protein kinase R (PKR)

Rnase L

54
Q

What is a dsRNA-dependent protein kinase which phosphorylates and inactivates cellular initiation factor eIF-2 preventing cellular and viral proteins?

A

proken kinase R (PKR)

55
Q

What is an interferon-induced ribonuclease which, upon activation, destroys all RNA in the cell (both cellular and viral)?

A

Rnase L

56
Q

Some viruses infect and damage cells of the immune system.. give an example

A

HIV infects T lymphocytes and destroy their ability to function

57
Q

Viruses may encode (blank) proteins that inhibit MHC function (adenoviruses, herpesviruses)

A

immunomodulatory proteins

58
Q

What does poxvirus and measles virus inhibit?

A

cytokine activity

59
Q

Viruses may mutate and change antigenic sites of (blank)

A

virion proteins (influenza, HIV)

60
Q

Infections are acute when a virus first infects a host, most infections are (blank)

A

self-limiting

61
Q

(blank) infections are those that give no overt sign of their presence

A

subclinical

62
Q

(blank) infections occur when replicating viruses can be continuously detected at low levels

A

chronic/persistent

63
Q

(blank) infections are those in which the virus persists in a hidden form, no new virus is produced.

A

latent

64
Q

There will be (blank) flare ups of clinical disease when a virus can be detected. You are then (blank)

A

intermittent

immunocompromised

65
Q

How does the latent herpesvirus infection work?

A

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
Q

Some viruses enter skin through abrasion. Which viruses do this?

A

poxviruses, papillomaviruses, herpes simplex viruses

67
Q

Some viruses are introduced by the bite of arthropod vectors. What virus does this?

A

arboviruses

68
Q

Some viruses are injected during blood transfusions or contaminated needles. What viruses do this?

A

Hep B

HIV

69
Q

Why do generalized skin rashes occur with viral infections?

A

they develop because virus spreads to the skin via the bloodstream following replication at some other site.

70
Q

Explain poliomyelitis infection

A
  • 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
Q

How do you prevent the spread of poliomyelitis to the CNS?

A

by antibodies from vaccination

72
Q

Viruses can gain access to the brain by the (blank) or (blank)

A

bloodstream

peripheral nerve fibers (neuronal spread)

73
Q

How can you get viruses to the brain through the bloodstream?

A

via viral replication in endothelia cells of cerebral vessels

74
Q

(blank) can be taken up at sensory nerve endings.

A

virions

75
Q

(blank) travels in axons to the dorsal root ganglion

A

herpesvirus

76
Q

Many viruses that infect the CNS can cause (blank) or (blank)

A

encephalitis

meningitis

77
Q

Viral CNS infections can cause pathological reactions that include what?

A

CNS cell necrosis
inflammation
phagocytosis by glial cells

78
Q

Most common viral route of infection is via the (blank) in aerosolized droplets or saliva

A

respiratory tract

79
Q

What are the host defenses in the respiratory tract that viruses overcome?

A

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

80
Q

Many respiratory infections remain localized to the lung, however some spread to develop characteristic symptoms. What viruses do this?

A

chickenpox
measles
rubella

81
Q

How do you get GI viral infections?

A

fecal oral route, through poorly cooked or contaminated food

82
Q

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?

A

naked

83
Q

(blank) is short term disease ranging from mild, watery diarrhea to severe febrile illness (vomiting, diarrhea, and prostration)

A

acute gastroenteritis

84
Q

(blank) and (blank) viruses are major causes of gastroenteritis.

A

rotaviruses

norwalk

85
Q

Most maternal viral infections do not result in (blank) and (blank)

A

viremia

fetal involvement

86
Q

If a virus crosses the placenta and infection occurs in utero, what will happen?

A

the fetus will be in serious danger

87
Q

(blank) and (blank) are presently the primary agents responsible for congenital defects in newborns.

A

rubella

cytomegalovirus

88
Q

What are the symptoms of congenital rubella syndrome?

A

deafness
eye abnormalities
congenital heart disease

89
Q

What is the leading cause of deafness, learning disabilities, and mental retardation in children?

A

congenital HCMV

90
Q

What is antiviral chemotherapy?

A

agents that are capable of inhibiting viral and not cellular function

91
Q

When do you use antivirals?

A

when vaccines aren’t available

92
Q

What are the most amenable stages of infection to target?

A
  • attachment of virus to host cells
  • uncoating of the viral genome
  • viral nucleic acid synthesis
  • translation of viral proteins
  • release of progeny virus
93
Q

What does this:

inhibits viral polymerase by incorporating a terminal nucleoside

A

nucleoside analog

94
Q

What does this:

binds to reverse transcriptase to disrupt enzymes catalytic site

A

reverse transcriptase inhibitor

95
Q

What does this:

inhibits the viral protease that is required at the late stage of the HIV replicative cycle

A

protease inhibitor

96
Q

What does this:

blocks viral and cellular membrane fusion step involved in entry of HIV into cells

A

fusion inhibitor

97
Q

viral (blank) utilize the immune response of the host to prevent viral disease

A

vaccines

98
Q

What is the most cost effective method of prevention of serious viral infections?

A

vaccinations

99
Q

What are common targets for vaccines?

A

surface viral glycoproteins

100
Q

(blank) is important in resistance to infection by viruses that replicate in mucosal membranes (influenza)

A

mucosal immunity (IgA)

101
Q

Viruses that have a viremic mode of spread need to be controlled with (blank)

A

serum antibodies (IgGs)

102
Q

(blank) is involved against systemic infections (control latent state)

A

cell-mediated immunity

103
Q

(blank) can complicate the development of an effective vaccine.

A

multiple viral serotypes (rhinoviruses)

104
Q

(blank) are challenging to produce an effective vaccine (HIV)

A

rapidly mutating virus

105
Q

What is a killed-virus vaccine?

A

virus is propagated then inactivated with minimal damage to the viral structural proteins

106
Q

How do killed-virus vaccines work?

A

stimulate development of circulating antibody against viral membrane proteins. A boost usually needs to be administered

107
Q

Parental administration of killed vaccine may not be ideal to protect (blank) or (blank) virus. Why?

A

respiratory or GI

IgG ad IgM are induced rather than IgA

108
Q

Cell mediated immunity to killed viruses is usually generally (blank)

A

poor

109
Q

What are attenuated live virus vaccines?

A

utilize virus mutants that antigenically overlap with wild-type virus

110
Q

How do you make an attenuated virus?

A

by serial passages in animals or cell cultures

111
Q

How do attenuated viruses work?

A

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
Q

do you need multiple or single doses for killed vaccines?

A

multiple for killed

single for live

113
Q

Which is better a killed vaccine or a live vaccine? why?

A

live because it has longer better immunity.

114
Q

What is the proper use of present vaccines?

A

-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
Q

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

A

T

116
Q

A variety of foreign proteins may stimulate immune responses after the (bank) and (blank) system

A

innate and intrinsic

117
Q

Humoral response begins with interaction of a specific receptor on precursor (blank) with antigen

A

B lymphocytes

118
Q

Binding of antigen promotes (blank) into antibody secreting cells (plasma cells).

A

differentiation

119
Q

Naïve T cells are activated in lymph nodes following (Blank) binding of viral peptides displayed on dendritic cells.

A

TCR

120
Q

(blank) is expressed on all cells except RBCs

A

MHC 1

121
Q

(blank) is expressed mainly on APCs (dendritic cells, macrophages, B cells)

A

MHC II

122
Q

What do TH cells do?

A

Help B cells differentiate into plasma cells

Help T cells differentiate into CTL that can kill infected cells

Block 6 Week 4 (9 decks)

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