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STEP Pathology > deck_4982595 > Flashcards

deck_4982595 Flashcards

1
Q

T or F. CMV, EBV, and KSHV (HHV8) are all herpes viruses

A

T.

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2
Q

All share a tropism for what?

A

lymphocytes

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3
Q

Which of the three are oncogenic viruses?

A

EBV and KSHV

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4
Q

Describe the structure of herpesviruses.

A

-icosahedral capsid surround by a lipid envelope containing ~12 virally derived glycoproteinstegumnet- has important proteins for replication

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5
Q

Describe the genome of herpesvirus.

A

large, linear, double-stranded DNA ca. 150-250 kilobase pairsCMV is largest

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6
Q

How do herpesviruses replicate?

A

genome is replicated and viruses assembled in the nucleus

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7
Q

T or F. In general, herpesviruses produce self-limiting infections in which the primary infection is often asymptomatic.

A

However, life-threatening infections or cancers can occur, especially in immune compromised hosts (neonates, AIDS, etc.)

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8
Q

Is the replicative cycle of herpesviruses lytic or lysogenic?

A

lytic in a variety of cell types

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9
Q

Following virus attachment, how does viral penetration occur?

A

by virus glycoprotein- mediated fusion of envelope and plasma membrane (pH independent)

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10
Q

What does the released nucleocapsid do after entering the cell?

A

migrates to nuclear envelope via microtubules, uncoats, and DNA enters the nucleus. Virion components act to shut off host macromolecular synthesis

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11
Q

Then what happens?

A

Programmed expression of viral genes- cascade regulation

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12
Q

What is the order of proteins transcribed in these viruses?

A
  • immediate early genes- early genes- late genes
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13
Q

What do immediate early (IE) genes encode?

A

virus-specific transcription factorsi. use host RNA polymerase IIii. stimulate transcription at virus early promoters

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14
Q

What do early genes encode?

A

many nonstructural proteins, enzymes

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15
Q

Specifically, what kinds of proteins/enzymes do early genes encode?

A

-DNA replication machinery, including viral DNA polymerase-thymidine kinase (tk) which phosphorylates a variety of nucleotides besides thymidine

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16
Q

What do late genes encode?

A

structural proteins (capsids, glycoproteins)

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17
Q

What is late gene transcription dependent on?

A

IE transcription factors and genome replication

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18
Q

Where does virus assembly occur?

A

nucleus- where nucleocapsids bud first into the perinuclear space

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19
Q

What happens after viral assembly?

A

virus particles migrate to the cell surface where they are released

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20
Q

What is latency?

A

situation in which entire genomes are maintained extrachromosomally in the host indefinitely, but no virus are produced

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21
Q

What are the stages of latency?

A

a. Establishmentb. Maintenancec. Reactivation

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22
Q

When does reactivation generally occur?

A

when there is a lapse in immunity and results in the production of virus particles and recurrent infection

23
Q

How many herpesviruses are there?

A

8- classified on basis of their genome arrangement and latency tropism

24
Q

Describe alphaherpesviruses.

A

neurotropic for latency, aggressive lytic growth

25
Q

What are some types of alphaherpesviruses?

A

a.Herpes simplex virus (HSV)-1b.HSV-2c.Varicella-zoster virus (VZV)

26
Q

Describe betaherpesviruses.

A

lymphotropic for latency, more insidious

27
Q

What are some types of betaherpesviruses?

A

a.Cytomegalovirus (CMV)b.Human herpesvirus-6 (HHV-6)c.HHV-7

28
Q

Describe gammaherpesviruses.

A

lymphotropic for latency, more insidious

29
Q

What are some types of gammaherpesviruses?

A

EBVHHV-8 (Kaposi’s sarcoma)

30
Q

T or F. CMV is highly contagious

A

F. Still, in low socioeconomic classes, infection is at 1 to 2 years of age and up to 80% of adult population is CMV positiveIn higher socioeconomic classes, CMV is typically acquired after 16 years of age and only about 50% of the adult population is CMV positive

31
Q

Where is CMV found in the body?

A
  • saliva-urine-breast milk-semen-cervical secretions-blood- transplant organs
32
Q

Who is at risk for CMV?

A
  • neonates- day care workers- pregnant workers- immunocompromised ppl- gay men
33
Q

How is CMV spread?

A

contact with secretions- not by aerosol

34
Q

Where does CMV replicate?

A

epithelial cells, followed by spread to lymphoid tissue

35
Q

CMV latently infects what cell types?

A

B-cells, T-cells, monocytes, and lymphocytes where it causes large, puffed up cells

36
Q

What are the symptoms of CMV infection in utero?

A
  • mostly asymptomatic- retardation and deafness possible
37
Q

What are the symptoms of CMV infection in adulthood?

A

-most asymptomatic-mononucleosis accompanied by fever can occur

38
Q

CMV is especially common in which patient population?

A

transplant recipients Can result from infection by CMV+ donor or by reactivation of CMV+ recipient

39
Q

CMV in transplant patients is often associated with what?

A

pneumonitis

40
Q

How can CMV infection in transplant patients be prevented?

A
  • prophylactic treatment with CMV Ig and ganciclovir
41
Q

AIDS patients with CMV are prone to what?

A

retinitiscolitispneumonitis

42
Q

How is CMV diagnosed?

A

-ELISA or PCR detection-Shell vial assay in which indirect immunofluorescence is used to detect an immediate early protein after 24 h of cell culture infection

43
Q

What are the treatment options for CMV?

A

-Ganciclovir-Foscarnet-Cidofovir

44
Q

What is Ganciclovir?

A

a guanosine analog similar to acyclovir, the prototype which is used in HSV, VZV, and EBV infections

45
Q

What does ganciclovir require for activity?

A

phosphorylation by viral kinaseTriphosphate form preferentially inhibits CMV polymerase but is more toxic to host than ACV

46
Q

Side effects of ganciclovir?

A

neutropeniaGI bleeding

47
Q

What is ganciclovir approved for?

A
  • treatment of transplant patients- treatment for CMV retinitis - treatment in AIDS patients
48
Q

What is Foscarnet approved to treat?

A
  • CMV retinitis in AIDS patients same for Cidofovir
49
Q

How does Foscarnet work?

A

Pyrophosphate analog that inhibits DNA polymerase, but does not require phosphorylation for activity

50
Q

How does Cidofovir work?

A

it is a deoxycytidine analog that is a competitive inhibitor of CMV (and HSV) DNA polymerase, but not does require viral kinase action for activity

51
Q

What is CMV possible linked to?

A

glioblastoma multiforme

52
Q

How does Acyclovir work?

A

guanosine analogue that enters the body and must have 3 phosphates put on it to work. The first is added by a virally derived thymidine kinase (thus, it is specific to only infected cells), and the last two by host kinases. Once incorporated, it disrupts DNA production

53
Q

T or F. Oncogenesis is the result of latency, not acute infection

A

T.

STEP Pathology (80 decks)

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