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4 PID Unit > 41 Herpes > Flashcards

41 Herpes Flashcards

1
Q

What is the genome like of herpes virus?

A

Large dsDNA (200nm)—LINEAR

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2
Q

T-F–herpes establishes a life long latency

A

True

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3
Q

T-F–herpes generally causes severe disease in healthy people?

A

False–severe in immunocompromised

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4
Q

HSV-1, HSV-2, VZV causes latency where?

A

in neurons

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5
Q

HCMV, HHV6, HHV7, EBV, KSHV causes latency where?

A

hematopoietic cells

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6
Q

What type of capsid does herpes have? enveloped?

A

icosehedral–Yes

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7
Q

What is tegument?

A

protein layer between capsid and envelope

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8
Q

T-F–herpes only contains one glycoprotein on surface of vision to facilitate entry?

A

False- several

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9
Q

What happens to herpes genome after it tracks to nucleus?

A

circularizes

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10
Q

Describe herpes virus genome transcription?

A

3 stages
1st- immediate genes needed for transcription
2nd-early- virus replication genes
3rd- late- virus particle genes

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11
Q

What is necessary for herpes virus to synthesize new viral DNA?

A

viral DNA polymerase

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12
Q

How does genome replicate in the herpes life cycle?

A

episomally and the episome is maintained in daughter cells

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13
Q

What is DNA that is able to replicate independent of the host chromosome and has an origin of replication?

A

episome

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14
Q

What is required for production of sufficient nucleotide substrates for virus replication? what is this a target for? What do they do?

A

1- viral nucleoside kinase

  1. antivirals
  2. phosphorylate nucleosides and nucleoside analogs
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15
Q

Does herpes have a lytic life cycle?

A

Yes

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16
Q

Where do herpes virus particles assemble? what does this mean? Where does it go next?

A
  1. In the nucleus
  2. Must transverse nuclear membrane
  3. Enters golgi and traffics to plasma membran
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17
Q

how do all herpes viruses enter an individual?

A

close contact with body secretions

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18
Q

Initiallly, herpes replication occurs in the cell type that is lytically infected. T cell response after a few weeks manages this. What happens next?

A

Virus passed to one or more secondary populations where latency occurs and remains there for hosts life

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19
Q

What are 3 steps/facts of herpes virus latency?

A
  1. viral lytic genes turned off
  2. late genes turned on- only a few genes
  3. resevoir population and productive viral factory population
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20
Q

T-F–HSV-1— is beta herpes virus, worldwide, close contact spread, and has asymptomatic and symptomatic shedding?

A

False- it is alpha herpesvirus–everything else is true

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21
Q

The initial HSV-1 infection and replication is at the mucocutaneous site—where is latency HSV-1?

A

Ganglion proximal to initial site (mouth initial infection will lead to trigeminal ganglion latent infection)

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22
Q

T-F–HSV-1 can traffic down the sensory neuron to infect epithelial cells at the site of the original infection- HSV-1?

A

True

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23
Q

T-F–the primary infection epidermal destruction is due to T cell infiltration and cytotoxic effects- HSV-1?

A

False- viral cytopathic effects—Reactivation is due to both

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24
Q

What is the cytopathic effect that gives away herpes HSV-1

A
  1. multinucleate giant cells

2. inclusion bodies

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25
Q

Where are the 4 sites of HSV-1 primary infection?

A
  1. gingivostomatitis
  2. ocular herpes
  3. herpetic whitlow
  4. genital herpes (mostly HSV-2)
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26
Q

What is conjunctivitis and corneal epithelial lesions stained with Rose bengal characteristic of?

A

primary herpes infection

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27
Q

Review the 6 points of reactive HSV-1 infection

A 
Virus travels back down neuron to target
1. asymptomatic
2. cold sore
3. herpes keratitis- disciform scar
4 herpes whitlow
5herpes encephalitis
6 Genital lesion
28
Q

What are the 3 HSV-1 and HSV-2 complications of immune impairment?

A
  1. sever local disease
  2. disease in other viscera–esophagus
  3. encephalitis
29
Q

Is there a vaccine for HSV-1

A

No

30
Q

What two types of antivirals do we use for HSV-1?

A

Nucleoside analogs and direct inhibitors of viral polymerase

31
Q

T-F– HSV-2 is worldwide, alpha herpesvirus, more prevalent than HSV-1 and usually effects more women than men? How many people are infected in US? Are most of them symptomatic?

A
  1. FAlse- less prevalent that HSV-1 and everything else is true
  2. 45 million
  3. No- less than a fourth
32
Q

What are the 4 results of primary HSV-2 infection?

A
  1. asymptomatic
  2. genital herpes
  3. neonatal herpes
  4. Primary gingivostomatits (mostly HSV-1 though)
33
Q

What are the 3 outcomes of HSV-2 reactive herpes?

A
  1. asymptomatic
  2. Genital herpes
  3. Cold sores (usually HSV-1 though)
34
Q

Does HSV-2 have a vaccine? Antivirals?

A
  1. No

2. Nucleoside analogues and viral polymerase inhibitor

35
Q

t-f– VZV is an alpha virus, found mostly in childhood, has no asymptomatic shedding, 98% of all children are seropositive by 18, and has a vaccine?

A

True

36
Q

What are the 3 key symptoms of VZV?

A
  1. diffuse vesicular rash
  2. fever
  3. Malaise
37
Q

Where does VZV replication occur?

A

macrophages and pneumocytes

38
Q

The infectious VZV virus is released from the rash, but how does it infect someone?

A

Respiratory system

39
Q

What is VZV reactivation commonly called?

A

shingles or zoster

40
Q

What is zoster (shingles associated with)?

A

Increased age (immunosupression)

41
Q

Does VZV have a vaccine? is it recommended for adults?

A

Yes and yes to prevent shingles

42
Q

T-F–VZV has nucleoside analogues (ACV-like drugs) for treatment?

A

True

43
Q

T-F– the EBV is gamma herpesvirus, highly prevalent, the kissing virus, and has asymptomatic and symptomatic shedding?

A

True

44
Q

Initial replication of EBV is in the oropharygeal cells- are the permissive to lytic infection? How is the virus spread? what does viremia result from? Where does latency occur?

A
  1. Yes
  2. Circulating B cells
  3. Productive replication in circulating B cells
  4. B cells– thought to be semi permissive for replication
45
Q

Reactivation of EBV in b cells leads to what? Can virus from both bcells and oropharygeal cells shed into saliva?

A
  1. spread of virus to oropharyngeal cells

2. Yes

46
Q

What is the EBV latency period outgrowth controlled by?

A

CD8 cell immune response- 1% of peripheral T cells are responding to EBV antigens

47
Q

What are the 2 types of primary infection of EBV?

A
  1. asymptomatic

2. Mononucleosis [fever, lymphadenopathy, spleomegaly, lymphocytosis, monospot-positive, adolescents]

48
Q

What is reactivation of EBV like?

A
  1. asymptomatic with shedding
  2. chronic lymphadenopathy
  3. some associate it with chronic fatigue syndrome
49
Q

What does the mono spot assay measure?

A
  1. heterophile antibody= spurious production of IgM to Paul-Bunnell antigen on animal erythrocytes
50
Q

What is the complication due to immune impairment for EBV?

A

lymphoproliferative disorder

51
Q

What EBV associated tmors contain latent virus?

A
  1. B cell lymphoma
  2. African Burkitt’s lymphoma (co-infect with malaria)
  3. Nasopharyngeal carcinoma
52
Q

How to we test EBV status acutely? Chronically?

A
  1. monospot postivity- IgM against capsid

2. EBNA seropositivty- IgG against capsid

53
Q

Vaccine for EBV?

A

No- antivirals usually nor required either

54
Q

T-F–CMV is a gamma herpesvirus, has high seroprevalence worldwide, sexual transmission, and asymptomatic and symptomatic shedding?

A

False- beta herpes virus and everything else is true

55
Q

CMV is like EBV mono. What is the difference?

A

No monospot postivity–not heterophile antibody

56
Q

What is the most common infectious cause of birth defects? What defects?

A
  1. CMV

2. deafness, sight impairment, developmental abnormalities etcs.

57
Q

What are the complications of immune impairment for CMV ?

A

retinitis, go ulcers, pneumonia, encephalitis [in HIV and transplant patients]

58
Q

Is there a vaccine for CMV?

A

No

59
Q

T-f–HHV-6 is a beta herpesvirus, is acquired by most children at 6-24 months, and has asymptomatic shedding only?

A

False- asymptomatic and symptomatic shedding, others are true

60
Q

What is vehicle of spread for HHV-6?

A

saliva

61
Q

Where is HHV-6 latency?

A

T cells and monocyte macrophages

62
Q

What is the effects of primary HHV6 infection?

A

Roseola (exanthem subitum) and Fever

Reactivation infection is usually asymptomatic

63
Q

Is immunization and antivirals found for HHV6?

A

No

64
Q

What is HHV8 also known as?

A

Kaposi’s sarcoma associated virus

65
Q

T-F– HHV8 has a high seroprevalence worldwide?

A

FALSE_VERY UNUSUAL FOR THE HERPES VIRUSES!!!!

66
Q

Where does HHV8 infect primarily? Latency?

A

Both in B cells—they cause endothelial tumors in immunocompromised individuals–think AIDS. Also associated with B cell lymphoma because it exists there

4 PID Unit (6 decks)

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