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

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

Flashcards in Cytomegalovirus, EBV, Kaposi's Sarcoma- Associated Herpesvirus II Deck (48):
1

When is EBV infection common?

Infection at early age in low socioeconomic setting

Infection in adolescence and early adulthood in higher socioeconomic setting

2

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

infectious mono

3

How much of the adult population have antibodies to EBV?

90 to 95% of adult population contains antibody to EBV

4

What can EBV cause in immunocompromised patients?

Oral hairy leukoplakia (think HIV!)

5

What can EBV cause in transplant patients?

Post-transplant lymphoproliferative disease

6

What cancers is EBV associated with?

-Burkitt
-nasopharyngeal carcinoma

-Hodgkin's (?)
-Multiple sclerosis (?)

7

How does EBV spread?

saliva (kissing)

8

What is the incubation period for EBV?

4-7 weeks

9

Where does the initial replication for EBV occur?

oropharyngeal epithelium then spread to lymphocytes and then liver and spleen

10

Where does EBV remain latent?

- throat epithelium
- B cells

Oral shedding of virus occurs for many weeks

11

What are the symptoms of EBV?

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

12

How is EBV diagnosed?

-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)

13

What would the large lymphocytes be indicative of?

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

14

What are some important antigenic markers of EBV?

-EBNA (EBV muclear antigens)
-VCA (viral capsid antigen)
-EA

15

What does conversion to anti-EBNA IgG indicate?

resolution of primary infection

16

What does anti-VCA IgM indicate?

primary infection

17

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

primary infection

18

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

past infection

19

What is EA?

early antigen

20

Where is EA detected?

cells that do not produce virus

21

What do heterophile antibodies do?

agglutinate sheep red blood cells

22

Are heterophiles antibodies present in all EBV patients?

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

23

What is the treatment of EBV? Oral leukoplakia?

-supportive for mono; withhold athletes due to possible spleen inflammation

-treatment for oral leukoplakia is acyclovir

24

How does EBV cause PTLD?

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

25

What patient population has the highest risk of PTLD?

seronegative transplant recipients in the first year

26

What is the treatment for PTLD?

a. stop immunosuppression

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

27

Burkitt lymphoma is associated with what three factors?

-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

T or F. Burkitt is treatable

T. Early detection allows cure rate of 80%

29

What cell line is neoplastic in nasopharyngeal carcinoma?

epithelial cells

30

Where is the association between nasopharyngeal carcinoma the highest?

High frequency in southern China: high salt diet likely cofactor

seen worldwide however

31

How does nasopharyngeal carcinoma present?

painless lump in neck

32

Prognosis for nasopharyngeal carcinoma?

At best, only 60% of patients survive ten years

33

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

T.

34

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

F. Thus, necessary but not sufficient alone.

35

What is the tropism for HHV-8?

-B cells
-endothelium

36

Where do KS tumors occur?

lining of the lymphatic system

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

37

Classical KS is seen in what patient population?

Mediterranean populations, also prevalent in sub-Saharan Africa

NOT sexually transmitted in these cases

38

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

AIDS

39

How is HHV-8 spread?

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

40

Where is HHV-8 virus present in the body?

-saliva
-not semen or vaginal secretions

41

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

10 yr

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

42

How does HHV-8 (KS) present?

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

43

What must infection be accompanied by to cause symptoms?

Infection must be accompanied by loss of immune system for disease symptoms
-Old age in classical forms
-AIDS in gay populations

44

When symptomatic, what is the treatment in AIDS patients?

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

45

What else can HHV-8 cause?

two B cell abnormalities:

-Primary effusion lymphoma
- Multicentric Castlman's disease (MCD)

46

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

non-hodgkin's B cell lymphoma

commonly found in body cavities

47

What is the mean survival time for Primary effusion lymphoma?

2-6 motnhs

48

What is MCD?

Lymph node tumors, not strictly a cancer