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Neuro > Poliovirus, Polyoma, Prions > Flashcards

Poliovirus, Polyoma, Prions Flashcards

1
Q

polio family and genus

A

picornaviridae

small rna virus

genus enterovirus
repliates in GI tract

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2
Q

characetristics of polivirus

A

nonenveloped, small, icosahedreal, spread by the fecal-oral route
3 serotypes

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3
Q

poliovirus causes

A

flaccid paralysis-poliomyelitis

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4
Q

course of poliovirus

A

7-14 day incubation
summer months-swimming pools

initially replicates in lymphoid tissue of pharynx and gut

virus present in throuat and feces

secondary viremia

to CNS and PNS

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5
Q

poliovirus in CNS and PNS

A

destroys motor neurons directly

causing flaccid paralysis

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6
Q

difference between poli method of damage

A

it is NOT the host immune response causing the damage-it is a lytic virus that directly causes neuronal cell injury

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7
Q

3 presentations of poliomyolitis

A

abortive-most common and symptomatic-mild no CNS inolvement 5%

aseptic meningitis-1-2%
-no paralysis,

paralytic poliomyeltis
-risk increases with age
any paralysis after 6 mos is permanent

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8
Q

post polio syndrome is

A

weakening of the muscles later in life

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9
Q

IgM response to polio replaced by

A

IgG-lifelong immunity

STRONG RESPONSE AND PRODUCITON TO SECRETORY IGA–> secreted by the gut into the mucosa-can nutralize the virus before shed in feces

thus preventing further transmission

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10
Q

diagnosis of polio virus

A

neutralization assays

vaccine strains can be distinguished from wild virus using specific antibodies

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11
Q

non-enveloped virus best inactivated by

A

formaldehyde or chlorine

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12
Q

types of polio vaccines 0general

A

live and inactivated

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13
Q

recommended type of vaccine in the US

A

inactivated

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14
Q

the name of the virus that prevents polio

A

SALK IPV-inactivated by formalin-killed no possibility of causing paralytic infection
by jonas salk

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15
Q

disdvantage of SALK IPV

A

protects against paralysis but not spread of wild virus

good IgG but not secretoy IgA-can still spread it in the fecal oral route0shed and spread

also takes 4 injections

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16
Q

do not use SALK IPV if allergic to

A

polymixin B, streptomycin, neomycin

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17
Q

SAYBIN vaccine advantages

A

chead
oral
porotects against paralysis and spread of virus wilde virus

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18
Q

difference between SALK and SABIN Polio viruses

A

the saybin makes a response strong enough to make an IgA response-> thus it inhibits shedding and spreading the IgA response inactivates the virus upon entering the GITract

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19
Q

disadvantage of the sabin virus

A

can revert to virulence during preparation or during replication in host and thus the otherwise attenuated virus can be shed–> can be given to others around them

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20
Q

disadvantage to OPV nationwide administration thingy

A

the OPV must be refrgierated—the africans dont have none of that over there

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21
Q

polyoma viruses are a member of the family

A

papovaviridae

> polyoma
papilloma
vacuoloating virus SV40

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22
Q

genome of the polyoma virus

A

non enveloped, icosahedral capsid

circular ds DNA small
5-8 kbp

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23
Q

can polyoma viruses remain in the environment

A

yes they are non enveloped

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24
Q

explain t antigen in polyoma viruses

A

since the virus is very small
it all begins at same ATG sequence

the t antigen, thanks to differential splicing can be clipped at three different spots

thiese are small T, middle T and Large T

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25
Q

one small genome with three distinc capsid proteins

A

polyoma virus

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26
Q

transformation of non-permissive cells and can make them cancerous

A

polyoma

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27
Q

to immortalize cells what is required from polyoma in transformaiton

A

large and small t antigen

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28
Q

what is required to transform the cell from an immortalized cell

A

small and middle t antigens

these cells have unchecked growth independent of growth factors THAT CAN BECOME TUMOR CELLS

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29
Q

“non-permissive” means

A

cell doesnt allow themselves to be lysed by the virus contained within

30
Q

2 known human polyoma viruses…

A

BK and JC

31
Q

do BK and JC cause tumors

A

no-human cells are permissive and allow themselves to be lysed

32
Q

50% of chuildren 3-4 are what

A

BK positive

*good thing it doesnt cause cancer in humans

33
Q

50% of 10-14 year olds are what

A

JC positive

*good that it doesnt caue cancer in humans

34
Q

in immunocompetent host what happens after primary and secondary viremia

A

it settles in kidneys and is latent

*inapaprent and silent infection

35
Q

in an immunocompromised host wehat happens with BK and JC viruses

A

reactivation after secondary viremia

BK to urine

JC to CNS

36
Q

BK outcome

A

BK-urine-does not cause significant disease in hmans once it has reactivated

37
Q

JC outcome in reactivation

A

JC-goes to CNS after reactivation

causes: progressive multifocal leukoencephalopathy

38
Q

describe PML by JC polyoma

demyelinating dz
mid to late life
death in 3-6 mos

A

reactivated JC virus infects and lyses oligodendrocytes

39
Q

diagnosis of JC

A

PCR amplification viral DNA in spinal fluid and brain tissue

MRI for white matter lesions

NO CELL CULTURE

40
Q

tx of JC polyoma

A

adjust HAART therapy to boost the immunosuppression

increases survival by 50%

41
Q

describe Transmissable spongiform ecephalopathies

A

typically long incubation period, then rapidly progressive

invariably fatal dimentia

multifocal spongiform changes

42
Q

path changes of TSE’s

A

mutifoca spingiform changes

astrogliosis

neuronal loss

amyloid plaques-but generally missing

minimal inflammatory response–> therefore the body likely reacting to something that is not that foreign to the body

43
Q

name the human TSE’s

A 
Kuru
CJD
GSS
FFI
variant CJD
44
Q

sheep TSE

A

scrappie

45
Q

cattle mad cow

A

Bovine spongiform ecephalopahty

46
Q

deer and elk

A

chronic wasting disease

47
Q

agents of TSE’s

A

infectious proteins

no nucleic acids, so it is not a virus

48
Q

prion protein conservancy in humans

A

chromosome 20

expressed as a 209 AA glycoprotein on the outside of the cell of neurons and lymphocytes

thus it is not surprising that the primary presentation deals with the CNS

49
Q

pathogenic prion

A

PRPsc

PRPres

PRPc-might actually inhibit pllaque formation in alzheimers
other wise the cellular form function unknown

50
Q

cellular and res forms can have_____ but can_____

A

same sequence but can can fold differntly

this varies the way scrapie proteins are cleaved by protease

51
Q

describe PRPsc

A

found in aggregates inside the vessicles of the cytoplasm

accumulation of scrapie leads to apooptosis of neurons

these have the same sequence as the cellular variant but fold differently and are much more stable and they aren’t cleaved very well so they can aggregate in vacuoles

52
Q

cannibalism prion

A

kuru

53
Q

most common human TSE

A

CJD

54
Q

clinical features of CJD

A

dementia
myoclonus
ataxia
mutism near death

very quick course

55
Q

most common cause of CJD

A

sporadic

60 yer old
no seasonality
no risk factors

realy rapid dath survival is 5-8 months

chance conversion of PRPc to PRPsc

56
Q

iatrogenic CJD from

pooled sources of graft material

also from survival in autoclave

A

dural graft
corneal grafts
human growth hormone

not by blood

shorter incubation period
1-2 years after documented contaminated grafts cources given to someone until the person has CJD

57
Q

familial CJD

different clnical features

A

autosomal dominant

specific alteration in PrP

average age 45-50

man survival=2-4 years

58
Q

dx of cjd

A

clinical-rapid diementia, myoclonus

histo-spongiform confirmed, lack of amyloid plauqes

rule out tertiary syphillis

characteristic EEG changes

59
Q

GSS

A

inherited, autosomeal dominant

AA 102 mutation in cellular form or PRP
more easily for confirmaitonal change to occur to make a new pathogenic protein

60
Q

GSS die quicker or shorters

A

longer-5 years
no eeg findings

less dementia

61
Q

amyloid plaques in GSS

A

positive—not there in CJD

62
Q

FFI

A

AD pattern
specific AA deletion
onset 50, 13 months to death

sleep disturbances
autonomic dysfiunction
rarely spondgiform changes

histopathology=less neruonal loss and less spongieform changes

63
Q

BLOOD transfusion and beef products

A

variant CJD

mad cow disease

64
Q

classical CJD limited to

A

CNS as a site for transmission

65
Q

vCJD can be found in

A 
CNS
lymph
tonsils, spleen, spleen, appendix, tonsils
blood
retina
DGR
spinal cord
66
Q

average age at vCJD and survival time

A

29 years-14 months

67
Q

main symptoms of vCJD

A

anxiety depression, akinetic mutism, sensory and visual abnormalities

68
Q

critical gene AA for vCJD

A

methionine at postiont 129 of PRPC

allowing these individuals to overcome specied barrier to cause BSE

69
Q

dx of vCJD

A

progressive neuropsychiatric dosroders more than 6 months

prion positive tonsillar biopsy

spongiforme in basal ganglia instead of cerebllum

florid appearanc

atypical EEG wihtout periodicity

70
Q

PRPsc summary

A

not sensitive to protease activity

aggregative

high beta sheet

intracellular vesicles

Neuro (19 decks)

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