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D2 Summer > Microbio Week 11 - Herpesviruses EBV CMV HHV6 HHV8 and Prions (Exam 3) > Flashcards

Microbio Week 11 - Herpesviruses EBV CMV HHV6 HHV8 and Prions (Exam 3) Flashcards

1
Q

How is Epstein-Barr virus (EBV) transmitted?

A

Saliva - mono is known as the kissing disease

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2
Q

By 35-40, almost all people in the US are infected with which disease?

A

EBV

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3
Q

EBV established latency in ___________ cells

A

memory B

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4
Q

T/F: People sporadically shed EBV in saliva throughout life after they are infected

A

True

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5
Q

In infectious mononucleosis, the virus initially divides in the _____________, causing a sore throat through _______ infection. It then infects its main target, B-cells.

A

oropharynx; lytic

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6
Q

What is known as heterophile antibody-positive mononucleosis?

A

EBV mononucleosis

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7
Q

What leads to heterophile antibody infection during EBV mononucleosis?

A

Generalized activation of B cells

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8
Q

Heterophile antibodies are _____________ antibodies that will react with certain animals, horses, and sheep, RBC.

A test for the presence of these antibodies is called the ____________ test

A

non-specific; monospot

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9
Q

What is the primary cause of all infectious mononucleosis symptoms?

A

Expansion of CTLs + their cytokines

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10
Q

How long is the incubation time for infectious mononucleosis?

A

Long, 4-6 weeks

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11
Q

Once the acute infection for infectious mononucleosis is over, some memory B cells have what? (ON EXAM)

A

Latent EBV genome

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12
Q

Memory B cells maintain their latency of infectious mononucleosis without producing what?

A

Proteins

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13
Q

When the B cells divide in infectious mononucleosis, they express a _______ ________ to make sure the viral genome goes into both cells.

A

viral protein

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14
Q

EBV can reactivate from what in order to make new infectious virus?

A

Memory B cell pool

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15
Q

What are the 3 complications of mononucleosis?

A
  1. Ruptured spleen
  2. Mild hepatitis
  3. Airway obstruction (enlarged tonsils)
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16
Q

What increases the chance of developing oral hairy leukoplakia?

A

EBV
Smoking

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17
Q

Benign, non-painful lesion on lateral border of tongue

A

Oral hairy leukoplakia

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18
Q

Can oral hairy leukoplakia be scraped off the tongue?

A

NO

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19
Q

Oral hairy leukoplakia can be the first sign that someone has an _______ infection or occurs in people taking immunosuppressive drugs

A

HIV

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20
Q

T/F: Certain drugs or acyclovir can be taken to clear lesions in oral hairy leukoplakia, and the lesions never come back

A

FALSE, the lesions usually come back within a few weeks of treatment cessation

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21
Q

When will oral hairy leukoplakia most likely clear up?

A

When CD4 count increases

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22
Q

T/F: Oral hairy leukoplakia can occur in immunocompetent people, but it is rare

A

True

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23
Q

What disease is rare in the US, and cases are often found in recent immigrants from certain parts of Africa, some Asian countries, and the native peoples of Alaska and Canada?

A

Nasopharyngeal Carcinoma

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24
Q

What causes Nasopharyngeal Carcinoma?

A

EBV

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25
Q

Is there a good chance of survival of Nasopharyngeal Carcinoma with treatment?

A

Yes, if caught early

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26
Q

In parts of central Africa, what is the causative agent in endemic Burkitt lymphoma and has a high incidence?

A

EBV

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27
Q

What is a very fast-growing, aggressive cancer?

A

Burkitt Lymphoma

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28
Q

Endemic Burkitt Lymphoma generally starts as a tumor of the ______ or __________. It is more likely to be in young children

A

face or jawbone

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29
Q

Burkitt Lymphoma is caused by a chromosomal translocation of the _________ gene to a
chromosome that has an immunoglobulin locus.

What does this cause?

A

c-myc

Unregulated c-myc expression -> uncontrolled cell growth

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30
Q

Sporadic Burkitt Lymphoma in the US usually starts in the ___________, not the jaw

A

abdomen

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31
Q

EBV-associated Burkitt Lymphoma is higher in people living with ________

A

HIV

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32
Q

Immunosuppression can increase the chance that EBV is associated with what?

A

Sporadic Burkitt Lymphoma

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33
Q

Most Cytomegalovirus (CMV) infections are asymptomatic, except what?

A

CMV mono-like syndrome
Congenital infections
Immunocompromised

34
Q

How is CMV transmitted?

A

Saliva
Urine
Blood
Breast milk
Semen
Cervical secretions

35
Q

T/F: There are many different strains of CMV, and it is possible to be infected with more than one strain

A

True

36
Q

What cells does CMV infect?

A

Wide range

37
Q

Where is CMV latency established in the body?

A

Myeloid precursor cells in bone marrow

38
Q

In people with AIDS, what is the most frequent problem with CMV?

A

Retinitis

39
Q

What disease is a significant problem in transplant recepients?

A

CMV

40
Q

In CMV mono like-syndrome, what does CMV activate?

A

T cells

(not B cells!!!)

41
Q

T/F: Because CMV mono-like syndrome does not infect B cells, there will be no generalized activation of antibodies and no production of heterophile antibodies

A

True!

42
Q

Will CMV mono-like syndrome be monospot positive or monospot negative?

A

Monospot negative, since it does not activate B cells nor cause production of heterophile antibodies

43
Q

Will CMV mono-like syndrome be heterophile AB positive or heterophile AB negative?

A

Heterophile AB negative, since it does not activate B cells nor cause production of heterophile antibodies

44
Q

What is the #1 congenital infection in the US?

A

Congenital CMV

45
Q

During pregnancy, what primary infection has a high risk of being transferred to the fetus?

A

CMV

46
Q

The risk of congenital CMV from an already CMV-positive woman is (high/low)

A

Low

47
Q

Babies born with asymptomatic CMV infections have a 10% risk of some __________ ________, which can be delayed and progressive

A

hearing loss

48
Q

Babies born with symptomatic CMV infection can develop what?

A

Motor and cognitive defects
Hearing loss
Vision loss

49
Q

Babies born with symptomatic CMV infection have (more/less) sequelae than babies born with asymptomatic infection

A

More

50
Q

T/F: Unless a baby is a very low birth weight or is immunosuppressed, CMV infections that are acquired at birth or through breastfeeding are not a problem

A

True

51
Q

What is a very common childhood infection?

A

HHV6

52
Q

What is the cause of Roseola and can cause febrile seizures?

A

HHV6

53
Q

What virus is present in large numbers in MSM, but much lower in the general population of the US?

A

HHV8

54
Q

HHV8 usually causes no symptoms unless co-infected with _______.

People with co-infections have a risk of developing what?

A

HIV

Kaposi sarcoma

55
Q

The risk of developing Kaposi sarcoma increases with what?

However, with an aging population infected with HIV, Kaposi’s sarcoma can also be seen with what?

A

Lower CD4 count

Higher CD4 count

56
Q

How is HHV8 spread?

A

Sex
Saliva

57
Q

What is often seen with Kaposi sarcoma?

A

Violet or brown oral lesions

58
Q

What was coined to highlight the fact that it was a proteinaceous infectious particle?

A

A prion

59
Q

What is a prion made of?

A

Protein

60
Q

The prion protein is a normal protein that is highly expressed where?

A

The brain

61
Q

What does the infectious prion look like?

A

Misfolded prion protein

62
Q

Normal prion protein

A

PrPc

63
Q

Misfolded infectious prion protein

A

PrPsc

64
Q

The PrPsc has a high number of what compared to PrPc?

A

Beta sheets

65
Q

The infectious PrPsc converts the cells PrPc into an altered form, causing what?

A

Aggregates that form amyloid plaques

66
Q

What do the aggregates that form amyloid plaques with the misfolded proteins cause?

A

Cell death -> releases the infectious misfolded prion

67
Q

PrPsc goes on to other cells and converts their PrPc protein to the misfolded form. What does this lead to?

A

Spongiform appearance in the brain

68
Q

There are lots of different kinds of prion disease. What are they all caused by?

A

Misfolded prions

69
Q

What is the most common prion disease?

A

Spontaneous Creutzfeldt-Jacob disease (CJD)

70
Q

What prion disease is a spontaneous mutation in the prion gene or a spontaneously misfolded protein that becomes ‘infectious’ to the normal prion proteins in the brain?

A

Spontaneous Creutzfeldt-Jacob disease (CJD)

71
Q

Is Spontaneous Creutzfeldt-Jacob disease (CJD) genetic?

A

No

72
Q

T/F: After symptoms of Spontaneous Creutzfeldt-Jacob disease (CJD) appear, life expectancy is rarely over a year. It is a fatal condition.

A

True

73
Q

T/F: It is easy to kill prions

A

FALSE!! It is very hard to kill prions! They are resistant to many disinfectants, proteases, and normal autoclaving

74
Q

A small sliver of Spontaneous Creutzfeldt-Jacob disease (CJD) is from “infectious” causes, meaning obtained from a source outside of the body. Name one potential source

A

Contaminated surgical instruments

75
Q

What disease is caused by eating beef contaminated with prion proteins?

A

Variant Creutzfeldt-Jacob disease (vCJD)

76
Q

T/F: Cases of Variant Creutzfeldt-Jacob disease (vCJD) from the UK were due to cows that had bovine spongiform encephalitis (Mad Cow Disease) entering the food chain

A

True

77
Q

Is Variant Creutzfeldt-Jacob disease (vCJD) fatal?

A

Yes, it is 100% fatal

78
Q

What is the incubation time for Variant Creutzfeldt-Jacob disease (vCJD)?

A

As short as 5 years

79
Q

What are most cases of Iatrogenic Creutzfeldt-Jacob disease (iCJD) from?

A

Material harvested from cadavers

80
Q

Dental instruments that come in contact with nerve tissue could potentially be contaminated with ___________ if not cleaned properly

A

prions

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