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micro exam 3 > Herpies Viruses > Flashcards

Herpies Viruses Flashcards

1
Q

What type of VIrus are Herpes Simple Virus Type 1 and Type 2 (HSV-1 and HSV-2)

A

Alphaherpesciridae (like varicella Zoster virus)

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2
Q

Host range of Alphaherpesvirus

A

Variable host range

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3
Q

Length of reproduction cycle of Alphaherpesvirus

A

Short

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4
Q

speed of culture spread of Alphaherpesvirus

A

Rapid Spread

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5
Q

Descruction efficiency of infected cells by Alphaherpesvirus

A

Efficient destruction (cyototix-can lyse cells)

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6
Q

where can Alphaherpesvirus establish latency

A

In sensory ganglia

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7
Q

Herpies virus type I infects where

A

waste up

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8
Q

Herpies virus Type II infects where

A

waste down

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9
Q

how does HSV-1 infect

A

oral-oral, oral-genital

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10
Q

amount of adults that are seropositive for HSV-1

A

nearly 2/3

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11
Q

How does HSV-2 infect

A

Primarily genital-genital, also oral-genital possible

prevealent with sexual activity

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12
Q

amount of adults with HSV-2

A

1/5 of adults are infected

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13
Q

where does HSV-1 and HSV-2 infected

A

Epithelial cells in the skin or mucosa (mucosa more susceptible)

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14
Q

Incubation of HSV-1 and 2

A

2-14 days, but typically 4-5 days

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15
Q

Symptoms of HSV 1 and 2

A

Flu-like, includes localized lesions (virus spreads to neighboring cells primarily)

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16
Q

who shows symptoms of HSV-1 and 2

A

1/3

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17
Q

can asymptomatic people transmit HSV-1 and 2

A

yes

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18
Q

how long does the Symptoms of HSV 1 and 2 last

A

8-12 days

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19
Q

Latency of Alphaherpesvirus occures where

A

In stationary cells

peripheral ganglia common site of latent infections

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20
Q

what occures in latency of Alphaherpesvirus

A

Genome circularizes and stays as an episome in the nucleus

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21
Q

what triggers latent Alphaherpesvirus

A

Sunburn, systemic infection, immune impairment, stresss

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22
Q

What immune response is used to fight Alphaherpesvirus

A

Cell mediated immune response required

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23
Q

can people who cant produce antibodies handle herpesvirus infections

A

YEs

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24
Q

what detects Alphaherpesvirus

A

T lymphocytes detect antigens presented by MHC I or II proteins

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25
Q

how does Alphaherpesvirus modulate the immune response to evade it

A

Viral proteins bind to Antibodies and complement proteins that counter effects of interferon

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26
Q

as people age are they more likely or less likely to be serum possitive for Alphaherpesvirus

A

more likely

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27
Q

Prevention of Alphaherpesvirus

A

Avoid contact (kissing, sex) during active herpes recurrence

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28
Q

Treating Alphaherpesvirus

A

Acyclovir can be used to limit virus replication, but will not eliminate latent infectinos

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29
Q

Host range of Betaherpesvirus

A

restricted

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30
Q

reproduction time of Betaherpesvirus

A

Long

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31
Q

profession in cell culture of Betaherpesvirus

A

Slow Progresion in cell culture

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32
Q

what does Betaherpesvirus do to infected cells

A

Cytomeglia (enlargement of infected cells)

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33
Q

what kind of culture does Betaherpesvirus lead to

A

Carrier cultures- cell line that keeps producing the virus without injury to cell

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34
Q

Where does Betaherpesvirus create a latent infection

A

In a variety of tissures

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35
Q

Cytomegalovirus is a member of what

A

Betaherpesvirus

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36
Q

Host range of Gammaherpesvirus

A

Restricted host range

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37
Q

What does Gammaherpesvirus target

A

T and B lymphocytes

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38
Q

what type of infection does Gammaherpesvirus create

A

Lytic infections

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39
Q

where does Gammaherpesvirus create latency

A

In lymphoid tissues

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40
Q

Epstein-Barr Virus (EBV)(mononucleosis) is part of what virus family

A

Gammaherpesvirus

41
Q

what does Beta/Gammaherpesvirus cause

A

EBV associated Carcinomas:
Burkett’s Lymphoma
Hodgkin’s Lymphoma

42
Q

the most common childhood cancer inequatorial africa

A

Burkett’s Lymphoma

43
Q

what does Burkett’s Lymphoma lead to

A

Tumor in jaw, eye socket, ovaries

44
Q

what is found in all causes of Burkett’s Lymphoma

A

All cases, tumor cells have monoclonal EBV episome

45
Q

Roll of EBV in Burkett’s Lymphoma

A

Spur B cell growth, mutation, or genes transform cells (not well understood)

46
Q

Type of Hodgkin’s Lymphoma

A

NL - Nodular Sclerosing
MC - Mixed Cellularity
LD - Lymphocy

47
Q

how often is EBV found in NL, MC, LD tumors

A

MC: 60-90%
LD: 60-90%
NL: 20-40%

48
Q

Role of EBV in Hodgkin’s Lymphoma

A

Unknown

49
Q

How does Beta/Gammaherpesvirus evade the immune system

A

Intrinsic
Innate
Adaptive

50
Q

Intrisic Immune Evasion

A

Block cell Death

Inhibit Apoptosis

51
Q

Innate Immune Evasion

A

Decrease NK cell activity

Inhibit NK receptor Activation

52
Q

Adaptive Immune Evasion

A

Decreased Antigen Presentation
Degrade MHC Class I and II
Block MHC class II and T-cell receptor interactions

53
Q

what Viruses Evade Immune system via Intrisic methods

A

HSV
CMV
EBV

54
Q

what Viruses Evade Immune system via Innate methods

A

HSV

CMV

55
Q

what Viruses Evade Immune system via adaptive methods

A

HSV
CMV
EBV

56
Q

Where does CMV persist in Vitro

A

In hematopoietic progenitor cells and macrophages

57
Q

How does CMV presist

A

as a chronic infection, not latency

58
Q

How is CMV Persistence controlled

A

By a healthy active immune system

59
Q

Where does EBV persist

A

genome persists in memory B cells

60
Q

What does EBV do to aid in its persistence

A

Virus PRoteins ensure B cell proliferation and EBV genome replication

61
Q

Commonality of Beat/gammaherpesvirus

A

Common

62
Q

Treating Beta?gammherpesvirus

A

Infections are usually self-limiting in immune competent individuals
antiviral therapy
Immunoprophylaxis
No vaccine

63
Q

When is Antiviral therapy recommended

A

For disseminated CMV and EBV in immune compromised individuals

64
Q

Types of antiviral therapy for Beta/Gammaherpesvirus

A

Ganciclovir, Foscarnet, Acyclovir

65
Q

how do Antivirals work to help with Beta/Gammaherpesvirus

A

Inhibit viral genome replication

66
Q

can resistance be developed against Antivirals by Beta/Gammaherpesvirus

A

Yes

67
Q

effectiveness of beta/gammaherpesvirus antivirals

A

Less effective treating EBV induced lymphoproliferation

Genome replication not essential for viral gene expression

68
Q

what kind of treatments can be done with Antiviral therapy for Beta/Gammaherpesvirus

A

Prophylactic or preemptive treatment

69
Q

who would get prophylactic or preeemptive treatment with Antiviral therapy for Beta/Gammaherpesvirus

A

TRansplant patients

70
Q

what is done in Immunoprophylaxis for Beta/gammaherpesvirus

A

The passive transfer of anibody for prevention of CMV infection
Transfer of EBV-specific T Lymphocytes

71
Q

Virus family for Human Papillomavirus

A

Papillomaviridae

72
Q

Genome for Human Papillomavirus

A

circular dsDNA

73
Q

Virion of Human Papillomavirus

A

Non-enveloped

74
Q

Proteins of Human Papillomavirus

A

L1 - cell attachment

L2 - membrane penetration

75
Q

How does Human Papillomavirus gain access to body

A

Through abrasion of the skin

76
Q

where does Human Papillomavirus first establish infection

A

In basal layer

77
Q

what is required for genome replication of Human Papillomavirus

A

Cell Polymerase

78
Q

where is Human Papillomavirus virus production done

A

in differentiating cells

79
Q

How is Human Papillomavirus released

A

Non, lytic

VIrus released with cell shedding

80
Q

Each type of Human Papillomavirus leads to a

A

different type of disease

81
Q

How does Human Papillomavirus spread

A

Direct skin to skin contact

Fomites

82
Q

strength of skin as a barrier

A

very strong (mucous membreanes more susceptible)

83
Q

What allows Human Papillomavirus to transmit via fomites

A

It is hardy to environmental stresses

84
Q

where are symptoms of Human Papillomavirus

A

Site of infection

85
Q

time it takes for Human Papillomavirus symptoms to manifest

A

months

86
Q

symptoms of Human Papillomavirus

A

Warts - raised or flat

87
Q

how does Human Papillomavirus warts go away

A

50% regress on their own in 2 years

88
Q

what serious disease can Human Papillomavirus cause

A

Respiratory papilllomatosis

89
Q

What is Respiratory papillomatosis

A

rare complication of Human Papillomavirus due to respired virus that can be lethal

90
Q

what is Oncogenesis

A

Cervical cancer caused by Human Papillomavirus

91
Q

does Human Papillomavirus need to replicate and produce progeny

A

actively replicating cells

92
Q

what does E7 from Human Papillomavirus do

A

blocks retinoblastoma (Rb) protein leading to continued cell proliferation

93
Q

what does E6 from Human Papillomavirus do

A

blocks the p53 tumor suppressor pathway

94
Q

how does Human Papillomavirus cause cancer

A

Unknown: viral transformation, cell proliferation leading to cancerous mutation

95
Q

what type of cancer is Human Papillomavirus responsible for

A

Cervical Cancer

96
Q

what types of HPV are most likely to cause cancer

A

HPV16 and HPV18

97
Q

treatment of Human Papillomavirus

A

ablative: liquid nitrogen, surgical excision, laser, caustic chem (may have to be repeated)

98
Q

condoms prevent Human Papillomavirus

A

lol, no, hit it raw

99
Q

Vaccination for Human Papillomavirus

A

Yes, protects against HPV-6, 11, 16, and 18

micro exam 3 (15 decks)

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