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Hematology Microbiology > CMV, EBV, KSHV > Flashcards

CMV, EBV, KSHV Flashcards

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Biology 101 flashcards
1
Q

What type of replication cycle does the herpes virus undergo?

A

Lytic replication

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2
Q

Describe structure of herpesvirus?

A

Icosahedral, enveloped, tegument contains the bad stuff (viral proteins)

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3
Q

Describe the attachment phase of the lytic replication cycle

A

herpes virus envlope fuses with the plasma membrane of the cell, nucleocapsid released and it goes to the nucleus

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4
Q

What are the 3 phases of the lytic replication cycle

A

Immediate early, Early, Late

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5
Q

What occurs during the immediate early phase?

A

viral transcription factors are transcribed.

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6
Q

Is the host RNA polymerase II used for this?

A

Yes.

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7
Q

What occurs during the early phase?

A

Replication proteins such as the viral DNA polymerase are transcribed. Thymidine kinase becomes thymidine

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8
Q

Late Phase

A 
Structural proteins (capsids, glycoproteins)
Viral glycoproteins are incorporated into virus envelope and transported to cell surface.
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9
Q

SUmmarize herpes lytic replication

A 
IE- transcrption factors
E- Replcation machinery (DNA poly)
L- Structural
Assembly occurs in nucleus.
Process is refered to as cascade regulation
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10
Q

Where are gnomes maintained during herpesvirus latency

A

extrachromosomally

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11
Q

Is virus produced during latency?

A

No

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12
Q

Three stages of latency

A

Establishment, Maintenance, Reactivation

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13
Q

When does reactivation occur?

A

During a lapse in immunity, results in the production of virus and recurrent infection

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14
Q

How is CMV spread?

A

STI, through anything liquid in the body….also THROUGH TRANSPLANTS

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15
Q

At risk populations?

A

neonates, day care workers, pregnant workers, gay men, immunocompromised patients

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16
Q

WHere does the primary replication of CMV occur?

A

Epithelial cells of throat then spreads to lymphoid tissue

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17
Q

Where does CMV become latent?

A

B and T cells, monocytes, lymphocytes.

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18
Q

What are the symptoms?

A

In neonates, mostly asymptomatic but can cause deafness and retardation
In adults, mostly asymptomatic but can cause mono.

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19
Q

Do most transplant patients develop CMV?

A

Yes.

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20
Q

What is a serious aspect of transplant acquired CMV

A

pneumonitis can be life-threatening.

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21
Q

How is it treated?

A

CMV Ig and Ganciclovir

22
Q

Diagnosis of CMV

A

PCR of ELISA….old way was SHell assay

23
Q

Three most common anti-virals for herpesvirus?

A

Acyclovir, Ganciclovir, Foscarnet

24
Q

WHich is most commonly used for CMV?

A

Ganciclovir- Guanosine analog, side effects are neutropenia and GI bleeds

25
Q

Is epstein barr virus common?

A

Yes

26
Q

What is one related symptom of EBV seen in AIDS patients

A

Oral hairy leukoplakia

27
Q

How is oral hairy leukoplakia caused by EBV treated?

A

Acyclovir.

28
Q

What two cancers is EBV associated with?

A

Nasopharyngeal carcinoma and Burkitts lymphoma

29
Q

How is EBV spread?

A

Saliva

30
Q

WHere does it lay latent?

A

Originally in the oropharyngeal epithehelium then moves to lymphocytes and then to liver and spleen

31
Q

Symptoms?

A

most asymptomatic. Some get mono.

32
Q

How is it diagnosed?

A

Monospot test or by symptoms and the appearance of 50% large lymphocytes with lobulated nuclei

33
Q

What is EBNA

A

Epstein barr nuclear antigen

34
Q

When does EBNA appear?

A

early in infection

35
Q

COnversion to what signals the end of primary infection?

A

Anti EBNA Ig

36
Q

What does VCA stand for

A

Viral capsid antigen

37
Q

Describe how VCA can help with diagnosis

A

Presence of Anti VCA IgM means primary infection
Presence og anti vca IgG without Anti EBNA indicates primary infection
Presence of anti vca IgG with anti EBNA IgG signals the end of primary infection.

38
Q

What does the monospot test look for?

A

Heterophile antibodies that agglutinate sheeps blood. This is the best test to differentiate EBV mono from CMV mono

39
Q

What is PTLD

A

Post transplant lymphoproliferative disorder

40
Q

What causes PTLD?

A

EBV modification of B cells causes them to proliferate out of control and in a post transplant patient taking immunosuppressive drugs, there is no immune response to these B cells.

41
Q

How do we treat PTLD

A

Take pt off immunosuppressive therapy…risky

42
Q

Burkitts lymphoma, describe it

A

Neoplasm of B cells that affects jaw bones. ENdemic in Central Africa and New Guinea. Three causes: EBV, Malaria, C-myc activation.

43
Q

Nasopharyngeal carcinoma affects what cells?

A

Epithelial cells. Most common insouth china. presents as painless lump in neck. very poor survival

44
Q

What is the role which KSHV plays in kaposi’s sarcoma

A

It is necessary but not sufficient to cause KS.

45
Q

Where is KSHV latent?

A

B cells and endothelial cells

46
Q

Where do KS tumors arise?

A

lining of lymphatic system.

47
Q

Most KS patients in US are aids pts?

A

True

48
Q

How is it spread?

A

Not quite sure. Its an STI but the virus is present in saliva

49
Q

What other B cell abnormalities does KSHV cause?

A

Primary Effusion Lymphoma

Castelemans disease

50
Q

HBow does Ganciclovir work?

A

Inhibits viral polymerase

51
Q

How does Foscarnet work?

A

Inhibits DNA polymerase, does not have to be phosphorylated.

52
Q

Where does EBV lay latent?
CMV
KSHV

A

EBV- Throat epithelial and B
CMV- B,T, mono, lymph
KSHV- lining of lymphoid

Hematology Microbiology (1 decks)

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