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Heme Week 2 > Cytomegalovirus, EBV, Kaposi's Sarcoma- Associated Herpesvirus II > Flashcards

Cytomegalovirus, EBV, Kaposi's Sarcoma- Associated Herpesvirus II Flashcards

1
Q

When is EBV infection common?

A

Infection at early age in low socioeconomic setting

Infection in adolescence and early adulthood in higher socioeconomic setting

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2
Q

Infection in adolescence and early adulthood in higher socioeconomic setting can lead to what?

A

infectious mono

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3
Q

How much of the adult population have antibodies to EBV?

A

90 to 95% of adult population contains antibody to EBV

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4
Q

What can EBV cause in immunocompromised patients?

A

Oral hairy leukoplakia (think HIV!)

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5
Q

What can EBV cause in transplant patients?

A

Post-transplant lymphoproliferative disease

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6
Q

What cancers is EBV associated with?

A
  • Burkitt
  • nasopharyngeal carcinoma
  • Hodgkin’s (?)
  • Multiple sclerosis (?)
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7
Q

How does EBV spread?

A

saliva (kissing)

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8
Q

What is the incubation period for EBV?

A

4-7 weeks

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9
Q

Where does the initial replication for EBV occur?

A

oropharyngeal epithelium then spread to lymphocytes and then liver and spleen

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10
Q

Where does EBV remain latent?

A
  • throat epithelium
  • B cells

Oral shedding of virus occurs for many weeks

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11
Q

What are the symptoms of EBV?

A
  • mostly asymptomatic

- infectious mono- fever for one to two weeks, malaise, LAD (recovery uneventful)

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12
Q

How is EBV diagnosed?

A
  • based on symptoms and presence of at least 50% atypical, large lymphocytes with lobulated nuclei
  • can also include looking for heterophilic antibodies (mono spot test)
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13
Q

What would the large lymphocytes be indicative of?

A

T-cells responding to infection, not the infected B cells

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14
Q

What are some important antigenic markers of EBV?

A
  • EBNA (EBV muclear antigens)
  • VCA (viral capsid antigen)
  • EA
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15
Q

What does conversion to anti-EBNA IgG indicate?

A

resolution of primary infection

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16
Q

What does anti-VCA IgM indicate?

A

primary infection

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17
Q

What does anti-VCA IgG without anti-EBNA indicate?

A

primary infection

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18
Q

What does anti-VCA IgG with anti-EBNA indicate?

A

past infection

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19
Q

What is EA?

A

early antigen

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20
Q

Where is EA detected?

A

cells that do not produce virus

21
Q

What do heterophile antibodies do?

A

agglutinate sheep red blood cells

22
Q

Are heterophiles antibodies present in all EBV patients?

A

No. If present, will distinguish EBV mono from CMV mono

23
Q

What is the treatment of EBV? Oral leukoplakia?

A
  • supportive for mono; withhold athletes due to possible spleen inflammation
  • treatment for oral leukoplakia is acyclovir
24
Q

How does EBV cause PTLD?

A

Uncontrolled proliferation of B cells due to their transformation by EBV and the absence of CTLs to control them

25
Q

What patient population has the highest risk of PTLD?

A

seronegative transplant recipients in the first year

26
Q

What is the treatment for PTLD?

A

a. stop immunosuppression

i. Must monitor for rejection
ii. ACV not useful because the infection is latent, virus is not replicating

27
Q

Burkitt lymphoma is associated with what three factors?

A
  • Early EBV infection leading to latency (a. Outside of Africa, only 20% of BL patients have EBV genomes in tumor)
  • Activation of c-myc
  • Malaria
28
Q

T or F. Burkitt is treatable

A

T. Early detection allows cure rate of 80%

29
Q

What cell line is neoplastic in nasopharyngeal carcinoma?

A

epithelial cells

30
Q

Where is the association between nasopharyngeal carcinoma the highest?

A

High frequency in southern China: high salt diet likely cofactor

seen worldwide however

31
Q

How does nasopharyngeal carcinoma present?

A

painless lump in neck

32
Q

Prognosis for nasopharyngeal carcinoma?

A

At best, only 60% of patients survive ten years

33
Q

T or F. HHV-8 infection is needed to cause Kaposi’s sarcoma

A

T.

34
Q

T or F. HHV-8 infection is sufficient to cause Kapok’s sarcoma

A

F. Thus, necessary but not sufficient alone.

35
Q

What is the tropism for HHV-8?

A
  • B cells

- endothelium

36
Q

Where do KS tumors occur?

A

lining of the lymphatic system

The lymphatic channels fill with blood cells, hence the bluish, bruised appearance of lesions

37
Q

Classical KS is seen in what patient population?

A

Mediterranean populations, also prevalent in sub-Saharan Africa

NOT sexually transmitted in these cases

38
Q

In the US, most KS patients are also ___ positive.

A

AIDS

39
Q

How is HHV-8 spread?

A

sexually transmitted (but virus is absent from semen and vaginal secretions)

40
Q

Where is HHV-8 virus present in the body?

A
  • saliva

- not semen or vaginal secretions

41
Q

How long is the typical incubation period for HHV-8 before KS onset?

A

10 yr

  • May be relatively mild
  • If patient is severely compromised, can be life-threatening
42
Q

How does HHV-8 (KS) present?

A

In AIDS and non-AIDS forms, 95% of infections are asymptomatic

43
Q

What must infection be accompanied by to cause symptoms?

A

Infection must be accompanied by loss of immune system for disease symptoms

  • Old age in classical forms
  • AIDS in gay populations
44
Q

When symptomatic, what is the treatment in AIDS patients?

A

tumor-specific (resection, chemo) or targets HIV, but not HHV-8

45
Q

What else can HHV-8 cause?

A

two B cell abnormalities:

  • Primary effusion lymphoma
  • Multicentric Castlman’s disease (MCD)
46
Q

What is Primary effusion lymphoma? and where is it commonly found in try body?

A

non-hodgkin’s B cell lymphoma

commonly found in body cavities

47
Q

What is the mean survival time for Primary effusion lymphoma?

A

2-6 motnhs

48
Q

What is MCD?

A

Lymph node tumors, not strictly a cancer

Heme Week 2 (18 decks)

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