Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

4 PID Unit > 41 Herpes > Flashcards

41 Herpes Flashcards

1
Q

What is the genome like of herpes virus?

A

Large dsDNA (200nm)—LINEAR

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

T-F–herpes establishes a life long latency

A

True

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

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

A

False–severe in immunocompromised

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

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

A

in neurons

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

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

A

hematopoietic cells

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

What type of capsid does herpes have? enveloped?

A

icosehedral–Yes

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

What is tegument?

A

protein layer between capsid and envelope

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

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

A

False- several

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

What happens to herpes genome after it tracks to nucleus?

A

circularizes

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

viral DNA polymerase

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

How does genome replicate in the herpes life cycle?

A

episomally and the episome is maintained in daughter cells

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

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

A

episome

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

Does herpes have a lytic life cycle?

A

Yes

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

how do all herpes viruses enter an individual?

A

close contact with body secretions

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

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

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

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

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

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

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

A
  1. multinucleate giant cells

2. inclusion bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Where are the 4 sites of HSV-1 primary infection?
1. gingivostomatitis 2. ocular herpes 3. herpetic whitlow 4. genital herpes (mostly HSV-2)
26
What is conjunctivitis and corneal epithelial lesions stained with Rose bengal characteristic of?
primary herpes infection
27
Review the 6 points of reactive HSV-1 infection
``` 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
What are the 3 HSV-1 and HSV-2 complications of immune impairment?
1. sever local disease 2. disease in other viscera--esophagus 3. encephalitis
29
Is there a vaccine for HSV-1
No
30
What two types of antivirals do we use for HSV-1?
Nucleoside analogs and direct inhibitors of viral polymerase
31
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?
1. FAlse- less prevalent that HSV-1 and everything else is true 2. 45 million 3. No- less than a fourth
32
What are the 4 results of primary HSV-2 infection?
1. asymptomatic 2. genital herpes 3. neonatal herpes 4. Primary gingivostomatits (mostly HSV-1 though)
33
What are the 3 outcomes of HSV-2 reactive herpes?
1. asymptomatic 2. Genital herpes 3. Cold sores (usually HSV-1 though)
34
Does HSV-2 have a vaccine? Antivirals?
1. No | 2. Nucleoside analogues and viral polymerase inhibitor
35
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?
True
36
What are the 3 key symptoms of VZV?
1. diffuse vesicular rash 2. fever 3. Malaise
37
Where does VZV replication occur?
macrophages and pneumocytes
38
The infectious VZV virus is released from the rash, but how does it infect someone?
Respiratory system
39
What is VZV reactivation commonly called?
shingles or zoster
40
What is zoster (shingles associated with)?
Increased age (immunosupression)
41
Does VZV have a vaccine? is it recommended for adults?
Yes and yes to prevent shingles
42
T-F--VZV has nucleoside analogues (ACV-like drugs) for treatment?
True
43
T-F-- the EBV is gamma herpesvirus, highly prevalent, the kissing virus, and has asymptomatic and symptomatic shedding?
True
44
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?
1. Yes 2. Circulating B cells 3. Productive replication in circulating B cells 4. B cells-- thought to be semi permissive for replication
45
Reactivation of EBV in b cells leads to what? Can virus from both bcells and oropharygeal cells shed into saliva?
1. spread of virus to oropharyngeal cells | 2. Yes
46
What is the EBV latency period outgrowth controlled by?
CD8 cell immune response- 1% of peripheral T cells are responding to EBV antigens
47
What are the 2 types of primary infection of EBV?
1. asymptomatic | 2. Mononucleosis [fever, lymphadenopathy, spleomegaly, lymphocytosis, monospot-positive, adolescents]
48
What is reactivation of EBV like?
1. asymptomatic with shedding 2. chronic lymphadenopathy 3. some associate it with chronic fatigue syndrome
49
What does the mono spot assay measure?
1. heterophile antibody= spurious production of IgM to Paul-Bunnell antigen on animal erythrocytes
50
What is the complication due to immune impairment for EBV?
lymphoproliferative disorder
51
What EBV associated tmors contain latent virus?
1. B cell lymphoma 2. African Burkitt's lymphoma (co-infect with malaria) 3. Nasopharyngeal carcinoma
52
How to we test EBV status acutely? Chronically?
1. monospot postivity- IgM against capsid | 2. EBNA seropositivty- IgG against capsid
53
Vaccine for EBV?
No- antivirals usually nor required either
54
T-F--CMV is a gamma herpesvirus, has high seroprevalence worldwide, sexual transmission, and asymptomatic and symptomatic shedding?
False- beta herpes virus and everything else is true
55
CMV is like EBV mono. What is the difference?
No monospot postivity--not heterophile antibody
56
What is the most common infectious cause of birth defects? What defects?
1. CMV | 2. deafness, sight impairment, developmental abnormalities etcs.
57
What are the complications of immune impairment for CMV ?
retinitis, go ulcers, pneumonia, encephalitis [in HIV and transplant patients]
58
Is there a vaccine for CMV?
No
59
T-f--HHV-6 is a beta herpesvirus, is acquired by most children at 6-24 months, and has asymptomatic shedding only?
False- asymptomatic and symptomatic shedding, others are true
60
What is vehicle of spread for HHV-6?
saliva
61
Where is HHV-6 latency?
T cells and monocyte macrophages
62
What is the effects of primary HHV6 infection?
Roseola (exanthem subitum) and Fever Reactivation infection is usually asymptomatic
63
Is immunization and antivirals found for HHV6?
No
64
What is HHV8 also known as?
Kaposi's sarcoma associated virus
65
T-F-- HHV8 has a high seroprevalence worldwide?
FALSE_VERY UNUSUAL FOR THE HERPES VIRUSES!!!!
66
Where does HHV8 infect primarily? Latency?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions