Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

characetristics of polivirus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

poliovirus causes

A

flaccid paralysis-poliomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

poliovirus in CNS and PNS

A

destroys motor neurons directly

causing flaccid paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

post polio syndrome is

A

weakening of the muscles later in life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diagnosis of polio virus

A

neutralization assays

vaccine strains can be distinguished from wild virus using specific antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

non-enveloped virus best inactivated by

A

formaldehyde or chlorine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

types of polio vaccines 0general

A

live and inactivated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

recommended type of vaccine in the US

A

inactivated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

do not use SALK IPV if allergic to

A

polymixin B, streptomycin, neomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SAYBIN vaccine advantages

A

chead
oral
porotects against paralysis and spread of virus wilde virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

disadvantage to OPV nationwide administration thingy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

polyoma viruses are a member of the family

A

papovaviridae

> polyoma
papilloma
vacuoloating virus SV40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

genome of the polyoma virus

A

non enveloped, icosahedral capsid

circular ds DNA small
5-8 kbp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

can polyoma viruses remain in the environment

A

yes they are non enveloped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
one small genome with three distinc capsid proteins
polyoma virus
26
transformation of non-permissive cells and can make them cancerous
polyoma
27
to immortalize cells what is required from polyoma in transformaiton
large and small t antigen
28
what is required to transform the cell from an immortalized cell
small and middle t antigens these cells have unchecked growth independent of growth factors THAT CAN BECOME TUMOR CELLS
29
"non-permissive" means
cell doesnt allow themselves to be lysed by the virus contained within
30
2 known human polyoma viruses...
BK and JC
31
do BK and JC cause tumors
no-human cells are permissive and allow themselves to be lysed
32
50% of chuildren 3-4 are what
BK positive | *good thing it doesnt cause cancer in humans
33
50% of 10-14 year olds are what
JC positive | *good that it doesnt caue cancer in humans
34
in immunocompetent host what happens after primary and secondary viremia
it settles in kidneys and is latent | *inapaprent and silent infection
35
in an immunocompromised host wehat happens with BK and JC viruses
reactivation after secondary viremia BK to urine JC to CNS
36
BK outcome
BK-urine-does not cause significant disease in hmans once it has reactivated
37
JC outcome in reactivation
JC-goes to CNS after reactivation causes: progressive multifocal leukoencephalopathy
38
describe PML by JC polyoma demyelinating dz mid to late life death in 3-6 mos
reactivated JC virus infects and lyses oligodendrocytes
39
diagnosis of JC
PCR amplification viral DNA in spinal fluid and brain tissue MRI for white matter lesions NO CELL CULTURE
40
tx of JC polyoma
adjust HAART therapy to boost the immunosuppression increases survival by 50%
41
describe Transmissable spongiform ecephalopathies
typically long incubation period, then rapidly progressive invariably fatal dimentia multifocal spongiform changes
42
path changes of TSE's
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
name the human TSE's
``` Kuru CJD GSS FFI variant CJD ```
44
sheep TSE
scrappie
45
cattle mad cow
Bovine spongiform ecephalopahty
46
deer and elk
chronic wasting disease
47
agents of TSE's
infectious proteins no nucleic acids, so it is not a virus
48
prion protein conservancy in humans
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
pathogenic prion
PRPsc PRPres PRPc-might actually inhibit pllaque formation in alzheimers other wise the cellular form function unknown
50
cellular and res forms can have_____ but can_____
same sequence but can can fold differntly this varies the way scrapie proteins are cleaved by protease
51
describe PRPsc
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
cannibalism prion
kuru
53
most common human TSE
CJD
54
clinical features of CJD
dementia myoclonus ataxia mutism near death very quick course
55
most common cause of CJD
sporadic 60 yer old no seasonality no risk factors realy rapid dath survival is 5-8 months chance conversion of PRPc to PRPsc
56
iatrogenic CJD from pooled sources of graft material also from survival in autoclave
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
familial CJD | different clnical features
autosomal dominant specific alteration in PrP average age 45-50 man survival=2-4 years
58
dx of cjd
clinical-rapid diementia, myoclonus histo-spongiform confirmed, lack of amyloid plauqes rule out tertiary syphillis characteristic EEG changes
59
GSS
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
GSS die quicker or shorters
longer-5 years no eeg findings less dementia
61
amyloid plaques in GSS
positive---not there in CJD
62
FFI
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
BLOOD transfusion and beef products
variant CJD mad cow disease
64
classical CJD limited to
CNS as a site for transmission
65
vCJD can be found in
``` CNS lymph tonsils, spleen, spleen, appendix, tonsils blood retina DGR spinal cord ```
66
average age at vCJD and survival time
29 years-14 months
67
main symptoms of vCJD
anxiety depression, akinetic mutism, sensory and visual abnormalities
68
critical gene AA for vCJD
methionine at postiont 129 of PRPC allowing these individuals to overcome specied barrier to cause BSE
69
dx of vCJD
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
PRPsc summary
not sensitive to protease activity aggregative high beta sheet intracellular vesicles

Neuro (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions