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herpes Flashcards

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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
latentcy of Usual Course of Herpes Simplex Virus Infection and Disease
maintentce of latent infections in Nn
26
recurrent disease of Usual Course of Herpes Simplex symptoms? caused by?
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
reactivation of various herpesviruses can be induced by:
``` Local trauma (surgery or nerve pressure) Mental tension Fatigue Menstruation Exposure to bright light Aging effects ```
28
Infections associated with Herpes Simplex Viruses
ocular, oral and genital herpes
29
Herpes keratitis
eye (can lead to scarring/blindness)
30
Herpetic stomatitis | could be confused with?
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
Herpes labialis (cold sore)
- reactivation of latent HSV-1 or HSV-2
32
Herpetic dermatitis and herpetic whitlow
HSV-1 or HSV-2
33
VZV can cause
chicken pox or shingles
34
VZV transmission
Aerosol transmission (90% of adults have VZV antibody (from time before vaccination)
35
VZV replication location
Local viral replication in the respiratory tract
36
VZV spread in body
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
VZV replication speed/ latentcy
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
VZV reactivation in older adults? path it takes? postherpetic neuralgia?
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
VZV recovery from primary disease what roles does Ab play? whys is this important? what plays the major role in recovery?
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
VZV primary infections of children vs adults
Childhood illness = Chickenpox Primary infection of adults more severe can cause interstitial pneumonia in 30% of adults and may be fatal
41
Epstein-Barr virus (EBV; HHV-4) infects?
infects B lymphocytes and epithelial cells
42
Cytomegalovirus (CMV; HHV-5) infects what cell types?
infects a wide variety of cells
43
EBV and CMV replication
EBV and CMV replication within host cells is very similar to general description of herpesvirus replication given previously
44
CMV latentcy
Establishment of CMV persistent/chronic infection, not truly latent/ low level of virus
45
Establishment of EBV latent infection
latent infection in memory B cells | virus proteins produced during latency promote B cell proliferation
46
Host defenses against CMV and EBV | how can risk of severe disease be increased?
both innate and adaptive immune responses are important | patients with primary immunodeficiencies have increased risk of severe disease
47
CMV and EBV infection commonality | asymptomatic?
95% of adults in developing world 50-60% of adults in United States usually asymptomatic when acquired early
48
EBV acquired how? symptomatic?
EBV acquired via saliva/sex Symptomatic infections when acquired after childhood: infectious mononucleosis
49
Congenital CMV
most common viral infection of the fetus in humans | leads to severe disease and permanent neurological damage, including hearing loss and learning disabilities
50
Persistent CMV and EBV infections associated with?
chronic inflammatory diseases and cancer | EBV: Hodgkin disease, African Burkitt lymphoma, and nasopharyngeal carcinoma
51
CMV diagnosis
large inclusions in tissue specimens (“owl eye” inclusions)
52
EBV diagnosis
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
CMV associated diseases
congenital | mononucleosis
54
EBV associated disease
mononucleosis
55
HHV 6 associated disease
roseola
56
HHV 7 associated disease
roseola
57
chicken pox oral manifestations
lesions may be found in mouth before skin rash develops
58
shingles oral manifestations
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
Epstein-Barr virus (EBV) oral manifestations
- 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
HHV-8 oral manifestations
Kaposi’s sarcoma lesions (endothelial tumor)
61
Herpesvirsuses and periodontal disease
Epstein-Barr virus (EBV) and cytomegalovirus (CMV) | present in majority of advanced periodontal lesions
62
Possible roles for herpesviruses in periodontal disease
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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