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OS Hematology/Oncology > Micro/CMV,EBV,KSHV > Flashcards

Micro/CMV,EBV,KSHV Flashcards

1
Q

CMV, EBV, and KSHV are latent in these types of cells

A

lymphocytes

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2
Q

Describe CMV,EBV,KSHV genome and structure

A

large, linear, dsDNA; icosahedral enveloped

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3
Q

CMV is this type of herpes virus

A

Betaherpesvirus

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4
Q

EBV is this type of herpesvirus

A

Gammaherpesvirus

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5
Q

Describe the genomic structure of HSV-1

A

Two unique regions (long and short) encoding viral gene products, each flanked by inverted repeat sequences

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6
Q

Describe the genomic structure of EBV

A

Multiple repeat region with amplified gene sequences; NO inverted repeats

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7
Q

Describe the genomic structure of CMV

A

Similar to HSV-1

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8
Q

Describe the lytic cycle

A

Initial infection occurs when virus attaches to heparin sulfate proteoglycans. It then binds more tightly another receptor.
Viral encelope fuses directly with the plasma membrane in a pH-indep event, releasing nucleocapsid inside the cell.
Nucleocapsid migrates along microtubules to nucleus where genomic DNA is released.

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9
Q

Describe the order of protein production when a herpesvirus infects a cell and what types of proteins are in each stage

A

1) Immediate early genes - transcription factors; use host RNA pol II
2) Early genes - nonstructural proteins; enzymes (make DNA pol; need IEs)
3) Late genes - structural (need IEs)

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10
Q

Describe the three phases of latency

A

Establishment; Maintenance; Reactivation

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11
Q

Are herpesviruses maintained in or out of the chromosome?

A

External to

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12
Q

Which viruses can cause mono?

A

CMV and EBV

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13
Q

How is CMV spread?

A

Through direct contact with secretions (saliva, urine, milk, semen, blood)
Considered an STI

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14
Q

Who is at risk for CMV infection?

A

Neonates, daycare workers, pregos, immunocompromised (AIDS, transplant), gay men

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15
Q

Can CMV be spread through aerosol?

A

NO

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16
Q

In utero infections with CMV may cause these defects

A

MR, deafness

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17
Q

Who is most at risk for CMV?

A

Transplant patients!

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18
Q

What is a common infection in immunocompromised patients infected with CMV?

A

Pneumonitis

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19
Q

How does pneuominitis occur in transplant patients with CMV?

A

Either through a positive donor or reactivated latent CMV

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20
Q

How do you prevent transplant patients from getting CMV infections?

A

Ig and ganciclovir

21
Q

What does CMV cause in AIDs patients?

A

Retinitis, pneumonitis

22
Q

How do you diagnose CMV infection?

A

Very large-looking lymphocytes; ELISA/PCR to detect DNA amplification; shell vial assay

23
Q

Explain the shell vial assay

A

Infect a monolayer of cells with potential CMV-infected source; after 12-18 hrs, check for antibody presence using IF

24
Q

When does pneumonitis usually present in transplant patients with CMV infection?

A

Several months after transplant

25
Q

What is the drug of choice for CMV treatment?

A

Gangciclovir

26
Q

What is the second line of therapy for CMV infections?

A

Acyclovir and foscarnet

27
Q

What treatment is best for AIDs patients with pneumonitis due to CMV?

A

Foscarnet

28
Q

What is unique about Foscarnet and Cidofovir compared to Ganciclovir?

A

They don’t require activation through kinase phosphorylation

29
Q

Describe Acyclovir MOA

A

Pro-drug guanosine analog requiring 3 phosphorylation events; first must be by viral kinase

30
Q

What percent of the adult population is seropositive for EBV?

A

~95%

31
Q

Which viruses causes hairy leukoplakia?

A

EBV

32
Q

Hairy leukoplakia is often a complication of what infection?

A

AIDS

33
Q

PTLD is caused by which virus?

A

EBV

34
Q

Describe the pathogenesis of EBV infection

A

Spread through saliva
Incubation period several weeks
Starts in oropharynx, then spleen
Oral shedding for many weeks

35
Q

What are the symptoms of mono?

A

Sore throat, fever 1-2 wks, malaise, lymphadenopathy

36
Q

How do you diagnose mono?

A

50% atypical, large lymphocytes with lobulated nuclei
and/or
use Monospot (heterophile antibody) test

37
Q

How does Monospot work?

A

Test for agglutination against sheep RBCs; positive test indicates EBV infection mono and not CMV mono

38
Q

EBV can cause which neoplasms?

A

PTLD, Burkitt’s, and nasopharyngeal carcinoma

39
Q

Who has the highest risk of contracting PTLD?

A

Seronegative EBV transplant recipients in the first year

40
Q

How do you treat PTLD?

A

Stop the immunosuppression and monitor for rejection

41
Q

Why doesn’t ACV work in PTLD?

A

Infection is latent; ACV requires replication to work

42
Q

Describe Burkitt’s lymphpoma and contributing factors

A

B-cell lymphoma affecting jaw (Africa); Associated with

1) Early EBV infection -> immort B cells
2) C-Myc activation to Ig promoter
3) Malaria

43
Q

Compare Burkitt’s and nasopharyngeal carcinoma in terms of EBV-related pathogenesis

A

NPC is 100% caused by EBV, whereas Burkitt’s has other causes

44
Q

What is the relationship between KSHV and Kaposi’s sarcoma

A

Necessary but not sufficient; need immunocompromise; KSHV DNA recovered from >95% of tumors

45
Q

How is KSHV spread and who is at risk?

A

AIDS patients at risk; STI spread but is not present in semen or vaginal secretions

46
Q

What does Kaposi’s look like?

A

Bluish, blue appearing lesions

47
Q

Where does KSHV become latent?

A

B cells and endothelium

48
Q

Beside’s Kaposi’s, KSHV/HHV-8 causes what B cell abnormalities?

A

Primary effusion lymphoma (NHL; body cavities; mean survival 2-6 mo); Castleman’s disease (nonmetastatic lymph node tumors)

OS Hematology/Oncology (14 decks)

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