Human Herpesviruses- Exam IV Flashcards
Describe the genome and structure of human herpesviruses:
double-stranded DNA genome; enveloped
How big is the genome of human herpesviruses?
125,000-236,000 base pairs
Herpesviridae family members share four significant biological properties including:
- encode a large array of enzymes
- synthesis of viral DNAs and capsid assembly occur in the nucleus, while final processing of virions occur in the cytoplasm
- production of virus results in destruction of the infected cell
- able to exist in a latent state in their natural hosts while retaining the capacity to replicate and reactivate
Herpesviridae family members encode a large array of enzymes involved in:
- nucleic acid metabolism (thymidine kinase)
- DNA synthesis (DNA polymerase)
- protein processing (protein kinases)
The nucleic acid metabolism enzymes produced by herpesviridae family members include:
thymidine kinase
Human herpes viruses can broadly be categorized as:
- alpha herpesviruses
- beta herpesviruses
- gamma herpesviruses
Alpha herpesviruses include:
- HSV-1 (HHV-1)
- HSV-2 (HHV-2)
- VZV (HHV-3)
herpes virus responsible for fever blisters:
HSV-1 (alpha)
herpes virus responsible sexually transmitted genital lesions:
HSV-2 (alpha)
herpes virus responsible chicken pox and shingles:
VZV (alpha)
herpes virus responsible for roseola:
HHV-6 and HHV-7 (beta)
List the beta human herpesviruses:
- cytomegalovirus (CMV)
- HHV-6
- HHV-7
List the gamma herpesviruses:
- epstein-barr virus (EBV) (HHV-4)
- kaposi’s sarcoma (HHV-8)
herpes virus responsible for infectious mononucleosis:
Epstein-Barr Virus (EBV)
Transmission of HSV-1 and HSV-2 occur through:
direct contact
Transmission of VZV occurs through:
inhalation & direct contact
Transmission of CMV and EBV occur through:
saliva & blood
The portal of entry for HSV-1 and HSV-2 is:
mucous membranes & skin
The portal of entry for VZV is:
respiratory tract and mucous membranes
The portal of entry for CMV & EBV is:
blood stream and mucous membranes
Herpes viruses are fragile, susceptible to heat & detergent & drying due to:
envelope
To become infected with a herpes virus, it generally requires:
direct inoculation
____ is more susceptible to herpes virus infection than ___.
mucous membranes; skin
CMV and EBV can be transmitted through:
infected leukocytes
VZV is mostly transmitted through:
aerosols
Similarly to the adenovirus, gene expression of herpes viruses occurs through:
a cascade
What happens upon release of herpes viruses:
attach to and infect adjacent cells
What involves in a local spread of herpes virus?
budding directly onto and into adjacent cells
Budding onto and into adjacent cells results in the local spread of herpes virus as well as:
syncytia formation (characteristic of herpesvirus)
Herpes viruses replicate and assemble in the:
cell nucleus
Because the herpes virus replicates and assembles in the nucleus, this causes some very severe changes in nuclear structures including:
- chromatin shifted to margins of nucleus
- Cowdry type A acidophilic intranuclear inclusion bodies
Under a microscope, stained cells infected with herpes virus show formation of:
syncytia
Multi-nucleated cells seen when viewing stained herpes virus:
Tzanck cells
Scraping from the base of a herpes lesion=
Tzanck smear
In addition to the Tzanck cells seen under a microscope, what else can be seen?
intranuclear inclusion bodies (darkly staining nuclear region)
Anti-herpesvirus antibodies play ___ in recovery from primary disease and on recurrent disease
BUT anti-herpesvirus antibodies can help prevent ____.
minor role; primary disease
What plays the major role in recovery in response to alpha-herpesvirus infections?
cell-mediated immune mechanisms
In the immune response to an alpha-herpes infection, MHC class I and II proteins displaying viral antigens on surface of infected cell activate:
T-lymphocytes
The T-lymphocytes activated by MHC class I and II proteins displaying viral antigens on surface of infected cell ultimately function to:
- directly all the infection cell
- secrete cytokines and chemokine to attract macrophages
The cell-mediated response to alpha-herpes viruses varies:
with age
Who is at most risk for problems associated with HSV infections? Who is most at risk for problems associated with VZV infections
neonates; elderly
HSV-1, HSV-2, and VZV evade the host immune response through:
envelope glycoproteins bind Fc domain of antibodies and complement components
HSV-1, HSV-2, and VZV evade the host immune response through envelope glycoproteins bind Fc domain of antibodies and complement components:
blocking their ability to promote an antiviral response
In order to evade the immune response, HSV proteins reduce ___ production and its downstream signaling pathway.
Type I interferon production
In order to evade the immune response, HSV proteins can prevent ____ from being expressed on the surface of infected cells
MHC Class I and II proteins
Results in no expression of viral proteins and therefore no peptides for MHC proteins to display:
Latency
facial or genital herpes, stomatitis, or keratitis, localized can all be described as:
acute disease of herpes simplex
How does the herpes virus gain entry into the host?
exposure of skin, mucosa, or cornea to secretions containing virus
What happens once herpes virus gains entry into host?
replication of virus in epithelial cells
The replication of herpes virus in epithelial cells causes:
vescular mucocutaneous lesions, stomatitis, or keratitis
What occurs after the replication of herpes virus in epithelial cells causing lesions?
spread to peripheral sensory or autonomic nerve endings and ganglia
- Herpes virus that is acquired very early in life
- 2/3 of adults are Ab positive
HSV-1
- Herpes virus mostly transmitted by genital contact
- Uncommon before adolescence
- 1/5 of adults are Ab positive
HSV-2
Most HSV-1 and HSV-2 infections :
asymptomatic
around ___ HSV infections have recognizable symptoms
1/3
Following the acute disease of herpes virus, what is the next phase?
recovery
Describe the recovery phase of herpes virus:
Healing of lesions and establishment of latent infections in neurons
Following the recovery phase of herpes virus, what is the next phase?
Latency
Describe the latency phase of herpes virus:
Maintenance of latent infections of neurons
Usual course of herpes simplex virus infection and disease includes:
- acute disease
- recovery
- latency
- recurrent disease
Reactivation of latent herpes simplex virus and distal spread:
recurrent disease
Recurrent phase of herpes disease can be characterized by:
cold sores, fever blisters, keratitis, or genital lesions localized
Recurrent herpes lesions are caused by:
virus replication in epithelial cells
Reactivation of various herpes viruses can be induced by:
- local trauma
- mental tension (stress)
- fatigue
- menstruation
- exposure to bright light
- aging effects
Infections associated with HSV include:
- ocular herpes
- oral herpes
- genital herpes
Describe the predominant virus type, frequency, age group, usual outcome and recurrence for ocular herpes:
HSV-1
Common
All
Resolution, visual impairment
Yes
Describe the predominant virus type, frequency, age group, usual outcome and recurrence oral herpes:
HSV-1 (sometimes HSV-2)
Very common
All
Resolution
Yes
Describe the predominant virus type, frequency, age group, usual outcome and recurrence genital herpes:
HSV-2 (sometimes HSV-1)
Common
Adolescents & Adults
Resoluation
Yes
Condition caused by herpes simplex virus that can lead to scarring/ blindness:
Herpes Keratitis - Eye
Most common viral infection of the mouth:
Herpetic stomatitis
Herpetic stomatitis is caused by:
primary infection by HSV-1 or HSV-2
Herpetic stomatitis is characterized by:
vesicles on oral mucosa, tongue, or gingivae
Herpetic stomatitis can often be confused with:
acute necrotizing ulcerative gingivitis (ANUG) when gingival is inflamed
Herpes labials (cold sore) is a result of:
reactivation of latent HSV-1 or HSV-2
Herpetic dermatitis and herpetic whitlow is a result of HSV-1 and HSV-2 infections that appears on the:
skin and fingers
Varicella-zoster virus (VZV) (HHV-3) is the cause of:
chicken pox and shingles
Transmission of VZV can be:
Aerosol (inhalation) and direct contact
____ % of adults have VZV antibody (from time before vaccination)
90%
Local VZV replication occurs in the:
respiratory tract
For VZV infections, local replication replication occurs in the respiratory tract and the virus then progresses to:
phagocytic cells via the bloodstream and lymphatic system
Following VZV progressing to phagocytic cells via the bloodstream and lymphatic system, ___ occurs and spreads the virus throughout the body
secondary viremia
Secondary viremia following VZV infection, spreads the virus throughout the body including the:
skin
When does secondary viremia following VZV infection occur?
11-13 days post infection
Where do the skin lesions appear from secondary viremia during VZV infection?
entire body
Compare the spread of VZV to the spread of HSV:
systemic spread for VZV (unlike herpes simplex virus)
Similarly to HSV, once the VZV is replicating in cells, it will spread:
cell-to-cell
VZV will spread cell-to-cell except for:
epithelial cells of lung keratinocytes and skin lesions, which can release virus
VZVs replication is similar to HSVs but:
slower
The smaller genome of HHVs:
VZV (~125,000 base pairs)
Where does the latent infection of VZV establish itself?
neurons, dorsal root ganglia, cranial nerve ganglia
VZV is often reactivated in older adults, why?
impaired cell-mediated immunity
When VZV is reactivated in older adults, the virus is released along:
entire neural pathway to infect the skin
Because VZV reactivation in older adults releases the virus along the entire neural pathway, this clinically presents as:
vesicular rash along the entire dermatome
VZV reactivation creates a vesicular rash along the entire dermatome =
herpes zoster or shingles
Post-herpetic neuralgia occurs in 30% of older patients and causes:
pain for months to years after zoster
Why is the entire dermatome affected by VZV reactivation?
because the dermatome is an area of skin innervated by fibers from a single dorsal root spinal nerve
What promotes recovery from primary VZV disease?
Host defenses
Anti-VZV antibodies play a ____ role in recovery from primary disease and on recurrent disease.
However, anti-VZV antibodies can help:
minor role; prevent primary disease
Is there a VZV vaccine? Is it effective?
yes
Anti-VZV antibodies limit:
viremic spread of virus
What plays the major role in recovery as for VZVs & HSVs?
Cell-mediated immune mechanisms
Childhood infection of VZV =
chicken pox
Primary infection of VZV in adults is ____ and can cause ____ in 30% of adults and can be fatal
more severe; interstitial pneumonia
Epstein-Barr VIrus (EBV; HHV-4) infects:
B lymphocytes and epithelial cells
Cytomegalovirus (CMV; HHV-5) infects:
a wide variety of cells
EBV and CMV replication within host cells is very similar to the replication of:
HSV
Establishment of CMV results in:
persistent/chronic infection (not a true latent infection)
Establishment of EBV results in:
latent infection
The establishment of a latent infection by EBC occurs in:
memory B cells
The EBV viral proteins produced during latency promote:
B-cell proliferation
CBV and EBV infections are very:
common
What percent of adults in the developing world are infected with CMV or EBV? What percent of adults in the United States are infected with CMV or EBV?
95%; 50-60%
When EBV and CMV are acquired early:
usually asymptomatic
EBV and CMV are acquired similarly. what is the difference?
Breast milk is NOT an important route of virus spread in EBV
When EBV is acquired after childhood, it results in:
infectious mononucleosis (infectious)
Most common viral infection of the fetus in humans:
congenital CMV
Congenital CMV leads to ___ and ___ including ___ and ___
severe disease; permanent neurological damage; hearing loss; learning disabilities
Persistant CMV and EBV infections are associated with:
chronic inflammatory diseases and cancer
Persistent EBV is specifically associated with:
- Hodgkin disease
- African Burkitt lymphoma
- Nasopharyngeal carcinoma
CMV have very characteristic cell changes including:
large inclusions in tissue specimens (Owl eye inclusions)
What test is used to determine EBV infection?
Heterophile antibody or monospot test (PCR test)
EBV infection induces production of large numbers of antibodies that recognize ___ of others species called ____.
RBC antigens; heterophiles antibodies
Agglutination of horse RBCs by heterophiles antibody in patients serum:
Monospot test
The syndromes associated with cytomegalovirus include:
congenital infection & mononucleosis
The syndrome associated with Epstein-barr virus include:
mononucleosis
The syndrome associated with herpesvirus type 6 include:
roseola
The syndrome associated herpesvirus type 7 include:
roseola
The syndrome associated with Kaposi’s sarcoma associated virus (HHV8) include:
Kaposi’s sarcoma
The oral manifestation of ____ includes lesions that may be found n both before skin rash develops:
VZV
VZV reactivation is associated with:
shingles
What is affected in 15% of shingles cases?
trigeminal nerve
What types of lesions are often involved in shingles (list them in order of occurrence)
ophthalmic –> maxillary –> mandibular
With ____, oral pain often precedes rash and mimics toothache pain
shingles
The most common intramural sites affected by shingles include:
- anterior half of tongue
- soft palate
- cheek
The cause of infectious mononucleosis:
EBV
- 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
infectious mononucleosis
Describe Kaposi’s Sarcoma associated virus oral manifestation:
Kaposi’s sarcoma lesions (endothelial tumor)
What viruses are present in majority of advanced periodontal lesions:
EBV & CMV
Possible roles for herpesviruses in periodontal disease:
- Viruses may cause DIRECT ___
- Gingival viruses may promote ___
- CMV and EBV can infect ___, ___, & ___, in lesions and impair cell function
- Viruses induce a pro inflammatory response that can result in ____
- Viruses can suppress host defenses ___ & ____
- cytopathic effects
- bacterial attachment/colonization
- monocytes, macrophages, & lymphocytes
- tissue destruction
- locally & systemically