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Block 3 Flashcards

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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
salk vs sabin admin
salk REQUIRES PARENTERAL sabin ==> oral. rep in intestines think salking teenager hates their parents (parenteral)
26
rash with central umbilication
COWPOX | pustules, vesicular
27
Roseola
fever, seizures then mobilliform rash (resembes measles)
28
Descending rash
measles and rubella. | rubella has more posterior cervical lymphoadeopathy
29
the only RNA virus that is double stranded
Reovirus
30
the only DNA virus that is single stranded
parvovirus
31
why is hepadnavirus special
circular, partially ds DNA virus | replicates in nucleus and cytoplasm
32
RNA all enveloped except
the ones that cause gut infections reovirus calcivirus (norovirus) picornavirus
33
all positive sense RNA are icosahdral except
coronavirus (helical)
34
SEGMENTED GENOMES thus can
undergo reassortment bunyavirus, orthomyxo, areno, reovirus BOAR
35
paramyxovirus shape
paranomal mixer has HELICAL DECORATIONS HANGING FROM THE PARTY helical shape enveloped (ghost wearing a ghost cloak)
36
requirement of viruses. the main goal
MAKE MORE MRNA and new viral genomes so need to make +mRNA from -mRNA genomic type defines nuclei acid detection and diagnostics
37
baltimore classification
genomic type | 6 classes -
38
plaque forming assay
plaque represents spread initiatited by a single infectious unit (pfu)
39
capsid vs enveloped
enveloped not stable in environemnt | capsid is stable
40
virion entry
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
M2
acifidication of endosome enables release of capsid and fusion of membarne with endocytic membrane to GET OUT OF THE ENDOSOME
42
viruses have to bring there own of these
RT (Rna to dan) rna dep rna pol HOST CELLS DONT HAVE RT ENZYMES THAT GO FROM RNA TO RNA
43
ALL VIRUSES
must make positive sense mRNA to make proteins | all viruses use HOST RIBOSOMES TO MAKE VIRAL PROTEINS
44
innate and adaptive responses to virus
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
innate is improtant bc
symptoms start BEFORE ADAPTIVE production of Interferons first, then NK cells, then T cell mediated killing (adaptive) peaks around 6 days after infection
46
NK cells
activated by IL12 from DC | IFNalpha and beta from epithelial cells
47
IFN treatment
IFNa ==> HCV IFNb => MS IFN gamma ==> leukemias, melanoma, carcinoma flu like symptoms can reduce blood counts
48
IFN alpha beta how does the response comes
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
Interferon genes
PKR OAS IFN gamma only made by T and NK cells IFN alpha and bet made by all cells
50
after IFN are made
they bind to receptors on nearby cells to induce an antiviral state BINDS TO RECEPTORS ==> stimulates synthesis of JAK and STAT
51
GUT VIRUSES
naked viruses | bc needs to be stable in acid
52
the only rna virus that replicates in nucleus
retrovirus, orthomyxovirus
53
only dna virus that replicates in cytoplasm
poxvirus
54
fecal oral transmission
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
acid labile
``` rhinovirus therefore it does not infect GI. respiratory disease (common cold) ```
56
enterovirus
IS ACID STABLE
57
intrinsic and extrinsic apoptogis converges at
caspase 3 activation extrinsic uses death ligand binding to FADD intrinsic uses mitochondrial release of cytochrome c
58
ICE inhibitors
prevents activation of IL1B IL1B drives inflamation ANTI INFLAMATROY EFFECT
59
AIDS patients
JC virus ==> PML
60
post transplant
BK ==> nephropathy
61
Lymph nodes
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
Measles pathogenesis
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
mumps clinical syndromes
fever, parotitis bilateral usually NO RASH CNS invovelment ==> CAN HAVE MENINGITIS!!!!
64
Prvovirus pathogenes
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
what is the cause of rash in parvovirus
``` immune complexxes (ab ag) DOESNT FIX COMPLEMENT BUT CAUSES ARTHRALGIA, ARTHIRITIS, RASH ```
66
COxsackie virus causes
aseptic meningitis, herpangina (sores in the mouth), hand foot mouth disease, MYOCARDITIS, PERICARDITIS
67
Issues with rotateq and rotarix
intisssceuption reversion to virulent strain shedding of virus by vaccine recipients immunosuppresd patients
68
norovirus characteristics "NOROWALK"
``` low infectious dose prolonged ASYMPTOMATIC SHEDDING environemntal stability STRAIN DIVERSYTI (MANY GENETIC AND ANTIGENIC TYPTES) dise can occur with REINFECTION NO LASTING IMMUNITY ```
69
VLP vaccines target
capsid proteins | VP1-4
70
mono
lymphadenopathy, fatigue, pharyngitis, hepatosplenomegaly
71
hepatomegaly
CMV,mono, acute viral hepatitis
72
papilledema
meningitis, increased ICP
73
SEGMENTED GENOME VIRUSES
enable ressortment ==> PANDEMICS INFLUENZA, REOVIRUS (rotavirus)
74
enterovirus
exits cell by LYSIS
75
Segmented genomes
are each transribed SEPARATELYD TO PRODUCE MONOCISTRONIC RNAS
76
comon cold
rhinovirus #1 cause | then coronavirus
77
adenovirus
exudative tonsillitis, adenopathy, conjunctivitis, hemoraghic cystitis
78
decrease risk of PTLD
donor gract contains T cells will decrease risk
79
Kaposi sarcoma
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
BK virus
renal transplant ==> nephropathy | BM transplant ==> hemorrhagic cystitis
81
EBV
Burkitts, hodkins lymphoma, nasopharyngeal carcinoma, hairy cell leukoplakia
82
Herpesviruses
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
Kaposi sarcoma vs merkel cell carcinoma lesions
MCC ==> pAINLESS dome shaped polyomavirus kapsoi ==> also painless, but PURPLE RAISED
84
hemoragic cystitis causes
immunosuppression, cyclophosphamide damages mucosa adenovirus BK virus JC VIRUS jab your bladder CIDOFOVIR TREATMENT
85
what did people use retrovirus for?
SCID bubble baby sydrome common gamma chain deficiency
86
HCC
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
Vaccinia virus
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
Other poxviruses
do not multiply in human cells more attenuated HIV vaccine trials canarypox modified vaccinia ankara
89
SSPE
seizures, visual disturbances, myoclonus | usually get mealses age 2, then latent for 6-8 years
90
rubella
mild rash, fever, postauricular lymphadenopathy, congenital rubella: cataracts, patent DA, deafness, heart defects, microencephaly
91
primary HSV
fever, lymphadenopathy, painful lesions on erthematous base
92
Preenting apoptosis
poxvirus and herpesvius encode soluble TNF receptors inhibitors of caspase block avarious proteolytic steps (poxvirus, herpesvirus, adenovirus) INHIBIT P53==> adenovirus
93
CMV congenital
``` 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
Hantavirus
from mouse rainfall plentiful food increased mouse population
95
CMV
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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