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Micro Block 3 > Block 3 > Flashcards

Block 3 Flashcards

1
Q

What viruses have natural onclytic tendencies

A

Reovirus
Parvovirus
Coxsackie

CPR (The essentials)

others:

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2
Q

genetically manipulated viruses to kill cancer cells

A

HSV
vaccinia
polio
adeno

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3
Q

How is polyomavirus special

A

circular dsDNA
early genes ==> large T antigen and small T anritgen
late genes ==> VP1-4

ALSO AFTER BEING ENDOCYTOSE GOES TO ER BEFORE NUCLEUS

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4
Q

BK virus

A

4 serotypes

disease upon immunosuppression
infection at young age
persistent in proximal renal tubular cells but can infect other T cells or other cells

10% of renal transplant polyomavirus associated nephorpaty

THINK TRANSPLANT IMMUNOSUPRESSION
10-25% BMT hemoraghic cystitis

cancer in animal modles not humans

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5
Q

JC virus

A

1 serotype

infections HUMAN GLIAL CELLS VIA SEROTONIN RECEPTOR

disease upon immunosupression like BK

persists in kidney, lymphocytes, bonne marrow cells

PML progressive multifocal leukoencephalopaty
DEMYELINATING DISEASE

cancer in animal models not humans

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6
Q

MCC

A

only PyV that can cause cancer in humans
starting during childhood
no cell culture systems

fast growing, PAINLESS, DOME SHAPED

RISK IN IMMUNOCOMPROMSIED, OLD PEOPLE SUN EXPSOED AREAS

integration into host chromosome in most MCC and mutation of LgT antigen in DDB

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7
Q

what causes cancer in MCC

A

integration into host chromosome and mutation in LgT

LgT expression in 98% of MCC

mutation in DBD of LgT

recall that LgT antigen (of early genes) consists of DNA binding domain, J domain (DNa replication), LXLCME, helicase domain

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8
Q

screen these viruses in pre engraftment

A 
HBV
HCV
HIV
CMV
EBV
syphilis
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9
Q

pre engraftment infections due to immunosupression

A

respriatoyr viruses
enteric viruses
HHV reactiv
HSV reactivation

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10
Q

post engraftment infections

30-100 days

A

CMV
adeno
HHV 6

RSV, IFV< PIV, MPV, RV (CA respiratory)

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11
Q

Retroviral mediated oncogenesis

A

non transforming and transforming

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12
Q

transforming oncogenesis

A

an oncogene is introduced

a MUTATED COPY OF A CELL GENE INVOLVD IN GROWTH CONTROL

infection introduces the mutated ONCOGENE ==> rapid tumor onset

Oncogenes include Src in the sarcoma virus

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13
Q

non transforming oncogenesis

A

ACTIVATING HOST GENES or INACTIVATING
dont transform culture cells
6 months - 1 year

promoter insertion
enhancer insertion (virus inserts in wrong directly opposite to gene but U3 is a strong viral enhancer that inappropriately turns on the cell promoter)
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14
Q

most viruses containing oncognes are

A

DEFECCTIVE

bc oncogene replaces some necessary viral genes

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15
Q

Basis for hiv strain tropism

A

envelope sequence of diff HIV have PREFERENCE FOR DIFF CO RECEPTORS

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16
Q

env interacts with CD4

A

induces CONFORMATIONAL CHANGE IN ENV
EXPOSES CO RECEPTOR BINDING SITE

gp41 FUSION DOMAINS EXPOSED. FUSION DOMAINS ENTER CELL MEMBRANE

co receptor engaged, gp41 snaps back
CAN YOU BLOCK SNAP BACK??? to block fusion

T20 blocks snapback of gp41

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17
Q

hiv infection pathogenesis

A

enters at mucosal surface
gets to the DC. DC brings HIV to the T cells in LYMPH NODES AND INFECTS T CELLS

replication within T cells, spills into circulation (viremia)

asymptomatic phase, FDC traps the virus and keeps viremia low BUT GALT is where REPLICATION IS HAPPENING

DC CAN CONTAIN THE VIRUS, BUT MOST REPLICATION IS STILL HAPPENING IN THE DLN

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18
Q

acute retroviral syndrome

A

sudden burst of virus production with decline in CD4 T cells

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19
Q

early vigorous CTL and humoral response helps clear viremia (along with FDC)

controlled it appears but high level persists in LN/GALT

A

HIV clinical features

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20
Q

progression of HIV

A

CD4:CD8 ratio, CD4 counts, viral load (RNA)

patients with a low set point have better prognosis

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21
Q

hiv diagnosis

A 
Ab ELISA (detects ab to virus, initial screening)
only 4-6 weeks after infection does it show positive. not detecting efore

Ag elisa (p24 capsid) 7-14 days after infection

WB ==> confifirmatory. detects HIV protein

rtPCR quantitatves RNA IN BLOOD

CAN DETECT BEFORE SEROCONVERSION

gauges viral load in ASYMPTOMATIC PATIENTS with low titers

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22
Q

ideal pathogen for vaccine

A

1) few serotypes
2) limitated mutageness of antigens
3) natural immunity after infection
4) acute infection that can be CLEARED FROM MOST IMMUNOCOMPETNET PEOPLE

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23
Q

How to make live vaccine

A

1) passage of a virus in animal host ca n make a weaker virus (Yellow fever)
2) isoalted virus from a diff species but provides cross protection
Cowpox/vaccinia to immunize smallpox
3) passage a pathogen in TC at a lower temp ==> select mutants that can’t replicate at BT (warmer)
aka flumist

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24
Q

inactiated virus

A

generates immune response BUT CAN’T MAKE INFECTIOUS VIRIONS

HAV, HBV, HPV, influenza, polio (salk), rabies

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25
Q

salk vs sabin admin

A

salk REQUIRES PARENTERAL
sabin ==> oral. rep in intestines

think salking teenager hates their parents (parenteral)

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26
Q

rash with central umbilication

A

COWPOX

pustules, vesicular

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27
Q

Roseola

A

fever, seizures then mobilliform rash (resembes measles)

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28
Q

Descending rash

A

measles and rubella.

rubella has more posterior cervical lymphoadeopathy

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29
Q

the only RNA virus that is double stranded

A

Reovirus

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30
Q

the only DNA virus that is single stranded

A

parvovirus

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31
Q

why is hepadnavirus special

A

circular, partially ds DNA virus

replicates in nucleus and cytoplasm

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32
Q

RNA all enveloped except

A

the ones that cause gut infections

reovirus
calcivirus (norovirus)
picornavirus

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33
Q

all positive sense RNA are icosahdral except

A

coronavirus (helical)

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34
Q

SEGMENTED GENOMES thus can

A

undergo reassortment

bunyavirus, orthomyxo, areno, reovirus

BOAR

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35
Q

paramyxovirus shape

A

paranomal mixer has HELICAL DECORATIONS HANGING FROM THE PARTY

helical shape
enveloped (ghost wearing a ghost cloak)

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36
Q

requirement of viruses. the main goal

A

MAKE MORE MRNA and new viral genomes
so need to make +mRNA from -mRNA

genomic type defines nuclei acid detection and diagnostics

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37
Q

baltimore classification

A

genomic type

6 classes -

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38
Q

plaque forming assay

A

plaque represents spread initiatited by a single infectious unit (pfu)

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39
Q

capsid vs enveloped

A

enveloped not stable in environemnt

capsid is stable

40
Q

virion entry

A

naked viruses use endocytusos

enveloped use glycoproteins to INDUCE USION WITH CELL MMBRAE
fusion releases capsid into the cytoplasm, traces of viral proteins left in the cytoplasm

41
Q

M2

A

acifidication of endosome enables release of capsid and fusion of membarne with endocytic membrane to GET OUT OF THE ENDOSOME

42
Q

viruses have to bring there own of these

A

RT (Rna to dan)
rna dep rna pol

HOST CELLS DONT HAVE
RT
ENZYMES THAT GO FROM RNA TO RNA

43
Q

ALL VIRUSES

A

must make positive sense mRNA to make proteins

all viruses use HOST RIBOSOMES TO MAKE VIRAL PROTEINS

44
Q

innate and adaptive responses to virus

A

innate (IFNs, cyrokines, chemokines) SOLUBLE MEDIATORS

recurtui macrophage, NK cells

apoptosis ==> TO PREVENT RELEASE OF INFECTIOUS VIRUS PARTICLES

adaptive (cell meaited and humoral)
humroal would be antibodies (enturalizing and complement fixing) d=
neuralizing blocks attachment and aentry

45
Q

innate is improtant bc

A

symptoms start BEFORE ADAPTIVE

production of Interferons first, then NK cells, then T cell mediated killing (adaptive) peaks around 6 days after infection

46
Q

NK cells

A

activated by IL12 from DC

IFNalpha and beta from epithelial cells

47
Q

IFN treatment

A

IFNa ==> HCV

IFNb => MS

IFN gamma ==> leukemias, melanoma, carcinoma

flu like symptoms
can reduce blood counts

48
Q

IFN alpha beta how does the response comes

A

PAMP binds to PRR
signaling thorugh adaptor and kinases

IRF factors bind to the ISRE
IRF acts like a transcription factor

SYNTHESIS AND SECRETOIN OF IFN ALPHA AND BETA

49
Q

Interferon genes

A

PKR
OAS

IFN gamma only made by T and NK cells
IFN alpha and bet made by all cells

50
Q

after IFN are made

A

they bind to receptors on nearby cells to induce an antiviral state

BINDS TO RECEPTORS ==> stimulates synthesis of JAK and STAT

51
Q

GUT VIRUSES

A

naked viruses

bc needs to be stable in acid

52
Q

the only rna virus that replicates in nucleus

A

retrovirus, orthomyxovirus

53
Q

only dna virus that replicates in cytoplasm

A

poxvirus

54
Q

fecal oral transmission

A

enterovrus(polio, coxsackie, echovirus which causes meningitis)

rotavirus

norovirus

polio is fecal oral, but replicates in nasopharynx and gut before travelling to the CNS

55
Q

acid labile

A 
rhinovirus
therefore it does not infect GI.
respiratory disease (common cold)
56
Q

enterovirus

A

IS ACID STABLE

57
Q

intrinsic and extrinsic apoptogis converges at

A

caspase 3 activation

extrinsic uses death ligand binding to FADD
intrinsic uses mitochondrial release of cytochrome c

58
Q

ICE inhibitors

A

prevents activation of IL1B

IL1B drives inflamation

ANTI INFLAMATROY EFFECT

59
Q

AIDS patients

A

JC virus ==> PML

60
Q

post transplant

A

BK ==> nephropathy

61
Q

Lymph nodes

A

enable virus to spread from inoculation / initialr eplicatoin site to go to the blood stream (Viremia) then carried to other parts of the body

62
Q

Measles pathogenesis

A

inoculation at respiratory tract ==> local replicatio ==> lymphatic spread ==> viremia == dissemiation ==> conjucntia, respiratory, urinary, sall blood vessels, CNS==> endothelall cells + Tcells CAUSES RASH

BASICALLY INCREASE VASCUMAR PERMEABILITY VIA CYTOKIEN RELEASE FROM T CELLS CAUSES RASH

after rash can have:

1) recovery (lifelong immunity)
2) post infectious encphalitis
3) SSPE
4) no resolution

63
Q

mumps clinical syndromes

A

fever, parotitis
bilateral usually

NO RASH

CNS invovelment ==> CAN HAVE MENINGITIS!!!!

64
Q

Prvovirus pathogenes

A

virus in URT==> local replication or goes to RBC prognietors in bone marrow. in normal hosts, slight drop in Hb
in those with hemolytic aneia, can get APLASTIC CRISIS

vriemia ==> rash and arthralgia

65
Q

what is the cause of rash in parvovirus

A 
immune complexxes (ab ag) 
DOESNT FIX COMPLEMENT BUT CAUSES ARTHRALGIA, ARTHIRITIS, RASH
66
Q

COxsackie virus causes

A

aseptic meningitis, herpangina (sores in the mouth), hand foot mouth disease, MYOCARDITIS, PERICARDITIS

67
Q

Issues with rotateq and rotarix

A

intisssceuption
reversion to virulent strain
shedding of virus by vaccine recipients
immunosuppresd patients

68
Q

norovirus characteristics “NOROWALK”

A 
low infectious dose
prolonged ASYMPTOMATIC SHEDDING
environemntal stability
STRAIN DIVERSYTI (MANY GENETIC AND ANTIGENIC TYPTES) 
dise can occur with REINFECTION
NO LASTING IMMUNITY
69
Q

VLP vaccines target

A

capsid proteins

VP1-4

70
Q

mono

A

lymphadenopathy, fatigue, pharyngitis, hepatosplenomegaly

71
Q

hepatomegaly

A

CMV,mono, acute viral hepatitis

72
Q

papilledema

A

meningitis, increased ICP

73
Q

SEGMENTED GENOME VIRUSES

A

enable ressortment ==> PANDEMICS

INFLUENZA, REOVIRUS (rotavirus)

74
Q

enterovirus

A

exits cell by LYSIS

75
Q

Segmented genomes

A

are each transribed SEPARATELYD TO PRODUCE MONOCISTRONIC RNAS

76
Q

comon cold

A

rhinovirus #1 cause

then coronavirus

77
Q

adenovirus

A

exudative tonsillitis, adenopathy, conjunctivitis, hemoraghic cystitis

78
Q

decrease risk of PTLD

A

donor gract contains T cells will decrease risk

79
Q

Kaposi sarcoma

A

most common aids malignancy
seen post transplant immunosupression
AIDS patients
IV Drug use

PURPLE, painless, raised plaques

torso, face, legs

AIDS patients ==> thrush, pneumonia

80
Q

BK virus

A

renal transplant ==> nephropathy

BM transplant ==> hemorrhagic cystitis

81
Q

EBV

A

Burkitts, hodkins lymphoma, nasopharyngeal carcinoma, hairy cell leukoplakia

82
Q

Herpesviruses

A

EBV replicates in nasopharynx

HSV1 and 2 replicate at the inoculation site in the mucosa and in sensory neurons. then retrograde trafficks to be latent in the ganglia

CMV EVERY WAY TRANSMISSION EXCEPT RESPIRATORY
breast feeding, fomites, shedding, genital, blood, transplant organs
usually gets in through GU, respiratory, GI tracts
lymphocytes circulate it around the body

VZV replicates in URT. respiratory secretion transmission (aerolized droplets)

83
Q

Kaposi sarcoma vs merkel cell carcinoma lesions

A

MCC ==> pAINLESS dome shaped
polyomavirus

kapsoi ==> also painless, but PURPLE RAISED

84
Q

hemoragic cystitis causes

A

immunosuppression, cyclophosphamide damages mucosa

adenovirus

BK virus

JC VIRUS

jab your bladder

CIDOFOVIR TREATMENT

85
Q

what did people use retrovirus for?

A

SCID
bubble baby sydrome
common gamma chain deficiency

86
Q

HCC

A

most commonly from chronic cirrhosis (HCV)

HBV can also cause HCC ut this is not from cirrhosis but integration into host genome causing malignant transformation

HBV is transmitted mainly during birth and sex
HCV think IVDU and blood transfusions (NOT THROUGH birthing)

87
Q

Vaccinia virus

A

poxvirus (DNA virus, but the only that replicates in cytoplasm not nucleus)

has its own replication machinery. replication competent

live attenuated virus for HBV
in contrast to subunit vaccine HbsAg (inactivated vaccine)

88
Q

Other poxviruses

A

do not multiply in human cells
more attenuated
HIV vaccine trials

canarypox
modified vaccinia ankara

89
Q

SSPE

A

seizures, visual disturbances, myoclonus

usually get mealses age 2, then latent for 6-8 years

90
Q

rubella

A

mild rash, fever, postauricular lymphadenopathy,

congenital rubella:
cataracts, patent DA, deafness, heart defects, microencephaly

91
Q

primary HSV

A

fever, lymphadenopathy, painful lesions on erthematous base

92
Q

Preenting apoptosis

A

poxvirus and herpesvius encode soluble TNF receptors

inhibitors of caspase block avarious proteolytic steps (poxvirus, herpesvirus, adenovirus)

INHIBIT P53==> adenovirus

93
Q

CMV congenital

A 
retinitis
microencephaly
jaundice
hepalosplenomegaly
hearing loss
petichiae
intracranial calcifications
seizures

perinatal/during birth from seronegative mother to fetus

after birth the nweborn sheds virus

like rubuella has CNS and ocular manifestation
(cataracts, deafness also in rubella)

94
Q

Hantavirus

A

from mouse

rainfall
plentiful food
increased mouse population

95
Q

CMV

A

associated with persistent infections ==> GBM atherosceloerisis
encodes own DNA POLYMERASE
alpha, beta, gamma genes

230kpb

BIG

Micro Block 3 (1 decks)

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