Viruses - CMV, EBV, KSHV Flashcards Preview

Heme > Viruses - CMV, EBV, KSHV > Flashcards

Flashcards in Viruses - CMV, EBV, KSHV Deck (95):
1

What is the structure of herpesvirus?

icosahedral capsid surrounded by a lipid envelope that contains about a dozen virus-encoded glycoproteins

2

What is the herpesvirus genome like?

large, linera, dsDNA

3

T or F. herpesviruses produce self-limiting infections in which the primary infection is often symptomatic?

F. primary infection is asymtomatic

4

Can life-threatening infections or cancers occur w/ herpesviruses?

yes, especially in immunocompromised pts.

5

What are examples of human herpesviruses?

CMV, EBV, HHV8, KSHV

6

What do herpesviruses undergo to propagate the virus?

lytic replication

7

What happens after virus attachment?

Virus penetrates via glycoprotein-mediated fusion of envelope and PM

8

What happens are the virus enters the cell?

Releases its nucleocapsid and migrates to nucleus envelope, incoats, and DNA enters nucleus.

9

How does the nucleocapside migrate to the nuclear envelope?

via microtubules

10

What is cascade regulation?

programmed expression of viral genes

11

What happens in the immediate early (IE) phagse?

-virus specific TFs use host RNA Pol II to stimulate transcription of early promoters

12

What do the early genes encode?

nonstructural proteins and enzymes
1. Create DNA replication machinery, viral DNA Pol
2. Thymidine kinase - phosphorylates variety of nucleotides besides thymidine

13

What do the late genes encode?

depend on IE transcription factors to encode structural proteins.

14

What happens to the newly encoded viral glycoproteins during late gene phase?

incorporated into the virus envelopes and transported to infected cell surface to cause syncytia

15

Where does virus assembly occur?

in the nucleus where nucleocapsids bud first into perinuclear space

16

T or F. All herpesvirses undergo latency?

True

17

What happens during latency?

genomes are maintained extrachromosomally in host but no virus are produced

18

What are the 3 stages of latency?

1. Establishment
2. Maintenance
3. Reactivation

19

What is the genome structure of HSV like?

2 unique regions (long and short) flanked by identical inverted repeats.

20

What does reactivation usually occur?

when there is a lapse in immunity so virus starts making particles and causes another infection

21

T or F. Anyone infected w/ a herpesvirus is infected for life.

True

22

What are the 3 types of herpesviruses?

1. Alpha (neurotropic)
2. Beta (lymphotropic)
3. Gamma (lymphotropic)

23

What are examples of beta viruses?

CMV, HHV6, HHV7

24

What are examples of gamma viruses?

EBV, HHV8

25

In low socioeconmic class, how many adults are CMV+?

80%

26

in higher socioeconomic classes, how many adults are CMV+?

50%

27

Where is CMV found?

saliva, breast milk, semen, cervical secretions, blood

28

Who is at risk for CMV?

neonates, day care workers, pregnant workers, immunocomprromised pts, gay men

29

What is the pathogenesis of CMV?

1. infection via contect w/ secretions
2. primary infection in epithelial cells then spreads to lymphoid tissues
3. latently infects B and T cells, monocytes, and lymphocytes

30

When do most symptoms of CMV occur in neonates?

in utero, most are asymptomatic

31

What can CMV in utero result in?

retardation and deafness

32

T or F. Most organ translant pts get CMV infection w/ pneumonitis.

True

33

Can mononucleuosis occur w/ CMv?

yes

34

What is the prophlyactic treatment for organ transplant pts to hopefully prevent CMV infection?

Give CMV Ig and ganciclovir

35

T or F. When you think transplant pt, think CMV!

True

36

What are AIDS pts prone to with viral related stuff?

CMV retinitis, colitis, and pneumonitis

37

What is used for the diagnosis for CMV?

ELISA, PCR detection, and Shell Vial Assay

38

What is a shell vial assay?

Indirect immunofloresence used to detect an immediate early protein after 24 hr of cell culture infection

39

Why is a shell vial assay beneficial?

normally CMV takes 2 wks to grow so this allows for early detection

40

What is the treatment for CMV? Going to more efficient to less

Ganciclovir, Foscarnet, Cidofovir

41

What is acyclovir?

a Guansine analog w/ phosphate

42

What is the PK of acyclovir and MOA?

its a pro-drug, needs to have 3 phosphate groups added to it to be used by viral DNA Pol and prevent chain elongation

43

What is ganciclovir?

guanosine analog similar to acyclovir, prodrug

44

In what viral infection is acyclovir used for?

HSV, VZV, and EBV

45

Is acyclovir more toxic than ganciclovir?

less

46

What is approved for CMV retinitis in AIDS pts.?

ganciclovir, foscarnet, and cidofovir

47

What are side effects of ganciclovir?

neutropenia and GI tract bleeding

48

How does foscarnet work?

pyrophosphate analog that inhibits DNA pol but isn't a pro-drug.

49

How does cidofovir work?

deoxycytidine analog, competitive inhibitors of CMV DNA Pol

50

Why can't these antivirals cure herpes or treat cancers caused by these viruses?

They inhibit virus replication to limit infection, but these viruses will undergo latency so there is no virus replication going on

51

Tell me about EBV infection is different socieconomic groups?

low setting -- at early age
higher setting -- adolescence and adulthood

52

How much of the adult population has an Ab to EBV?

90-95%

53

What can EBV cause in immunocompromised hosts?

oral hairy leukoplakia

54

What are 2 cancers that ENV are associted w/?

Burkitt's lymphoma and nasopharyngeal carcinoma

55

How is EBV spread?

through saliva -- kissing

56

what is the incubation period for EBV?

4-7 weeks

57

where is the initial replication of EBV after infection?

oropharyngeal epithelium

58

Where can EBV spread to?

lymphocytes and then liver and spleen

59

Where will EBV remain latent?

throat epithelium and B cells

60

How long does oral shedding of EBV last?

week or even months

61

T or F. Most EBV infections are symptomatic.

F

62

What is symptoms of infection mononucleosis?

sore throat, fever for one to two wks, malaise, lymphadenopathy

63

What is the diagnosis of EBV based on?

symptoms and presence of at least 50% atypical large lymphocytes w/ lobulated nuclei

64

What is the role of the large lymphocytes in mono?

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

65

What are important Antigenic Markers of EBV?

1. EBNA
2. VCA
3. EA

66

When does one see EBNA? (EBV nuclear antigens)

early in primary infection, it maintains genome replication in dividing B cells

67

What does anti-VCA IgM indicate?

primary infection

68

What does anti-VCA IgG indicate?

- w/out anti- EBNA indicates primary infection
- w/ anti-ENBA indicates past infection

69

When is EA seen? (early antigen)

detected in cells that don't produce virus

70

How do you diagnose EBV infection?

Monospot test, aka Heterophile Antibodies

71

What do the Abs agglutinate w/ monospot test?

sheep red blood cells

72

What is the treatment for mono?

supportive, tell athletes to not to do physical activity due to enlarged spleen.

73

What is PTLD?

uncontrolled proliferation of B cells due to their transformation by EBV and absence of CTLS to control them

74

What is the treatment for PTLD?

stop immunosuppression, monitor for rejection and acyclovir is not useful b/c infection is latent

75

When is the highest risk for PTLD?

in seronegative EBV transplant recipients in the 1st year

76

What is Burkitt's Lymphoma?

neoplasm of B cells that affect bones of the jaw, endemic in central Africa and New Guinea

77

What are the 3 associated factors w/ Burkitt's Lymphoma?

1. early EBV infection leading to latency
2. activation of c-myc
3. malaria

78

What does early detection of Burkitt's lymphoma allow?

cure rate of 80%

79

How many people have EBV genomes in Burkitt's outside Africa?

20%

80

What is nasopharyngeal carcinoma?

neoplasm of epithelial cells

81

Where is nasopharyneal carcinoma common?

southern china-- high salt diet likely cofactor

82

What is the initial presentation of nasopharyngeal carcinoma?

painless lump in the neck

83

How many people survive ten years if they have nasopharyngeal carcinoma?

60%

84

What can cause Kaposi's sarcoma?

HHV8 is necessary but not sufficient

85

What happens w/ the B cells and the endothelial latency tropism w/ HHV8?

KS tumors are in lining of lymphatic system, the lymphatic channels fill w/ blood cells --> causes bluish, bruised appearance of lesion

86

In US, who usually has KS?

AIDS patients

87

How does HHV8 spread?

1. sexually-transmitted but virus is absent from semen and vaginal secretions, it's found in saliva

88

What is the incubation of HHV8 before onset of KS?

10 years

89

is HHV8 symptomatic in AIDS and in non-AIDS?

no, asymptomatic

90

When will HHV8 infection by symptomatic?

- must be accompanied by loss of immune system so common in old age and AIDS in gay populations

91

When symptomatic, what is the treatment of HHV8 in AIDS?

there is no treatment for HHV8 but instead aim is to treat AIDS patients for tumor specific or targets of HIV

92

What other cancers can HHV8 cause?

1. primary effusion lymphoma
2. multicentric Castleman's diseas

93

What is primary effusion lymphoma?

NHL B cell, found in body cavities, mean survival time 2-6 months

94

What is multicentric Castleman's disease?

lymph node tumors, not strictly a cancer (not metastatic)

95

T or F. KSHV is found in virtually all tumors of HIV+ pts.

T