Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Heme Micro > CMV, EBV, KSHV > Flashcards

CMV, EBV, KSHV Flashcards

1
Q

CMV, EBV, and human herpesvirus-8 or KSHV all fall into what category?

A

Human herpesviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the general structure of a herpesvirus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What’s the genome of a herpesvirus like?

A

Large, linear, double stranded DNA (150-250 kbp)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Herpesvirus genomes are replicated in the (cytoplasm/nucleus).

A

Nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Herpes viruses produce _________ in which the primary infection is often asymptomatic. But _________ can occur especially in immune-compromised hosts.

A

Self-limiting infections; life-threatening infections or cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of replication do herpesviruses undergo?

A

Lytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Following virus attachment, penetration occurs by _________.

A

Virus glycoprotein-mediated fusion of envelope and plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Herpesvirus penetration occurs by a (pH dependent/pH independent) event.

A

pH independent event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens after the released nucleocapsid gets in the cell?

A
  1. Migrates to nuclear envelope via microtubules
  2. Uncoats
  3. DNA enters the nucleus
  4. Virion components shut off host macromolecular synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the parts of the cascade regulation of viral genes?

A
  1. Immediate early (IE) gene expression
  2. Early gene expression
  3. Late gene expression
  4. Virus assembly
  5. Virus particle release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are immediate early genes?

A

Virus-specific transcription factors that use host RNA pol II and stimulate transcription at virus early promotors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are early genes?

A

Genes that encode many nonstructural proteins and enzymes and use viral DNA pol and thymidine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are late genes?

A

Genes that encode structural proteins and are dependent on IE TFs plus genome replication for expression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Viral glycoproteins can be transported to the infected cell surface where they cause _______.

A

Syncytia formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where in the cell does virus assembly occur?

A

In the nucleus where nucleocapsids bud first into the perinuclear space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T or F: All herpesviruses undergo latency.

A

T: entire genomes are maintained extrachromosomally in the host indefinitely, but no viruses are produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the three stages of latency?

A
  1. Establishment
  2. Maintenance
  3. Reactivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When does reactivation generally occur?

A

When there’s a lapse in immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Reactivation results in ______ and ______.

A

Production of virus particles and recurrent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T or F: Anyone infected with a herpesvirus is in the club fo life.

A

True dat (risk of recurrent infections or other sequelae)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is acyclovir?

A

An antiviral prodrug that prevents chain elongation from continuing on an actively replicating virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the alphaherpesvirinae (3)?

A
  1. HSV-1
  2. HSV-2
  3. VZV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The alphaherpesvirinae are (neurotropic/lymphotropic) for latency and have (aggressive/insidious) growth.

A

Neurotropic, aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

The betaherpesvirinae are (neurotropic/lymphotropic) for latency and have (aggressive/insidious) growth.

A

Lymphotropic, insidious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the betaherpesvirinae? (3)

A
  1. CMV
  2. HHV-6
  3. HHV-7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the gammaherpesvirinae? (2)

A
  1. EBV

2. HHV-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The gammaherpesvirinae are (neurotropic/lymphotropic) for latency and have (aggressive/insidious) growth.

A

Lymphotropic, insidious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

T or F: CMV is highly contagious.

A

F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CMV is more prevalent in (lower/higher) socioeconomic classes.

A

Lower (80% of adults in lower class, 50% of adults in higher class)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the general steps of the lytic cycle? (6)

A
  1. Virus attachment
  2. Penetration
  3. Uncoating
  4. Programmed expression of viral genes
  5. Assembly
  6. Release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where is CMV found?

A

Saliva, urine, breastmilk, semen, cervical secretions, blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Who’s the most at risk for CMV?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Neonatal CMV infections can result in ________.

A

Retardation and deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CMV infection occurs through _________.

A

Direct contact with secretions (not by aerosol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where is primary CMV replication taking place? Secondary?

A

Primary in epithelial cells followed by spread to lymphoid tissue

36
Q

What do CMV-infected cells look like?

A

Large, puffed up

37
Q

T or F: Most CMV infections in neonates and adults are asymptomatic.

A

T

38
Q

Most _________ get CMV infection with pnemonitis.

A

Organ transplant patients. Don’t forget this!

39
Q

AIDS patients are prone to CMV _____, _____, and ______.

A

Retinitis, colitis, pneumonitis

40
Q

How can you diagnose CMV?

A

ELISA, PCR, Shell vial assay (indirect immunofluorescent used to detect an immediate early protein after 24 hours of cell culture infection)

41
Q

What can you use to limit complications of CMV in transplant patients?

A

CMV Ig and ganciclovir

42
Q

What is ganciclovir?

A

Guanosine analog that requires phosphorylation by viral kinase for activity
-Triphosphate form inhibitys CMV polymerase

43
Q

What is the downside of the triphosphate form of ganciclovir?

A

It is more toxic to the host than acyclovir

44
Q

Side effects of ganciclovir

A

Neutropenia and GI bleeding

45
Q

_______ are approved for CMV retinitis treatment in AIDS patients.

A

Gancyclovir, Cidofovir, Foscarnet

46
Q

What is foscarnet?

A

A pyrophosphate analog that inhibits DNA polymerase but doesn’t require phosphorylation for activity

47
Q

What is cidofovir?

A

A competitive inhibitor of CMV DNA pol that does not require viral kinase action for activity (like ganciclovir does)

48
Q

Who typically gets EBV infection at an early age?

A

People in a low socioeconomic setting

49
Q

EBV can lead to what common disease?

A

Infectious mononucleosis

50
Q

_____% of the adult population contains Ab to EBV.

A

95%

51
Q

EBV can cause ________ in immunocompromised hosts.

A

Oral hairy leukoplakia (productive infection of tongue epithelial cells)

52
Q

____________ from EBV is seen in some transplant patients.

A

Posttransplant lymphoproliferative disease (PTLD)

53
Q

Which cancers is EBV associated with?

A

Burkitt’s lymphoma and nasopharyngeal carcinoma

54
Q

How does EBV spread from person to person?

A

Through saliva by kissing <3

55
Q

What is EBV’s incubation period?

A

4-7 weeks

56
Q

Initial replication of EBV occurs in _______, then spreads to _______.

A

Initial replication in oropharyngeal epithelium –> lymphocytes –> liver and spleen

57
Q

Where does EBV remain latent?

A

Throat epithelium and B cells

58
Q

T or F: Oral shedding of EBV occurs for many months.

A

F: occurs for many weeks

59
Q

T or F: Most EBV infections are asymptomatic.

A

T

60
Q

What are the symptoms of infectious mononucleosis?

A

Sore throat, fever, malaise, lymphadenopathy

61
Q

How can you diagnose EBV?

A

Symptoms and presence of at least 50% atypical large lymphocytes with lobulated nuclei

62
Q

What is EBNA and what does it indicate?

A

An EBV antigenic marker

  • EBNA 1 maintains genome replication in dividing B cells
  • Conversion to anti-EBNA IgG indicates resolution of primary infection
63
Q

Where will you find VCA?

A

It’s a viral capsid antigen on EBV

64
Q

Anti-VCA IgM indicates _______.

A

Primary infection

65
Q

Anti-VCA IgG without ________ indicates primary infection.

A

anti-EBNA

66
Q

Anti-VCA IgGa with anti-EBNA indicates ______.

A

Past infection

67
Q

Where will you detect EA (early antigen)?

A

In cells that do not produce virus

68
Q

What does the monospot test look at?

A

Heterophile antibodies that agglutinate sheep RBCs (distinguishes EBV mono from CMV mono)

69
Q

How do you treat oral leukoplakia?

A

Acyclovir

70
Q

How do you treat PTLD?

A

Stop immunosuppression and monitor for rejection

71
Q

What is PTLD?

A

Uncontrolled proliferation of B cells due to their transformation of EBV and no CTLs to control them

72
Q

Where is Burkitt’s lymphoma endemic?

A

Central Africa and New Guinea

73
Q

What three factors is Burkitt’s lymphoma associated with?

A
  1. Early EBV infection –> latency
  2. C-MYC activation
  3. Malaria
74
Q

T or F: Association of nasopharyngeal carcinoma with EBV is worldwide.

A

T

75
Q

Where does nasopharyngeal carcinoma have the highest frequency and what’s a possible reason for this?

A

Southern China – dat high salt diet

76
Q

How does nasopharyngeal carcinoma present?

A

Painless lump in the neck

77
Q

T or F: HHV-8 is necessary and sufficient to cause Kaposi’s sarcoma (KS) ?

A

F: Necessary but not sufficient

78
Q

Human herpes virus 8 is aka ______.

A

KSHV

79
Q

Where do KS tumors occur?

A

In the lining of the lymphatic system (fill lymphatic channels with blood cells –> bluish, bruised lesions)

80
Q

Where is KS prevalent?

A

Mediterranean and sub-Saharan Africa (not sexually transmitted in these populations)

81
Q

In the US, who are most of the KS patients? How is it transmitted?

A

AIDS patients, Sexually transmitted/via saliva (not present in semen and vaginal secretions)

82
Q

Whats the typical incubation period for KS?

A

10 years

83
Q

T or F: When symptomatic for KS, treatment in AIDS patients targets the tumor or HIV but not HHV-8.

A

T

84
Q

Other than KS, what B cell abnormalities does HHV-8 cause?

A
  1. Primary effusion lymphoma

2. Castleman’s disease

85
Q

What is primary effusion lymphoma?

A

KSHV+ NHL commonly found in body cavities (mean survival 2-6 months)

86
Q

What is Castleman’s disease?

A

Lymph node tumors that are KSHV+ (not strictly cancer)

Heme Micro (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions