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Immunology 3 > #18 Viral infection and Transplants > Flashcards

#18 Viral infection and Transplants Flashcards

1
Q

Polyomaviruses
genome
enveloped

A

non enveloped
dsDNA
2 distinct transcript units

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2
Q

origin of polyomaviruse has:

A

viral promoters and origin of DNA replication

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3
Q

function of miRNA in polyomavirus

A

shuts of early gene expression

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4
Q

The most potent oncoprotein in polyomavirus

A

Large T antigen

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5
Q

J Domain:

A

DNAreplication

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6
Q

binds and disrupts tumor suppressor proteins RB, p130, p107 promoting cell proliferation

A

LXCXE:

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7
Q

Helicase in polyomavirus :

A

binds and disrupts

tumor suppressor protein p53

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8
Q

binds and disrupts

tumor suppressor protein p53

A

helicase

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9
Q

LXCXE:

A

binds and disrupts tumor suppressor proteins RB, p130, p107 promoting cell proliferation

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10
Q

Genome replication by:

A

large T- antigen

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11
Q

alter activity of cellular protein phosphatase

A

Small T antigen:

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12
Q

Tropism Defined by

A

Host Cell Surface Gangliosides

our VP1

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13
Q

First isolated (1971) from the urine of a renal transplant patient (BK

A

BK polyomavirus (BKPyV)

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14
Q

Infection of BK polyomavirus

A
  • Benign in healthy individuals
  • Disease upon immunosuppression
  • Infection occurs at young age
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15
Q

Mechanism of transmission for BK polyomavirus

A

respiratory,urino-oral, fecal-oral routes?

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16
Q

Where does the BK virus like to hang out once you get it?

A

• Likely persistent in proximal renal tubular cells, but capable of infecting lymphocytes and other cells.

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17
Q

Disease seen from BK polyomavirus

A

10% of Renal transplant-polyomavirus
associated nephropathy (PVAN)
0-25% of BMT-haemorrhagic cystitis (HC)

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18
Q

10% of Renal transplant-polyomavirus
associated nephropathy (PVAN)
0-25% of BMT-haemorrhagic cystitis (HC)

A

diesase from BK polyomavirus

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19
Q

BK polyomavirus has ___ serotypes

A

4

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20
Q

Where does JC polyomavirus grow

A

Grows in human glial cells in culture, 5-HT2A serotonin receptor

21
Q

How many serotypes does JC have

A

1

22
Q

when do we see disease from JC polyomoavirus

A

immunosuppreison at young age

23
Q

Where does JCPyV persist

A

kidneys, lymphocytes, bone marrow

24
Q

What disease does JCPyV cause

A

Progressive multifocalencepholopathy seen in 5-8% of AIDS encephalopathies

25
Q

Progressive multifocalencepholopathy seen in 5-8% of AIDS encephalopathies

A

from JCPyV

26
Q

Only PyV classified as a causative agent of a human malignancy

A

Merckel Cell polyomavirus

27
Q

do we contain antiBs to meckel cell polyomavirus

A

yes, 80% adults to

28
Q

Progression of Merkel Cell Carcinoma

A

fast growing, painless, dome shaped

29
Q

Risk in immunocompromised, >60 yr old, often

occurs on sun-exposed areas

A

MCC

30
Q

Clonal integration into host chromosome in most MCC and mutation of _____antigen in DDB

A

LgT

31
Q

•_______ (oncoprotein) expression in ~97% of

MCC

A

LgT antigen

32
Q

Phase I: Pre engraftment

A

Screen to identify potential infections that may put the patient at risk of death following the immunosuppression that precedes transplant
both donor and receipt

33
Q

Key screenings are for

A
  • Hepatitis C virus (HCV)
  • Hepatitis B virus (HBV)
  • Human immunodeficiency virus (HIV)
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV)
  • Syphilis
34
Q

Pre-transplant chemotherapy and radiation and the post-transplant immune suppression: cyclosporine, tacrolimus put the patient at risk of infections
• Pre-engraftment infections due to :

A

immunosuppression

35
Q
  • Respiratory viruses
  • Enteric viruses ‘
  • Human herpesvirus 6 (HHV6) reactivation
  • Herpes simplex virus (HSV) reactivation
A

pre-engraftment infections

36
Q

Phase II: Post-Engraftment
Days 30-100
worry about:

A

• Cytomegalovirus (CMV) reactivation
• Adenovirus infection
• Human herpesvirus 6 (HHV6) reactivation
• Community-acquired respiratory viruses:
influenza/respiratory/humanmetapneum/picorna

37
Q

Phase II: Post-Engraftment >100 days

presence of GVHD requires constant _______ during post transplant

A

GVHD

38
Q

Chronic GVHD and it’s treatment are issues

A

ongoing cellular/humoral immunity defects in pts

39
Q

Phase II:

Chronic GVHD compromises skin, mucous membranes and GI thus infections during Phase II are usulaly

A

in lungs, skin, URT

-

40
Q

During Phase II, viral infections, especially secondary to VZV, are responsible for

A

more then 40% of infections

41
Q

Late phase III:

see lots of______

A

VZV infections secondary to reactivation

usually 5 months after transplant

42
Q

85% pts with reactivated VZV devo ____

15% devo ______

A

herpes zoster

chx pox

43
Q

pts that devo ch pox have increased risk for

A

systemic infction like pnemonia, hepatitis

44
Q

Hemorrhagic cystisis: from BK, JC and adenovirus occur:

A

Following irradiation, cyclophosphamide or busulfan in the pre-transplantation regimen, and prolonged aplasia after transplantation

45
Q

Early development of Hemorrhagic cystisi associated with

A

high- dose cyclophosphamide before transplantation

46
Q

Late-onset hemorrhagic cystitis (> day 15) from

A

BK, JC virus, or adenoviruses

47
Q

TX for BK or adenovirus associated with hemorrhagic cystitis

A

Cidofovir successfully will treat BK or adenovirus–associated hemorrhagic cystitis.

48
Q

Goals of devo of effective intervention therapies

A

more effective antivirals
virus specific vaccines
immune modulation

Immunology 3 (20 decks)

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