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x virology term 2 quiz 4 > mumps, measles and slow viruses > Flashcards

mumps, measles and slow viruses Flashcards

1
Q

review of structure of paramyxoviruses

  • enveloped?
  • nucleocapsid symmetry?
  • genome structure?
  • -/+ stranded?
A

enveloped virion
helical symmetry
genome consists of a single molecule of RNA
RNA genome is minus-stranded

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2
Q

what type of virus are mumps and measles?

A

paramyxoviruses

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3
Q

are mumps and measles antigenically related to parainfluenza viruses?

A

mumps is

measles is not

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4
Q

describe mumps and measles:

  • nucleocapsid
  • genome
  • +/-
  • envelope?
A

helical nucleocapsid
minus-stranded RNA
envelope with virus-specified glycoproteins

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5
Q

do mumps and measles hemagglutinate red cells?

A

yes

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6
Q

do paramyxoviruses carry an RNA polymerase?

A

yes

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7
Q

can measles and mumps viruses reassort? why or why not?

A

since the RNA is only one piece, genetic reassortment is impossible
as a result, no significant antigenic variation has been seen

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8
Q

what types of infections do mumps and measles (and paramyxoviruses) cause?

A

systemic infections with viremia as an essential step in pathogenesis

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9
Q

what is an essential step in the pathogenesis of mumps and measles

A

viremia

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10
Q

what kinds of infections do orthomyxoviruses and paramyxoviruses generally cause?

A

local, nonsystemic noviremic infections

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11
Q

what is the significance of the fact that mumps and measles cause systemic infection (summary)?

A

incubation period is longer for mumps and measles because cycles of multiplication in several sites in sucession are required
lifelong immunity occurs in individuals who have had the disease - obligatory viremia allows neutralization by IgG

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12
Q

how does the incubation period of mumps and measles compare with that of orthomyxoviruses and paramyxoviruses (so flu and paraflu)?

A

it’s longer because the cycles of multiplication is several sites in succession are required to establish infection in mumps and measles

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13
Q

how long is immunity to mumps and measles after infection?

A

lifelong

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14
Q

what antibody type is involved in the reaction to mumps and measles?

A

obligatory viremia allows for neutralization by IgG

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15
Q

how many serotypes of mumps are there?

A

only one

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16
Q

how many types of species can mumps infect?

A

humans are the sole reservoir of mumps

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17
Q

how is mumps transmitted?

A

by respiratory droplets

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18
Q

how long is the average incubation period of mumps before symptoms appear?

A

18 days

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19
Q

what are the symptoms of mumps? what would allow you to diagnose mumps (ie what would you look for)?

A

around 18 days, a prodromal period of fever, malaise, and anorexia is followed by unilateral or bilateral swelling of the parotid gland (parotiditis) = usual presenting clinical symptom
will have inflamed parotid duct (stensens duct) in mouth
also get orchitis in males after age of puberty

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20
Q

what is paratiditis

A

caused by mumps
infection of the parotid gland
the virus grows in the enlarged parotid salivary glands
becomes painful
is excreted in saliva several days before and after swelling of the gland begins

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21
Q

why does mumps cause pain?

A

pressure and swelling within organs in tight capusles, so ones like the parotid gland and testis (orchitis) after puberty

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22
Q

are most mumps infections symptomatic or asymptomatic?

A

most are symptomatic - only 30% are subclinical/asymptomatic

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23
Q

where does mumps virus multiply, primarily?

A

in respiratory epithelium and local lymph nodes

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24
Q

what is the result of primary mumps multiplicaton (ie what’s the secondary step in infection)?

A

in viremia that spreads to the salivary glands and other organs

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25
Q

where do most of the infectious virions in mumps come from?

A

they are produced in the salivary glands

they go down the duct to the mouth and are spread by coughs and sneezes

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26
Q

how long does it take for parotiditis to begin in a mumps infection?

A

about 18-21 days = a three week incubation period

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27
Q

how frequent is orchitis in mumps infections?

A

occurs in about 30% of infected males past puberty

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28
Q

what is orchitis?
does it resolve?
who can get it?

A

painful inflammation of the testicles
caused by mumps
unilateral orchitis resolves with no other complicatoins
bilateral can result in sterility or subfertility but this outcome is uncommon
only in adults after puberty because children don’t have fibrous capsule yet

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29
Q

what organs are affected by mumps?

A

testicles, parotid gland
uncommonly the pancrease and ovary
more commonly the meninges (aseptic meningitis)
all have a generally benign course

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30
Q

how long is the immunity to mumps after infection?

A

generally lifelong, even after subclinical infection

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31
Q

is there an antiviral therapy for mumps?

A

no

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32
Q

is there a vaccine for mumps? if there is, what kind of vaccine is it and how is it administered (timing)?

A

yes, there is a live-attenuated vaccine
it’s administered as a component of the MMR pediatric vaccine
given twice to confer protection without serious side effects
incidence of infection has fallen in developed countries because of childhood immunization

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33
Q

what has been the incidence of mumps infection in developed countries recently?

A

the incidence has fallen markedly because of childhood immunization but there have been some recent epidemics

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34
Q

what kind of virus is measles? is it antigenically related to other viruses of its type?

A

measles is a paramyxovirus

it is unrelated to any other paramyxoviruses in humans

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35
Q

how often does measles cause subclinical infections?

A

almost never

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36
Q

pre-vaccination, how often were there measles epidemics?

A

local epidemics occured generally every three years in the winter

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37
Q

what were the causes of measles epidemics?

A

1: the number of nonimmune susceptibles increases because of births
2: epidemics occur when the number of nonimmune susceptibles becomes sufficient to break down herd immunity
note: there is no antigenic variation between the strain that causes epidemic and other strains, unlike flu

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38
Q

how is measles transmitted?

A

respiratory droplets

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39
Q

how/where does measles infect?

A

via the respiratory tract

initially multiplies in the epithelium and local lymph nodes and conjunctiva

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40
Q

what are the prodromal symptoms of measles?

A

fever, cold-like symptoms, runny nose, red eyes

photophobia is also a common symptom

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41
Q

what is the definitive symptom of measles?

A

rash
Koplik spots - bright red lesions with a white central spot on the buccal mucosa - appear first and then rash appears in a day or two
the rash is described as a generalized maculopapular erythematous rash

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42
Q

at what point after measles infection would you expect to see a rash appear?

A

after a 14-day incubation period

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43
Q

what, besides the virus, plays a role in the development of the rash seen in measles?

A

the immune response

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44
Q

how and when is measles virus excreted?

A

excreted from the respiratory tract and in tears and urine

for a few days before and after appearance of the rash

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45
Q

how common are complications from measles infection in developed countries?

A

can be mild to severe (death)

death rate in us from measles infection is 1 to 3 deaths per 1000 cases

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46
Q

what are common complications of measles in developed countries?

A

1: 1 in 20 result in pneumonia (sometimes due to a secondary bacterial infection
2: otitis media (generally bacterial)
3: acute encephalitis in about 1 to 2 per 1000 cases

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47
Q

in what cohort of patients would you expect to see complications from measles?

A

in adults and in those who are immune compromised

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48
Q

how is measles treated?

A

there is no specific treatment, but could give antibodies to measles from the sera of immune individuals to help a bit

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49
Q

what is the effect of the immune response to measles (ie is it effective and for how long)?

A

immune response eliminates viral excretion

confers life-long immunity without requiring restimulation by contact with exogenous virus

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50
Q

what is the pathology of measles virus?

A

measles causes the formation of multinucleated giant cells in lymphoid tissue and respiratory mucosa (virus-induced cell fusion)

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51
Q

what is the mechanism behind the pathology of the measles virus?

A

the measles fusion protein is inserted into infected cell plasma membranes, causing it to fuse with surrounding cells

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52
Q

what is the effect of measles on cell-mediated immunity?

A

measles infection suppresses cell-mediated immunity
eg: delayed hypersensitivity skin tests (such as the TB test) become negative for a few weeks or even months in a child who was positive before contracting measles = anergy

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53
Q

what is anergy and in what viral infection does it occur?

A

transient loss of cell-mediated immunity

occurs in measles infections

54
Q

<p>

| what type of environment (think population) does measles need to survive?</p>

A

<p>
a large, concentrated human population since it&#39;s enveloped, it&#39;s unstable and so must be growing in some individual at all times</p>

55
Q

how many resivoirs for the measles virus are there? how many serotypes?

A

only one - humans

there’s also only one serotype

56
Q

do immune individuals excrete infectious measles virus?

A

no

57
Q

what is the occurence of measles virus in small isolated populations like?

A

the virus disappears because continuous transmission is blocked by immunity or herd immunity

58
Q

what are the potential complications of measles virus and when do they occur?

A

though complications are rare, giant-cell pneumonia can occur
this is lethal, and occurs without a measles rash
occurs when cell-mediated immunity is defective (proof that cell-mediated immunity plays a role in the genesis of the rash)

59
Q

review of cell-mediated immunity

A

at least as important as antibodies in immunity to viral disease
viral proteins are synthesized on cellular ribosomes in the cytoplasm and these are occasionally partially degraded and antigenic fragments are displayed on MHCI proteins
this antigen presentation triggers an attack by MCHI-restricted cytotoxic T cells that are specific for the viral antigen

60
Q

what is congenital agammaglobulinemia? what diseases are patients with this disorder usually susceptible to and which ones can they recover from?

A

a defect in the ability to make antibody but still have normal cell-mediated immunity
subject to recurrent bacterial infection but usually recover from viral infections and develop long-term immunity to these infections

61
Q

what is the mortality rate due to measles in developing countries?

A

5-25% mortality rate
still causes more than 160,000 childhood deaths each year (down from 600,000 10 years ago)
progress in reducing deaths due to measles vaccination initiative

62
Q

what is symptom is seen in fatal cases of measles?

A

a severe hemorrhagic rash

63
Q

why does measles cause death? what can reduce mortality?

A

likely results from fatal synergism of measles and malnutrition
evidence for this: treatment with vitamin A can reduce mortality from measles (but also reduces overall childhood mortality rates)
also formation of multinucelated giant cells (syncytia) - don’t need to know mechanism, but antibodies won’t inhibit and immune system will have to clear out all the damaged tissue - t-cell immunity must be used to do so

64
Q

how is measles treated?

A

there is no specific antiviral therapy available

65
Q

is there a vaccine for measles? if so, what type is it and how is it administered?

A

there is an injected live-attenuated vaccine
given as a component of the MMR pediatric vaccine
given twice

66
Q

how does herd immunity to measles compare to that of other viruses?

A

since measles is highly infective, establishing and sustaining herd immunity is more difficult

67
Q

how frequent are measles cases in the US today?

A

it has been eradicated in the US, but about 50 to 100 imported cases occur every year

68
Q

what are the challenges of measles eradication?

A

in developing countries, many cases occur before 12 months of age, making immunization extremely difficult because of maternal antibody

69
Q

what are general characteristics of slow viruses caused by conventional viruses? (summary card)

A

1: have a long incubation period (usually years)
2: follow a slow but relentless course leading to death
3: tend to have a genetic predisposition
4: often re-emerge from latency during immune suppression

70
Q

how long is the incubation period of most slow viruses?

A

usually years

71
Q

how do genetics contribute to slow viruses?

A

those caused by conventional agents usually have a genetic predisposition
those caused by prions may have a genetic predisposition

72
Q

what are some examples of slow viruses caused by conventional viruses (list)?

A

HIV
JC virus - causes PML
SSPE

73
Q

what family of viruses does JC virus belong to?

A

papovavirus

74
Q

what does JC virus cause?

A

progressive multifocal leukoencephalopathy (PML)

75
Q

what types of patients does PML occur in?

A

it’s present in 75% of normal human sera, but only becomes a problem in immunocompromised individuals
especially AIDS patients and those receiving cancer chemotherapy and immunosuppresive drugs following organ transplantation
some patients undergoing MS treatment with monoclonal antibody natalizumab

76
Q

what are effects of PML?

  • cell types affected
  • symptoms and final outcome
A

it’s a progressive demyelinating disease of the brain (JC infects oligodendroglia)
causes demyelination by killing oligodendrocytes
neurons are unaffected
no inflammation is seen
progresses to blindness, dementia, coma
patients die within 6 months
initial symptoms include visual field defects, mental status changes, and weakness

77
Q

what is thought to cause PML in those infected with JC virus?

A

originates via the reactivation of JC virus

cases have been reported in patients undergoing immune treatment for MS

78
Q

what are the effects/results of subacute sclerosing panencephalitis (SSPE)?

A

intellecutal deterioration, psychological disturbances with slow decline interrupted by remissions
starts with mild changes in personality
generally fatal with terminal paralysis and blindness

79
Q

what virus causes subacute sclerosing panencephalitis (SSPE)?

A

measles

due to a recurrent infection that can’t repeat its replication (lev)

80
Q

what is seen by electron microscope in SSPE patients?

A

inclusion bodies

helical nucleocapsids were seen in these - suggested viral etiology

81
Q

what Ab titer and antigen results would you expect to see in a patient with SSPE?

A

high Ab titers to measles virus (much higher than in normal immune state)
CNS contains measles virus antigen

82
Q

what is the relationship between measles and SSPE?

A

all patients with SSPE had an uncomplicated case of measles 4 to 17 years before developing SSPE
many had measles at age 2 or younger
all have high antibody titer to measles and measles antigen in their CNS
the virus can be isolated from SSPE brains
however, how measles virus causes SSPE is not well understood

83
Q

can SSPE occur in individuals who have been vaccinated?

A

yes, but the incidence is less than one per million, which is much lower than the incidence following natural measles (one per 100000) (so basically you’re still better off getting vaccinated

84
Q

what are general characteristics of slow diseases caused by unconventional agents (prions)? (summary)

A

1: long incubation period (usually years)
2: follow a slow but relentless course leading to death
3: cause diseases confined to CNS
4: produce a spongiform encephalopathy
5: may have a genetic predisposition

85
Q

what are prions?

A

they’re hypothesized to be infectious proteins
protein-containing particles that lack any detectable nucleic acid
highly resistant to proteolytic enzymes
resistant to temperatures usually employed in cooking - may be important in suspected ability to be transmitted by food

86
Q

what are human prion-mediated diseases called?

A

transmissible spongiform encephalopahties
(note: spongiform refers to spongy, swiss-cheese like hose seen in brain parenchyma that are caused by the death of the neurons - levinson)

87
Q

what are the five known human transmissible spongiform encephalopathies due to prions? (list)

A

1: KURU
2: creutzfeld-jacob disease (CDJ)
3: variant CDJ
4: gerstmann-Straussler-scheinker syndrome (GSS)
5: fatal familial insomnia

88
Q

scrapie (summary card)

A

chronic progressive CNS (usually cerebellum) disorder of adult sheep
no pathological evidence of an infectious process
certain inbred lines are much more susceptible
agent that causes the disease has been transfered to mice with an incubation period of less than one year
resistant to uv irradiation, formaldehyde, alkylating agents, etc. - no known virus would survive these treatments

89
Q

in what species and part of the body does scrapie act?

A

in adult sheep

chronic progressive CNS disorder - usually in the cerebellum

90
Q

what makes sheep genetically predisposed to scrapie?

A

being the descendent of certain inbred lines

91
Q

can scrapie infect other animals?

A

yes, it has been transfered to mice

92
Q

what is the incubation period of scrapie?

A

in the strains that have been transfered to mice, an incubation period of less than a year has been observed

93
Q

what treatments is scrapie resistant to?

A

UV irradiation
formaldehyde
alkylating agents
no know virus would survive these

94
Q

what species and part of the body does Kuru affect?

A

it’s a progressive degenerative disorder of the CNS, especially the cerebellum, in humans

95
Q

in what population is the Kuru virus seen?

A

limited to a small stone-age tribe in New Guinea (the Fore people)

96
Q

what are the symptoms/effects of Kuru?

  • what cells it affects
  • symptoms
A

spongiform encephalopathy - death of neurons (rather than demylenation as with JC virus)
at it’s peak caused 1/2 of the mortality rate of the fore tribe that it effects
symptoms = progressive tremors and ataxia, but not dementia

97
Q

how can the kuru disease be transmitted?

A

by ingestion of infected brains
the symptoms and neuropathy were reproduced in chimps that were infected by intracerebral injection of brain material from human cases
could also be transmitted through cuts while the brains were prepared

98
Q

what other prion does Kuru resemble?

A

scrapie, in terms of the properties of the infectious agent

99
Q

what is the incidence of Kuru today?

A

now low because of reduced cannibalism

100
Q

what is the most common human spongiform encephalopathy?

A

creutzfeld-jacob disease (CJD)

101
Q

what are the causes of creutzfeld-jacob disease (CJD)?

A 
some are due to an inherited mutation (15% of cases; autosomal dominant; called fCJD), but most are spontaneous with no established cause (called sCJD)
some iatrogenic (inadvertently caused by physicians) cases have been caused by corneal transplants and other medical procedures
102
Q

what are iatrogenic cases of a disease?

A

cases inadvertently caused by physicians
example: cases of CJD due to corneal transplants from a donor with undiagnosed disease or contaminated surgical instruments or to GH prepared from the pituitary glands of undiagnosed patients

103
Q

what is variant CJD (aka vCJD), and how is it spread?

A

this is mad cow disease
it’s a spongiform encephalopathy of cows
reached epidemic status in britain as a result of using brains and bone marrow from cows and sheep to manufacture of bovine food
outbreak in humans was linked to eating beef from these infected cows

104
Q

what can inactivate prions?

A

protein and lipid-disrupting agents such as phenol, ether, NaOH, and hypochlorite

105
Q

what is the mechanism by which prions affect neuronal signaling (levinson)?

A

normally in alpha helical conformation (known as PRPc)
when to changes to beta-pleated sheet (now known as PrPsc or prion protein scrapie) these aggregate into filaments - disrupt neuronal function and cause cell death
beta-pleated form can recruit alpha helical forms and cause them to change their concentration

106
Q

are there virus particles in the brains of people with spongiform encephalopathies?

A

no

107
Q

what is an encephalopathy (levinson)?

A

pathologic process in the brain without signs of inflammation

108
Q

what is encephalitis (lev)?

A

an inflammatory brain process in which either neutrophils or lymphocytes are present

109
Q

how are prions acquired/transmitted? what do they do once they are (ie how do they spread throughout the body)? (lev)

A

ingested
must survive digestion in intestinal tract and penetrate gut mucosa
amplified within follicle dendritic cells in lymphatic tissue, such as peyer’s patches
spread to spleen - carried by migrating dendritic cells
spread to CNS, probably via sympathetic nerves
could also reach the brain via lymphocytes

110
Q

what are polyomaviruses (enveloped?; genome structure?)? what is an example of one?

A

nonenveloped viruses with a circular, double-stranded DNA genome
JC virus is one
this is according to levinson - our course notes classify JC virus as a papovavirus

111
Q

how would you diagnose JC virus? (lev)

A

usually by PCR assay of a brain biopsy specimen or spinal fluid

112
Q

what are the clincal findings of CJD? (lev)

A

dementia, including behavioral changes, memory loss, and confusion
myoclonic jerking
ataxia
aphasia
visual loss
hemiparesis
symptoms appear gradually and progress inexorably
in terminal stage - patient mute and akinetic, then comatose
80% die within 1 year

113
Q

how can CJD be diagnosed? (lev)

A

presumptively by detecting spongivform changes in brain biopsy specimen
would see neuronal loss and gliosis and sometimes amyloid plaques
brain imaging and eeg may show changes
specific diagnosis by immunohistochemistry for prions (make antibodies in other animals because humans don’t make antibodies for the prions that infect them - so no serological tests can be used)

114
Q

how can vCJD be diagnosed? (lev)

A

presumptive diagnosis via brain biopsy specimen
would see “florid” plaques composed of flowerlike amyloid plaques surrounded by a halo of vacuoles
brain imaging and eeg may show changes
can look at tonsilar tissue using monoclonal antibody-based assays

115
Q

what is familial fatal insomnia?

A

one of the slow diseases caused by prions
characterized by progressive insomnia, dysautonomia, resulting in dementia, death
patients have specific mutation in prion protein

116
Q

what is different about variant CJD than CJD? ie why is it variant? (lev)

A

occurs in much younger people

has certain clinical and pathologic findings different from those found in typical form of disease

117
Q

what genetic profile must someone have to contract vCJD?

A

can only be contacted by people who have a native prion protein that is homozygous for methionine at AA 129

118
Q

what are the symptoms of scrapie?

A

sheep get tremors, ataxia, itching - sheep scrape their wool off against fence posts
spongiform degeneration without inflammation

119
Q

describe the replicative cycle of measles and mumps (lev)

A

adsorption to the cell surface via hemagglutinin
penetrates and uncoats
virion RNA polymerase transcribes the negative-strand genome into mRNA
multiple mRNAs are synthesized
each translated into the specific viral proteins
helical nucleopcapsid is assembled
matrix protein mediates teh interaction with the envelope
virus released by budding from the cell membrane

120
Q

what is the result of measles infection in pregnant women? (lev)

A

usually results in stillbirth

121
Q

why shouldn’t the MMR vaccine be given before 15 months of age?

A

maternal antibodies could neutralize the virus, preventing an immune response

122
Q

what ways can genetic variation in viruses occur? (review)

what forms of influenza can this occur in and why?

A
  • genetic reassortment - mixing between viruses of different species
    influenza A can undergo shifts in antigenicity but B and C don’t because B and C don’t exist in birds or pigs, where the reassortment is suspected to occur since birds and pigs can host human forms of influenza A
  • can have classical genetic recombination
    not with single-stranded RNA viruses
  • simple mutation
    RNA viruses have higher rate - paramyxoviruses
123
Q

what is the only thing that changes the death rate of humans?

A

influenza A (just a random interesting fact)

124
Q

why does the antibody for measles not appear until after 14 days? (what is the normal length of time for occurence?)

A

normally takes 7 days for antibodies to appear

125
Q

what are koplick spots?

A

spots in the mouth
appear 14 days after infection
definitive of measles

126
Q

where can measles virus grow? what will the infection cause in some of these tissue types?

A 
can grow everywhere
so also grows in eyes
causes photophobia - pupils huge
often have tears
in respiratory tract so potential for pneumonia
in skin so rash
ear infections
encephalitis because can grow in NS
fever
127
Q

what age group is measles infection most severe?

A

older children and adults

128
Q

what is anergy and in what virus does it occur?

A

anergy is lack of immune response to infected cells

in measles indicates that there’s a defect in T-cell response to the virus

129
Q

what is giant cell pneumonia and when does it occur?

A

only occurs in kids infected by measles with a genetic defect in cell-mediated immunity
no measles rash!
kills kids cause get syncytia in lung

130
Q

what can increase deadliness of measles (epidemiological factors)?

A

living in close proximity - in Glasgow rates of death increased significantly with the more people living/room - also socioeconomic though
malnourished
rickets
vitamin A
protein
give any of these things get reduction in deaths

x virology term 2 quiz 4 (6 decks)

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