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microbiology > herpes > Flashcards

herpes Flashcards

1
Q

Human Herpesviruses
genome
eveveloped?
geometry

A

dsDNA
enveloped
iscoshedral

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2
Q

herpes genome size

A

125,000 - 236,000 base pairs

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3
Q

Herpesviridae family members share four significant biological properties:

A
  1. Encode a large array of enzymes involved in
    a. nucleic acid metabolism (thymidine kinase)
    b. DNA synthesis (DNA polymerase, helicase, primase)
    c. protein processing (protein kinases)
  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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4
Q

groups of herpes virus

A

Alpha, beta and gamma

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5
Q

alpha herpes viruses

A
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6
Q

beta herpes viruses

A
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7
Q

gamma herpes viruses

A
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8
Q

HSV 1, 2 transmission/ POE

A

direct contact

mucus membranes and skin

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9
Q

VZV transmission and POE

A

inhalation/ direct contact

respiratory tract and mucus membrane

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10
Q

CMV transmission and POE

A

saliva and blood

mucus membrane and bloodstream

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11
Q

EBV transmission and POE

A

saliva and blood

mucus membrane and bloodstream

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12
Q

fragility of herpes virus

A

Herpes viruses are fragile (enveloped)

susceptible to heat, detergent, drying

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13
Q

herpes virus infection usually requires?
why mucus membranes?
CMV/EBV can transmit thru?
VZV mainly transmitted thru?

A

Generally require direct inoculation
mucous membranes more susceptible than skin
CMV and EBV can be transmitted through infected leukocytes
VZV is mostly transmitted by aerosols

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14
Q 
Herpesvirus infection of cells
entry?
nucleus involved? 
gene expression? 
where is capsid assembly?
envelope?
lytic? 
adjacent cells affected?
A

similar to adenovirus- entry and uncoating with factors and nucleporteins entering the nucleus

cascade of gene expression occurs with transcription regulators present

capsid assembly occurs in nucleus

budding at ER to acquire envelope

releases at cell mem- lytic cycle

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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15
Q

herpesvirus and nuclei
alter of nuclei?
syncitia?
Tzanck cells?

A

Virus replicates and assembles in the cell nucleus
Get changes in nuclear structure - chromatin shifted to margins of nucleus
Cowdry type A acidophilic intranuclear inclusion bodies

Stained cells infected with a herpes virus show syncytia formation (multinucleated
cells)(= Tzanck cells from Tzanck smear (scraping from the base of the lesion) and
intranuclear inclusion bodies (darkly staining nuclear region).

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16
Q

anti herpes Ab role

A

Anti-herpesvirus antibodies play minor role in recovery from primary disease and
on recurrent disease
But anti-herpesvirus antibodies can help prevent primary disease=VZV vaccine is effective

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17
Q

Host response to alpha-herpesvirus infections (HSV-1, HSV-2, and VZV)
ages and issues with certain viruses?

A

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- directly kill the infected cell or secrete cytokines and chemokines to attract macrophages, etc.

Cell-mediated immune response varies with age: neonates: problems with HSVs; elderly: problems with VZV

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18
Q 
herpes immune evasion
effect on Ab's?
interferons? 
MHC? 
latentcy effect for this?
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.

HSV proteins reduce type I interferon production and its downstream signaling
pathway

HSV proteins can prevent MHC class I and II proteins from being expressed on the
surface of infected cells

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

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19
Q

Usual Course of Herpes Simplex Virus Infection and Disease stages

A

acute disease
recovery
latency
recurrent disease

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20
Q 
acute disease of Usual Course of Herpes Simplex 
due to exposure to? 
outcomes? 
viral replication where? 
spreads to?
A

facial or genital herpes, stomatitis, mucocutaneous lesions, or keratitis= localized

Exposure of skin, mucosa, or cornea to secretions containing virus

Replication of virus in epithelial cells, causing vescular mucocutaneous lesions, stomatitis, or keratitis

Spread to peripheral sensory or autonomic nerve endings and ganglia

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21
Q

HSV 1 often acquired when?

A

HSV-1 acquired very early in life (e.g. kissing)

2/3 of adults are Ab+

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22
Q

HSV 2 acquired how/when usually?

A

HSV-2 mostly transmitted by genital contact
uncommon before adolescence
1/5 of adults are Ab+

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23
Q

HSV 1 and 2 infections always symptomatic?

A

Most HSV-1 and HSV-2 infections are
asymptomatic
~1/3 of infections have recognizable symptoms

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24
Q

recovery of Usual Course of Herpes Simplex Virus Infection and Disease

A

Healing of lesions and establishment of latent

infections in neurons

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25
Q

latentcy of Usual Course of Herpes Simplex Virus Infection and Disease

A

maintentce of latent infections in Nn

26
Q

recurrent disease of Usual Course of Herpes Simplex
symptoms?
caused by?

A

cold sores, fever blisters, keratitis, or genital lesions= localized

Reactivation of latent virus and distal spread

Recurrent lesions caused by virus replication in epithelial cells

27
Q

reactivation of various herpesviruses can be induced by:

A 
Local trauma (surgery or nerve pressure)
Mental tension
Fatigue
Menstruation
Exposure to bright light
Aging effects
28
Q

Infections associated with Herpes Simplex Viruses

A

ocular, oral and genital herpes

29
Q

Herpes keratitis

A

eye (can lead to scarring/blindness)

30
Q

Herpetic stomatitis

could be confused with?

A

most common viral infection of the mouth- Primary infection by HSV-1 or HSV-2
vesicles on oral mucosa, the tongue, and gingivae
confused with acute necrotizing ulcerative gingivitis (ANUG) when gingivae inflamed

31
Q

Herpes labialis (cold sore)

A
  • reactivation of latent HSV-1 or HSV-2
32
Q

Herpetic dermatitis and herpetic whitlow

A

HSV-1 or HSV-2

33
Q

VZV can cause

A

chicken pox or shingles

34
Q

VZV transmission

A

Aerosol transmission (90% of adults have VZV antibody (from time before vaccination)

35
Q

VZV replication location

A

Local viral replication in the respiratory tract

36
Q

VZV spread in body

A

Virus progresses to phagocytic cells via the bloodstream and lymphatic system
Secondary viremia spreads the virus throughout the body, including the skin- occurs 11-13 days post infection
skin lesions appear over the entire body
systemic spread is different from herpes simplex viruses

Virus spreads cell-to-cell like HSVs
except epithelial cells of lung keratinocytes and skins lesions, which can release virus

37
Q

VZV replication speed/ latentcy

A

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

38
Q

VZV reactivation in older adults?
path it takes?
postherpetic neuralgia?

A

VZV reactivated in older adults with impaired cell-mediated immunity

virus is released along the entire neural pathway to infect the skin causes a vesicular rash along the entire dermatome = herpes zoster or shingles

postherpetic neuralgia in 30% of older patients
pain for months to years after zoster

39
Q

VZV recovery from primary disease
what roles does Ab play? whys is this important?
what plays the major role in recovery?

A

Host defenses promote recovery from primary disease

Anti-VZV antibodies play minor role in recovery from primary disease and on recurrent disease

But anti-VZV antibodies can help prevent primary disease= VZV vaccine is effective

And anti-VZV antibodies limit viremic spread of virus

Cell-mediated immune mechanisms play the major role in recovery as for HSVs

40
Q

VZV primary infections of children vs adults

A

Childhood illness = Chickenpox
Primary infection of adults more severe
can cause interstitial pneumonia in 30% of adults and may be fatal

41
Q

Epstein-Barr virus (EBV; HHV-4) infects?

A

infects B lymphocytes and epithelial cells

42
Q

Cytomegalovirus (CMV; HHV-5) infects what cell types?

A

infects a wide variety of cells

43
Q

EBV and CMV replication

A

EBV and CMV replication within host cells is very similar to general description of
herpesvirus replication given previously

44
Q

CMV latentcy

A

Establishment of CMV persistent/chronic infection, not truly latent/ low level of virus

45
Q

Establishment of EBV latent infection

A

latent infection in memory B cells

virus proteins produced during latency promote B cell proliferation

46
Q

Host defenses against CMV and EBV

how can risk of severe disease be increased?

A

both innate and adaptive immune responses are important

patients with primary immunodeficiencies have increased risk of severe disease

47
Q

CMV and EBV infection commonality

asymptomatic?

A

95% of adults in developing world
50-60% of adults in United States
usually asymptomatic when acquired early

48
Q

EBV acquired how? symptomatic?

A

EBV acquired via saliva/sex
Symptomatic infections when acquired after childhood:
infectious mononucleosis

49
Q

Congenital CMV

A

most common viral infection of the fetus in humans

leads to severe disease and permanent neurological damage, including hearing loss and learning disabilities

50
Q

Persistent CMV and EBV infections associated with?

A

chronic inflammatory diseases and cancer

EBV: Hodgkin disease, African Burkitt lymphoma, and nasopharyngeal carcinoma

51
Q

CMV diagnosis

A

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

52
Q

EBV diagnosis

A

PCR
heterophile antibody or “monospot” test
EBV infection induces production of large number of antibodies that recognize RBC
antigens of other species (“heterophile antibodies”)
Monospot test: agglutination of horse RBCs by heterophile antibody in patient’s serum

53
Q

CMV associated diseases

A

congenital

mononucleosis

54
Q

EBV associated disease

A

mononucleosis

55
Q

HHV 6 associated disease

56
Q

HHV 7 associated disease

57
Q

chicken pox oral manifestations

A

lesions may be found in mouth before skin rash develops

58
Q

shingles oral manifestations

A

trigeminal nerve affected in 15% of cases
Ophthalmic > maxillary > mandibular divisions involved (lesions)
oral pain often precedes rash and mimics toothache pain

most common intraoral sites affected:
anterior half of tongue
soft palate
cheek

59
Q

Epstein-Barr virus (EBV) oral manifestations

A
  • infectious mononucleosis

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

60
Q

HHV-8 oral manifestations

A

Kaposi’s sarcoma lesions (endothelial tumor)

61
Q

Herpesvirsuses and periodontal disease

A

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

present in majority of advanced periodontal lesions

62
Q

Possible roles for herpesviruses in periodontal disease

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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