Gastro-Adeno-Papilloma Flashcards

(52 cards)

1
Q

Viral Gastroenteritis
inflamm of?
important diseased of?
leading cause of?

A

– Inflammation of stomach or intestines
– important disease of infants and children
– leading cause of childhood death in developing countries

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2
Q

viral cause of gastroeneritis

A
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3
Q

rotavirus and group A, b and c genomes

A

segemented dsRNA

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4
Q

medical significance of group A reovirdiae

A

major cause of diarrhea in infants

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5
Q

norovirus significance

A

major cause of diarrhea outbreaks in adults/children

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6
Q

~____% of diarrhea cases still have unknown etiology

A

50

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7
Q

Norwalk identification

A

1st virus identified from stool samples by electron microscopic examination (1972)

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8
Q

Rotaviruses are members of the_________family

A

Reovirus= Respiratory Enteric Orphan viruses

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9
Q

Reovirus family envelope/caspids

A

nonenveloped with inner/outer capsids

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10
Q

rotavirus/reovirus replication

A

enters via endocytosis
full genome replication
uses own RNA poly
buds from ER

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11
Q

genome of rotaviruses

A

11 segments of double-stranded RNA (dsRNA)

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12
Q

end result rotavirus infection on cell

A

Lysis of infected cells

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13
Q

Rotaviruses may cause?

A
  • potentially fatal dehydration
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14
Q

transmission of rotaviruses
what allows them to be transmitted this way?
how infectious?

A

fecal-oral transmission
acid stability conferred by double capsid structure
up to 10^12 virus particles per ml stool and as few as 10 virus particles can cause infection

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15
Q

how do rotaviruses cause potentially fatal diarrhea

A

virus produces an enterotoxin
binds integrins; signaling results secretion of chloride and water
infected gut epithelial cells destroyed & replaced by immature epithelial cells (reduced uptake of ions, water; less absorption of foods molecules (carbs))

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16
Q

most common group of rotaviruses in US

A

group A

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17
Q

rotavirus vax?

A

Rotavirus vaccine for infants (>75% effective)

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18
Q

norovirus genome/ strucutre

A

+ RNA

naked capsid virions

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19
Q

norovirus replication, similar to what other virus?

A

Replication similar to picornaviruses (poliovirus) except 2nd phase of translation involves subgenomic RNAs (like coronaviruses).

Has a 5VPg protein on RNA (like picornaviruses)

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20
Q

Adenovirus
genome
structure/ geometry

A

linear dsDNA
non enveloped
iscohedral

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21
Q

adenovirus cell entry

A

•Adenovirus attaches to receptors on surface of host cells (CAR = coxsackievirus
adenovirus receptor)
•most cells express CAR
•receptor-mediated endocytosis
•pH drop in endosome induces viral uncoating
•endosome ruptures, releasing contents into cytoplasm
•viral nucleoprotein complex enter cell nucleus

22
Q

adenovirus gene expression and transcription regulators

where does viral DNA go?

A

Adenovirus gene expression temporal regulation: pre-early, early, late genes
RNAs are spliced

transcriptional regulators produced during one phase act to promote transcription of genes of subsequent phase

VIRAL DNA ENTERS NUCLEUS

23
Q

adenovirus DNA replication, priming?

A

only one of the 2 DNA strands is copied at each replication fork no discontinuous replication (lagging strand replication)
priming is by a viral protein, pTP (preterminal protein)
strand not copied can self bind and be primed for replication

24
Q

what primes adenovirus DNA syn

A

Priming of DNA synthesis by pTP serine residue

25
adenovirus infections commonality? | symptoms?
widespread: 5-10% of all viral infections | similar to common cold
26
adenovirus vax type | targets which serotypes?
Vaccine (live virus) given to new military recruits | targets serotypes 4 and 7
27
acute respiratory disease (ARD) caused by what virus/serotypes
adenovirus serotypes 4, 7, and 21
28
adenovirus interference with host cell function
interefers with gene expression to reduce mRNA transport/ translation= stops host cell pro synthesis
29
adenovirus Mechanisms for evasion of host defense
block MHC class I mRNA production block transport of MHC class I proteins to the cell surface viral E3gp19K protein does this= results in block of killing by cytotoxic T cells
30
Adenovirus | E3 region
cluster of genes mediating evasion of host defense
31
adenovirus will drive the host cell into? why? proteins used? actions? can potentially lead to what state?
Adenovirus drives the host cell into cell division necessary for adenovirus to replicate (needs cellular S phase factors) Adenovirus E1a and E1b proteins interfere with cell division controllers E1b sequesters p53 and E1a sequesters Rb (retinoblastoma protein) Viral infection can potentially drive a cell toward a cancerous state
32
Brief background on cell cycle factors: Rb and E2F example
Example: DNA damage during G1 P53 recognizes DNA damage and activates P21 (p53 recognizes certain types of DNA mismatches) P21 binds and inactivates the cyclin-CDK complex which has already begun to be produced in response to different signals DNA repaired, p53 decreases, P21 no longer blocks cyclin-CDK, cell cycle progression P53 act as a checkpoint controller to stop cell-cycle progression
33
Inactivation of p53 by adenovirus
done by E1b protein- prevents activation of p21 (and Bax)
34
Adenovirus E1a protein
binding to Rb complex prevents Rb from negatively regulating E2f
35
Human papillomaviruses | genomes and strucutres
circular dsDNA | non enveloped
36
Human papilloma viruses (HPV) serotypes
100s
37
types of HPV
mucosal or cutaneous
38
HPV infection process timeframe
3-4 month process (usually)
39
HPV access into body | what stimulates early growth?
HPV accesses basal layer through breaks in skin | Viral early genes stimulate cell growth (which facilitates viral replication)
40
``` HPV reproduction coordinated with? HPV gene expression? late proteins made when? Assembly? nuclear remnants shed? ```
HPV reproduction coordinated with development of keratinocytes (Keratinocytes = nondividing, physical barrier; nuclear) As cells move through skin layers HPV gene expression and DNA replication begins (uses cellular DNA polymerase) Late proteins (capsid proteins) only made in differentiated layers Assembly occurs in nucleus during keratinocyte development Nuclear remnant with viral particles shed at skin surface. HPVs are not lytic.
41
Koilocytes
enlarged keratinocytes with clear halos around enlarged nuclei - characteristic of HPV infection
42
HPV spread by?
skin-to-skin contact: breaks in skin or example, scratching mucous membranes more susceptible sexual contact During birth
43
HPV oral/ airway symptoms
Warts of oropharynx laryngeal papillomas (HPV-6 and -11) respiratory papillomatosis: hoarseness is usual symptom (signify obstructing HPV lesions) respiratory distress and secondary bacterial pneumonia in children
44
most benign tumors of oral cavities
HPV Single oral papillomas are the most benign epithelial tumors of the oral cavity
45
Anogenital warts, main strains?
condylomata acuminata (90% caused by HPV-6 and -11)
46
Cervical papillomas %? strains?
HPV is present in 99.7% of a cervical cancers >85% of cervical carcinomas contain integrated HPV DNA HPV 16 and 18 (and 31& 45) are high-risk types
47
detection of cervical cancer
Koilocytic cells in Pap smears indicate HPV
48
HPV infection often visable?
Often infections are not recognizable (asymptomatic) up to 50% of a population positive for HPV DNA but majority have no visible evidence of infection
49
HPV prevention
vax available for strains 16 and 18, prevention of cervical cancer
50
HPV proteins important in cancer
The HPV E6 and E7 proteins are important for cancer development. They are the only 2 HPV proteins always expressed in cervical cancer cells.
51
HPV E6 protein action
Inactivation of p53: leads to ubiquitination of p53 and degradation
52
E7 protein action
prevents Rb from controlling cell division these proteins bind Rb complex and prevent Rb from negatively regulating E2f E2f is now free to activate transcription of cellular DNA synthesis genes.