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Heme > Viruses - CMV, EBV, KSHV > Flashcards

Viruses - CMV, EBV, KSHV Flashcards

1
Q

What is the structure of herpesvirus?

A

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

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2
Q

What is the herpesvirus genome like?

A

large, linera, dsDNA

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3
Q

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

A

F. primary infection is asymtomatic

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4
Q

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

A

yes, especially in immunocompromised pts.

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5
Q

What are examples of human herpesviruses?

A

CMV, EBV, HHV8, KSHV

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6
Q

What do herpesviruses undergo to propagate the virus?

A

lytic replication

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7
Q

What happens after virus attachment?

A

Virus penetrates via glycoprotein-mediated fusion of envelope and PM

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8
Q

What happens are the virus enters the cell?

A

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

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9
Q

How does the nucleocapside migrate to the nuclear envelope?

A

via microtubules

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10
Q

What is cascade regulation?

A

programmed expression of viral genes

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11
Q

What happens in the immediate early (IE) phagse?

A

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

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12
Q

What do the early genes encode?

A

nonstructural proteins and enzymes

  1. Create DNA replication machinery, viral DNA Pol
  2. Thymidine kinase - phosphorylates variety of nucleotides besides thymidine
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13
Q

What do the late genes encode?

A

depend on IE transcription factors to encode structural proteins.

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14
Q

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

A

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

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15
Q

Where does virus assembly occur?

A

in the nucleus where nucleocapsids bud first into perinuclear space

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16
Q

T or F. All herpesvirses undergo latency?

A

True

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17
Q

What happens during latency?

A

genomes are maintained extrachromosomally in host but no virus are produced

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18
Q

What are the 3 stages of latency?

A
  1. Establishment
  2. Maintenance
  3. Reactivation
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19
Q

What is the genome structure of HSV like?

A

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

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20
Q

What does reactivation usually occur?

A

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

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21
Q

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

A

True

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22
Q

What are the 3 types of herpesviruses?

A
  1. Alpha (neurotropic)
  2. Beta (lymphotropic)
  3. Gamma (lymphotropic)
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23
Q

What are examples of beta viruses?

A

CMV, HHV6, HHV7

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24
Q

What are examples of gamma viruses?

A

EBV, HHV8

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25
Q

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

A

80%

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26
Q

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

A

50%

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27
Q

Where is CMV found?

A

saliva, breast milk, semen, cervical secretions, blood

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28
Q

Who is at risk for CMV?

A

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

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29
Q

What is the pathogenesis of CMV?

A
  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
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30
Q

When do most symptoms of CMV occur in neonates?

A

in utero, most are asymptomatic

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31
Q

What can CMV in utero result in?

A

retardation and deafness

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32
Q

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

A

True

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33
Q

Can mononucleuosis occur w/ CMv?

A

yes

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34
Q

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

A

Give CMV Ig and ganciclovir

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35
Q

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

A

True

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36
Q

What are AIDS pts prone to with viral related stuff?

A

CMV retinitis, colitis, and pneumonitis

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37
Q

What is used for the diagnosis for CMV?

A

ELISA, PCR detection, and Shell Vial Assay

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38
Q

What is a shell vial assay?

A

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

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39
Q

Why is a shell vial assay beneficial?

A

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

40
Q

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

A

Ganciclovir, Foscarnet, Cidofovir

41
Q

What is acyclovir?

A

a Guansine analog w/ phosphate

42
Q

What is the PK of acyclovir and MOA?

A

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
Q

What is ganciclovir?

A

guanosine analog similar to acyclovir, prodrug

44
Q

In what viral infection is acyclovir used for?

A

HSV, VZV, and EBV

45
Q

Is acyclovir more toxic than ganciclovir?

A

less

46
Q

What is approved for CMV retinitis in AIDS pts.?

A

ganciclovir, foscarnet, and cidofovir

47
Q

What are side effects of ganciclovir?

A

neutropenia and GI tract bleeding

48
Q

How does foscarnet work?

A

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

49
Q

How does cidofovir work?

A

deoxycytidine analog, competitive inhibitors of CMV DNA Pol

50
Q

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

A

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

51
Q

Tell me about EBV infection is different socieconomic groups?

A

low setting – at early age

higher setting – adolescence and adulthood

52
Q

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

A

90-95%

53
Q

What can EBV cause in immunocompromised hosts?

A

oral hairy leukoplakia

54
Q

What are 2 cancers that ENV are associted w/?

A

Burkitt’s lymphoma and nasopharyngeal carcinoma

55
Q

How is EBV spread?

A

through saliva – kissing

56
Q

what is the incubation period for EBV?

A

4-7 weeks

57
Q

where is the initial replication of EBV after infection?

A

oropharyngeal epithelium

58
Q

Where can EBV spread to?

A

lymphocytes and then liver and spleen

59
Q

Where will EBV remain latent?

A

throat epithelium and B cells

60
Q

How long does oral shedding of EBV last?

A

week or even months

61
Q

T or F. Most EBV infections are symptomatic.

A

F

62
Q

What is symptoms of infection mononucleosis?

A

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

63
Q

What is the diagnosis of EBV based on?

A

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

64
Q

What is the role of the large lymphocytes in mono?

A

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

65
Q

What are important Antigenic Markers of EBV?

A
  1. EBNA
  2. VCA
  3. EA
66
Q

When does one see EBNA? (EBV nuclear antigens)

A

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

67
Q

What does anti-VCA IgM indicate?

A

primary infection

68
Q

What does anti-VCA IgG indicate?

A
  • w/out anti- EBNA indicates primary infection

- w/ anti-ENBA indicates past infection

69
Q

When is EA seen? (early antigen)

A

detected in cells that don’t produce virus

70
Q

How do you diagnose EBV infection?

A

Monospot test, aka Heterophile Antibodies

71
Q

What do the Abs agglutinate w/ monospot test?

A

sheep red blood cells

72
Q

What is the treatment for mono?

A

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

73
Q

What is PTLD?

A

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

74
Q

What is the treatment for PTLD?

A

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

75
Q

When is the highest risk for PTLD?

A

in seronegative EBV transplant recipients in the 1st year

76
Q

What is Burkitt’s Lymphoma?

A

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

77
Q

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

A
  1. early EBV infection leading to latency
  2. activation of c-myc
  3. malaria
78
Q

What does early detection of Burkitt’s lymphoma allow?

A

cure rate of 80%

79
Q

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

A

20%

80
Q

What is nasopharyngeal carcinoma?

A

neoplasm of epithelial cells

81
Q

Where is nasopharyneal carcinoma common?

A

southern china– high salt diet likely cofactor

82
Q

What is the initial presentation of nasopharyngeal carcinoma?

A

painless lump in the neck

83
Q

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

A

60%

84
Q

What can cause Kaposi’s sarcoma?

A

HHV8 is necessary but not sufficient

85
Q

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

A

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

86
Q

In US, who usually has KS?

A

AIDS patients

87
Q

How does HHV8 spread?

A
  1. sexually-transmitted but virus is absent from semen and vaginal secretions, it’s found in saliva
88
Q

What is the incubation of HHV8 before onset of KS?

A

10 years

89
Q

is HHV8 symptomatic in AIDS and in non-AIDS?

A

no, asymptomatic

90
Q

When will HHV8 infection by symptomatic?

A
  • must be accompanied by loss of immune system so common in old age and AIDS in gay populations
91
Q

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

A

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

92
Q

What other cancers can HHV8 cause?

A
  1. primary effusion lymphoma

2. multicentric Castleman’s diseas

93
Q

What is primary effusion lymphoma?

A

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

94
Q

What is multicentric Castleman’s disease?

A

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

95
Q

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

A

T

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