Gastro-Adeno-Papilloma- Exam IV Flashcards

1
Q
  • inflammation of stomach or intestines
  • important disease of infants and children
  • leading cause of childhood death in developing countries
A

viral gastroenteritis

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2
Q

The naming of viral gastroenteritis is named based on:

A

tissue tropism; not viral structure

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3
Q

viral gastroenteritis is an important disease of ___ & ___

A

infants and children

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4
Q

The leading cause of childhood death in developing countries:

A

viral gastroenteritis

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5
Q

Etiological agents of viral gastroenteritis in humans include: (6)

A
  1. rotavirus (Groups A,B & C)
  2. Norovirus
  3. Sapovirus
  4. Enteric adenovirus
  5. Astrovirus
  6. Aichi virus
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6
Q

Describe the genomic structure of groups A, B, and C rotaviruses:

A

segmented double stranded RNA

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7
Q

Describe the genomic structures of Norovirus, Sapovirus, Astrovirus and Aichi virus:

A

positive sense single stranded RNA

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8
Q

Describe the genomic structure of enteric adenovirus:

A

linear double stranded DNA

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9
Q

Major cause of diarrhea in children 6-24 months:

A

Group A rotavirus

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10
Q

Major cause of diarrhea outbreaks in children and adults:

A

Norovirus

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11
Q

~50% of diarrhea cases still have:

A

unknown etiology (meaning we likely still have yet to discover many pathogens)

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12
Q

first virus identified from stool samples by electron microscopic examination in 1972:

A

Norwalk

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13
Q

What family of viruses does Rotaviruses belong too?

A

Reovirus family

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14
Q

What does Reovirus stand for:

A

Respiratory Enteric Orphan virus

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15
Q

Describe the characteristic structure of rotaviruses:

A
  • nonenveloped
  • inner and outer capsids
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16
Q

How do rotaviruses enter host cells?

A

endocytosis

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17
Q

What happens once rotaviruses have been endocytosed into the host cell?

A

exit the phagosome

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18
Q

What allows for the ds-RNA genome of the rotavirus to be copied inside the host cell?

A

RNA dependent RNA polymerase

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19
Q

What does the viral protein produced by the mRNA of rotavirus assemble into?

A

capsid structures

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20
Q

Where does the viral replication of rotavirus complete?

A

inside capsid structures

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21
Q

How rotavirus acquire an envelope? (recall it is originally unenveloped upon entering host cell)

A

by budding into ER

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22
Q

Following acquiring the viral envelope via the ER, when does rotavirus shed the envelope?

A

Sheds envelope as the second capsid layer is build and the virus is released

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23
Q

What does the release of the rotavirus envelope involve?

A

Lysis of infected cells

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24
Q

What is responsible for the tissue damage associated with Rotaviruses?

A

lysis of infected cells

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25
Q

What is responsible for the fatality of infection rotaviruses?

A

dehydration

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26
Q

Discuss the transmission mode of rotavirus?

A

fecal-oral transmission

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27
Q

What is responsible for the acid stability seen in rotavirus?

A

double capsid structure

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28
Q

During an active infection of rotavirus, how many particles can be shed per ml of stool?

A

10^12 viral particles

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29
Q

How many viral particles are necessary to initiate infection of rotavirus?

A

as few as 10

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30
Q

What is the characteristic symptoms of infection with rotavirus?

A

watery-diarrhea

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31
Q

Rotavirus produces a ___.

A

enterotoxin

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32
Q

The enterotoxin produced by rotavirus binds ____, resulting in ___.

A

integrins, signaling that causes secretion of chloride and water

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33
Q

The enterotoxin produced by rotavirus ultimately results in:

A

secretion of chloride and water

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34
Q

During rotavirus infection, what happens to infected gut epithelial cells?

A

these cells are destroyed and replaced by immature epithelial cells

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35
Q

During a rotavirus infection, what is the significance of the infected gut epithelial cells being replaced with immature epithelial cells:

A
  1. reduced uptake of ions
  2. reduced water uptake
  3. less absorption of food molecules (carbs)
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36
Q

What is the most common type of rotavirus in the U.S?

A

Group A

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37
Q

Is there a vaccine for rotavirus?

A

Yes- for infants and greater than 75% effective

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38
Q

Describe the genomic structure of Noroviruses:

A
  • positive single stranded RNA genome
  • ~7,500 bases in lengths
    ~ Naked Capside virions
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39
Q

Describe the virions produced by Noroviruses:

A

naked capside virions

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40
Q

The replication of Noroviruses are similar to ____ except for ____.

A

picornavirus (polioviruses); except for 2nd phase of translation

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41
Q

How does the 2nd phase of translation of Noroviruses differ from the replication of picornaviruses (poliovirus)?

A

The second phase of translation involves subgenomic RNAs

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42
Q

The second phase of translation of noroviruses involve subgenomic RNAs being produce. What other virus is this similar to?

A

coronaviruses

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43
Q

Similar to picornaviruses, Noroviruses have a ____ on the RNA.

A

5’ VPg protein

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44
Q

Since the Noroviruses is a naked capsid virus, infection will result in:

A

tissue damage

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45
Q

Virus that is a characteristically a positive agent of infection in big group confined settings such as cruise ships:

A

Noroviruses

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46
Q

Describe the genomic structure of adenovirus:

A
  • linear double stranded DNA genome
  • nonenveloped
  • icosahedral capsid
47
Q

Discuss the location of viral replication characteristic of most DNA viruses (including adenovirus):

A

the nucleus is involved

48
Q

Follow the endosome rupture during adenovirus replication, what occurs:

A

viral nucleoprotein complex enters the cell nucleus

49
Q

DNA viruses have larger genomes and more genes and they end up having a cascade of gene expression and this typically involves three waves. What are waves of gene expression in the adenovirus?

A

pre-early, early, and late genes

50
Q

Adenovirus displays ____, meaning replication occurs in waves.

A

temporal regulation

51
Q

Adenovirus along with most DNA viruses produces ____ during viral gene expression

A

transcriptional regulators

52
Q

Transcriptional regulators produced during one phase of gene expression/viral replication act to:

A

promote transcription of genes of subsequent phase

53
Q

Describe the priming of DNA synthesis in adenovirus:

A

by pTP serine residue (pre-terminal protein)

54
Q

Adenovirus DNA Replication:

  1. Only ____ is copied at each replication fork
  2. No ____ replication
  3. Priming is by ___.
A
  1. one of the two DNA strands
  2. discontinuous
  3. viral protein (pTP)
55
Q

Adenovirus infections can be described as ____. Explain

A

widespread; 5-10% of all viral infections

56
Q

Symptoms of adenovirus usually resemble:

A

common cold symptoms

57
Q

Adenovirus are one of the causative agents for:

A

common cold

58
Q

Is there an adenovirus vaccine? If so, describe:

A

vaccine, live virus, given to new military recruits for serotypes 4 & 7

59
Q

What virus causes ARD (acute respiratory disease):

A

adenovirus serotypes 4 & 7

60
Q

ARD:

A

acute respiratory disease

61
Q

Discuss the mechanisms for evasion of host defenses used by Adenovirus:

A
  1. block MHC class I mRNA production
  2. block transport of MHC class I proteins to cell surface
62
Q

How does adenovirus block transport of MHC class I proteins to cell surface in order to evade host defense?

A

viral E3gp19K protein does this and results in the block of killing by cytotoxic T cells

63
Q

One thing we will encounter with most DNA viruses including adenovirus is their ability to drive host cell into:

A

cell division

64
Q

Adenovirus drives the host cell into cell division which is necessary for:

A

adenovirus replication

65
Q

What aspect of host cell division is necessary for adenovirus to replicate?

A

S phase factors

66
Q

What aspects of adenovirus interfere with cell division controllers?

A

proteins E1a and E1b

67
Q

What is the function of adenovirus proteins E1b and E1a?

A

both interfere with cell division controllers but specifically E1b sequesters p53 and E1a sequesters Rb (retinoblastoma protein)

68
Q

Adenovirus protein E1b:

A

sequesters p53

69
Q

Adenovirus protein E1a:

A

sequesters Rb (retinoblastoma protein)

70
Q

Because of the interference with cell division controllers, adenovirus infection can potentially:

A

drive a cell toward cancerous state

71
Q

In typical cell cycle, ____ recognizes DNA damage and activates ____.

A

P53; P21

72
Q

P53 recognizes DNA damage and activates P21 which will bind and inactivate the ____.

A

cyclin-CDK complex

73
Q

As DNA damage is repaired, what happens to P53 and P21?

A

P53 decreases; P21 no longer blocks cyclin CDK, cell-cycle progression

74
Q

Acts as a checkpoint controller to stop cell-cycle progression:

A

P53

75
Q

Inactivation of p53 by adenovirus E1b protein prevents:

A

activation of p21 (and Bax)

76
Q

Adenovirus E1a protein binds to:

A

Rb complex

77
Q

When adenovirus E1a protein binds to Rb complex, this:

A

prevents Rb from negatively regulating E2F

78
Q

What is E2F responsible for in the cell cycle:

A

transcribing a number of different genes for DNA synthesis

79
Q

Describe HPV genome and viral structure:

A
  • double stranded circular DNA molecule
  • nonenveloped viral particles
80
Q

How many types of HPV are there and what are the broad categories?

A

at least 100 different types; cutaneous HPV or mucosal HPV

81
Q

The infection process of HPV usually takes:

A

3-4 months

82
Q

HPV accesses ____ through breaks in skin

A

basal layer

83
Q

In HPV infection, viral early genes stimulate ____ which facilitates ___.

A

cell growth; viral replication

84
Q

HPV reproduction is coordinated with:

A

development of keratinocytes

85
Q

non dividing, physical barrier; anuclear:

A

keratinocytes

86
Q

In HPV infection, as cells move through skin layers:

A

HPV gene expression and DNA replication begins

87
Q

For HPV gene expression and DNA replication, ___ is used

A

cellular DNA polymerase

88
Q

In HPV infection, ____ are only made in differentiated layers

A

late proteins (capsid proteins)

89
Q

In HPV infection, assembly occurs in ___ during ___ development

A

nucleus; keratinocyte

90
Q

In HPV infection, as the nucleus breaks down you end up with nuclear remnants with ____ shed at ___.

A

viral particles; skin surface

91
Q

HPVs are not considered:

A

lytic

92
Q

HPVs are not considered lytic, as they simply rely on ___ to create a viral release event

A

the natural production of keratinocytes

93
Q

enlarged keratinocytes with clear halos around enlarged nuclei; characteristic of an HPV infection

A

koilocytes

94
Q

HPV spread is by _____ contact especially:

A

skin-to-skin; breaks in skin, mucous membranes, during birth

95
Q

HPV may cause warts of the ____ which is a dental concern of HPV.

A

warts of the oropharynx

96
Q

HPV-6 and HPV-11 are responsible for:

A

laryngeal papillomas

97
Q

Laryngeal papillomas caused by HPV-6 and HPV-11 may lead to ____.

A

respiratory papillomatosis

98
Q

Caused by HPV-6 and HPV-11, occurs in young children leading to respiratory distress; hoarseness is a usual symptom which signifies the obstructing HPV lesions; and secondary bacterial pneumonia can result.

A

respiratory papillomatosis

99
Q

The most benign epithelial tumors of the oral cavity caused by HPV:

A

single oral papillomas

100
Q

condylomata acuminata is commonly referred to as:

A

anogenital warts

101
Q

90% of ___ are caused by HPV-6 and HPV-11:

A

anogenital warts (condylomata acuminata)

102
Q

HPV is present in ___% of cervical cancers

A

99.7%

103
Q

Greater than 85% of cervical carcinomas contain:

A

integrated HPV DNA

104
Q

What are the high risk types of HPV that are associated with cervical papillomas?

A

16 & 18 (and 31& 45)

105
Q

Cells are scraped from the crevice and examined under a microscope to check for disease and other problems:

A

pap smear

106
Q

What cells determine if a Pap smear is abnormal?

A

koilocytic cells

107
Q

Are there vaccinations for HPV? If so explain:

A

yes; vaccination protects against HPV-16 and HPV-18 (leading strains for cervical cancer)

108
Q

The HPV proteins ____ & ____ are important for cancer development

A

E6 & E7

109
Q

What are the only two HPV proteins that are ALWAYS expressed in cervical cancer cells?

A

E6 & E7

110
Q

How does HPV E6 protein work to induce cancer?

A

inactivation of p53 (E6 signals the binding of ubiquination factors to bind to p53 and target its destruction)

111
Q

How does HPV E7 protein work to induce cancer?

A

prevents Rb from controlling cell division (E7 binds to Rb complex and prevents Rb from negatively regulating E2f)

112
Q

HPV E7 protein acts like the ____ protein which promotes disassembly of ____.

A

SV40 virus LT protein; Rb-E2f complex

113
Q

SV40LT (similar to HPV E7 protein) promotes the disassembly of Rb-E2f complex which allows Ef2 to:

A

be free & activate transcription of cellular DNA synthesis genes