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4.41 Flashcards

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1
Q

Human Herpesviruses

characteristics (3)

A

Double-stranded DNA genome
enveloped
Genome = 125,000 - 236,000 base pairs

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2
Q

Herpesviridae family members share four significant biological properties: (4)

A
  1. Encode a large array of enzymes involved in
  2. Synthesis of viral DNAs and capsid assembly occur in the nucleus, while
    final processing of virions occurs in the cytoplasm
  3. Production of virus results in destruction of the infected cell
  4. Able to exist in a latent state in their natural hosts while retaining the
    capacity to replicate and cause disease upon reactivation
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3
Q
  1. Encode a large array of enzymes involved in (3)
A

a. nucleic acid metabolism (thymidine kinase,)
b. DNA synthesis (DNA polymerase)
c. protein processing (protein kinases)

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4
Q

Alpha

herpesviruses (3)

A

HSV1
HSV2
VZV

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5
Q

Beta

herpesviruses (3)

A

cytomegalovirus
HHV6
HHV7

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6
Q

Gamma

herpesviruses (2)

A

EBV

HHV8

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7
Q

HSV1

A

fever blisters

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8
Q

HSV2

A

sexually transmitted genital lesions

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9
Q

VZV (HHV3)

A

chicken pox and shingles

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10
Q

HHV5, 6, 7

A

roseola

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11
Q

EBV (HHV4)

A

infectious mononucleosis

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12
Q

virus: HSV1
means of transmission
portal of entry

A

direct contact

mucous membranes, skin

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13
Q

virus: HSV2
means of transmission
portal of entry

A

direct contact

mucous membranes, skin

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14
Q

virus: VZV
means of transmission
portal of entry

A

inhalation, direct contact

respiratory tract, mucous membranes

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15
Q

virus: CMV
means of transmission
portal of entry

A

saliva, blood

bloodstream, mucous membranes

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16
Q

virus: EBV
means of transmission
portal of entry

A

saliva, blood

mucous membranes, bloodstream

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17
Q 
Herpes viruses are fragile (enveloped)
susceptible to (3)
A

heat, detergent, drying

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18
Q

Generally require direct —

— more susceptible than skin

A

inoculation

mucous membranes

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19
Q

CMV and EBV can be transmitted through

A

infected leukocytes

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20
Q

VZV is mostly transmitted by —

A

aerosols

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21
Q

Herpesvirus
Lytic cycle
Cascade of gene expression (3)

A 
Attach to and infect adjacent cells upon
release
Budding directly onto and into adjacent cells
Therefore get a local spread of virus
(predominantly)
Syncytia can form
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22
Q

Virus replicates and assembles in the cell nucleus

Get changes in nuclear structure -

A

chromatin shifted to margins of nucleus

Cowdry type A acidophilic intranuclear inclusion bodies

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23
Q

Stained cells infected with a herpes virus show — formation (multinucleated

cells) (= Tzanck cells from Tzanck smear (scraping from the base of the lesion) and
- – (darkly staining nuclear region)

A

syncytia

intranuclear inclusion bodies

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24
Q

Host defenses promote recovery from primary disease
— antibodies play minor role in recovery from primary disease and on recurrent disease
But anti-herpesvirus antibodies can help prevent

A

Anti-herpesvirus

primary disease: VZV vaccine is effective

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25
Q

Host response to alpha-herpesvirus infections (HSV-1, HSV-2, and VZV)
Cell-mediated immune mechanisms play the major role in recovery
MHC class I and II proteins displaying viral antigens on surface of infected cell
activate T lymphocytes (2)

A

directly kill the infected cell or

secrete cytokines and chemokines to attract macrophages, etc

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26
Q

Cell-mediated immune response varies with — (2)

A

age

neonates: problems with HSVs;
elderly: problems with VZV

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27
Q

Immune evasion by herpesviruses

A

HSV-1, HSV-2, and VZV envelope glycoproteins bind Fc domain of antibodies and
complement components, blocking their ability to promote an antiviral response

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28
Q

HSV proteins reduce

A

type I interferon production and its downstream signaling

pathway

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29
Q

HSV proteins can prevent

A 
MHC class I and II proteins from being expressed on the
surface of infected cells
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30
Q

Latency results in

A

no expression of viral proteins and therefore no peptides for
MHC proteins to display

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31
Q
  1. Acute disease (4)
A

facial or genital herpes, stomatitis, or keratitis

localizied

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32
Q 
1. Acute disease 
Exposure of (4)
A

skin, mucosa, or cornea to secretions

containing virus

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33
Q
  1. Acute disease
    Replication of virus in epithelial cells, causing
    (3)
A

vescular mucocutaneous lesions, stomatitis, or

keratitis

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34
Q 
1. Acute disease 
Spread to (2)
A

peripheral sensory or autonomic nerve

endings and ganglia

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35
Q
  1. Acute disease
    HSV-1 acquired —
    — of adults are Ab+
A

very early in life (e.g. kissing)

2/3

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36
Q
  1. Acute disease
    HSV-2 mostly transmitted by —
    — of adults are Ab+
A

genital contact
uncommon before adolescence

1/5

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37
Q
  1. Acute disease
    Most HSV-1 and HSV-2 infections are —
    ~— of infections have recognizable symptoms
A

asymptomatic

1/3

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38
Q

Usual Course of Herpes Simplex Virus Infection and Disease (continued)
2. Recovery

A

Healing of lesions and establishment of latent

infections in neurons

39
Q

Usual Course of Herpes Simplex Virus Infection and Disease (continued)
3.

A

Latency Maintenance of latent infections in neurons

40
Q

Usual Course of Herpes Simplex Virus Infection and Disease (continued)
4. Recurrent disease (4)

A

cold sores, fever blisters, keratitis, or genital lesions
localizied
Reactivation of latent virus and distal spread
Recurrent lesions caused by virus replication in
epithelial cell

41
Q

reactivation of various herpesviruses

can be induced by: (6)

A 
Local trauma (surgery or nerve pressure)
Mental tension
Fatigue
Menstruation
Exposure to bright light
Aging effects
42
Q 
infection: occular herpes 
predominant virus type:
frequency:
age group:
usual outcome:
recurrence:
A 
1
common
all
resolution, visual impairment 
yes
43
Q 
infection: oral herpes 
predominant virus type:
frequency:
age group:
usual outcome:
recurrence:
A 
1>2
very common
all
resolution
yes
44
Q 
infection: genital herpes 
predominant virus type:
frequency:
age group:
usual outcome:
recurrence:
A 
2>1
common 
adolescents, adults 
resolution
yes
45
Q

Herpes keratitis -

A

eye (can lead to scarring/blindness)

46
Q

most common viral infection of the mouth

A

Herpetic stomatitis

47
Q

Herpetic stomatitis
Primary infection by (2)
vesicles on (3)

A

HSV-1 or HSV-2

oral mucosa, the tongue, and gingivae

48
Q

Herpetic stomatitis -

confused with — when gingivae inflamed

A

acute necrotizing ulcerative gingivitis (ANUG)

49
Q

Herpes labialis (cold sore) -

A

reactivation of latent HSV-1 or HSV-2

50
Q

VZV (HHV-3) (2)

A

chicken pox

shingles

51
Q

VZV

— transmission (—% of adults have VZV antibody (from time before vaccination)

A

Aerosol

90

52
Q

VZV

Local viral replication in —

A

respiratory tract

53
Q

VZV

Virus progresses to phagocytic cells via the (2)

A

bloodstream and lymphatic system

54
Q

VZV

— spreads the virus throughout the body, including the skin

A

Secondary viremia

55
Q 
VZV
Secondary viremia spreads the virus throughout the body, including the skin
occurs --- days post infection
skin lesions appear over the ---
systemic spread is different from ---
A

11-13
entire body
herpes simplex viruses

56
Q

VZV

Virus spreads cell-to-cell like —

A

HSVs

except epithelial cells of lung keratinocytes and skins lesions, which can release virus

57
Q

VZV replication is similar to HSVs but —

2

A

slower [smallest genome of HHVs (~125,000 bp)]
also establishes latent infection of neurons
dorsal root ganglia or cranial nerve ganglia

58
Q

VZV reactivated in older adults with impaired –

A

cell-mediated immunity

59
Q

VZV reactivated in older adults with impaired cell-mediated immunity
virus is released along the entire — pathway to infect the skin

A

neural

60
Q

VZV reactivated in older adults with impaired cell-mediated immunity
causes a vesicular rash along the entire dermatome =

A

herpes zoster or shingles

61
Q

VZV reactivated in older adults with impaired cell-mediated immunity
postherpetic neuralgia in —% of older patients
pain for — after zoster

A

30

months to years

62
Q

Dermatome is area of skin

innervated by

A

fibers from a single

dorsal root spinal nerve

63
Q

Host defenses promote recovery from primary disease

  • – play minor role in recovery from primary disease and on recurrent disease
  • – mechanisms play the major role in recovery as for HSVs
A

Anti-VZV antibodies

Cell-mediated immune

64
Q

Anti-VZV antibodies play minor role in recovery from primary disease and on
recurrent disease
But anti-VZV antibodies can help prevent —
And anti-VZV antibodies limit — spread of virus

A

primary disease
VZV vaccine is effective

viremic

65
Q

Childhood illness = —

A

Chickenpox

66
Q

Primary infection of adults more severe

can cause

A

interstitial pneumonia in 30% of adults and may be fatal

67
Q

Epstein-Barr virus (EBV; HHV-4)

infects (2)

A

B lymphocytes and epithelial cells

68
Q

Cytomegalovirus (CMV; HHV-5)

A

infects a wide variety of cells

69
Q

EBV and CMV replication within host cells is very similar to

A

general description of

herpesvirus replication given previously

70
Q

Establishment of CMV:

A

persistent/chronic infection

71
Q

Establishment of EBV latent infection (2)

A

latent infection in memory B cells

virus proteins produced during latency promote B cell proliferation

72
Q

CMV and EBV infections are very common
—% of adults in developing world
—% of adults in United States
usually — when acquired early

A

95
50-60
asymptomatic

73
Q

EBV acquired similarly, except — not a important route of virus spread

A

breast milk

74
Q

Symptomatic infections when acquired after childhood:

A

infectious mononucleosis

75
Q

most common viral infection of the fetus in humans

A

Congenital CMV

76
Q

Congenital CMV

leads to

A

severe disease and permanent neurological damage,

including hearing loss and learning disabilities

77
Q

Persistent CMV and EBV infections associated with (2)

EBV: (3)

A

chronic inflammatory diseases and cancer

Hodgkin disease, African Burkitt lymphoma, and nasopharyngeal carcinoma

78
Q

Diagnosis

CMV:

A

large inclusions in tissue specimens (“owl eye” inclusions)

79
Q

Diagnosis

EBV: (2)

A

PCR

heterophile antibody or “monospot” test

80
Q

heterophile antibody or “monospot” test (2)

A

EBV infection induces production of large number of antibodies that recognize RBC
antigens of other species (“heterophile antibodies”)
Monospot test

81
Q

Monospot test:

A

agglutination of horse RBCs by heterophile antibody in patient’s serum

82
Q

virus: cytomegalovirus (2)
syndrome:

A

congenital infection

monocucleosis

83
Q

virus: EBV
syndrome:

A

mononucleosis

84
Q

virus: herpesvirus type 6
syndrome:

A

roseola

85
Q

virus: herpesvirus type 7
syndrome:

A

rosela

86
Q

virus: kaposis sarcoma associate virus
syndrome:

A

kaposis sarcoma?

87
Q

Oral manifestation of other herpes virus infections

Chickenpox (VZV) -

A

lesions may be found in mouth before skin rash develops

88
Q

Oral manifestation of other herpes virus infections

Shingles (VZV reactivation) (2)

A

trigeminal nerve affected in 15% of cases

Ophthalmic > maxillary > mandibular divisions involved (lesions)

89
Q

Oral manifestation of other herpes virus infections

Ophthalmic > maxillary > mandibular divisions involved (lesions)

A 
oral pain often precedes rash and mimics toothache pain
most common intraoral sites affected:
anterior half of tongue
soft palate
cheek
90
Q

Shingles (VZV reactivation)

most common intraoral sites affected: (3)

A

anterior half of tongue
soft palate
cheek

91
Q

Oral manifestation of other herpes virus infections

Epstein-Barr virus (EBV) - infectious mononucleosis (3)

A

painful sore throat at onset of infection
rash may be present at junction of hard and soft palates (fine petechial hemorrhages)
White pseudomembrane may develop on tonsils and other parts of oral mucosa

92
Q

Oral manifestation of other herpes virus infections

HHV-8 (Kaposi’s sarcoma-associated virus)

A

Kaposi’s sarcoma lesions (endothelial tumor)

93
Q

Herpesvirsuses and periodontal disease

• (2) present in majority of advanced periodontal lesions

A

Epstein-Barr virus (EBV) and cytomegalovirus (CMV)

94
Q

Possible roles for herpesviruses in periodontal disease: (5)

A
  1. Viruses may cause direct cytopathic effects
  2. Gingival viruses may promote bacterial attachment/colonization
  3. CMV and EBV can infect monocytes, macrophages, and
    lymphocytes in lesions and impair cell function.
  4. Viruses induce a proinflammatory response that can result in
    tissue destruction.
  5. Viruses can suppress host defenses locally and systemically

Microbiology (42 decks)

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