Herpes Viruses (EXAM IV) Flashcards by Annabella Moody

Describe the genome & structure of human herpes viruses:

Double-stranded DNA genome
enveloped

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How big is the genome of human herpes viruses?

125,000-236,000 basepairs

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Herpesviridae family members share four significant biological properties including:

Encode a large array of enzymes
Synthesis of viral DNAs & capsid assembly occur in nucleus, while final processes sing of virions occurs in the cytoplasm
Production of virus results in destruction of infected cell
Able exist in latent state in natural hosts while capacity to replicate & reactivate

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Herpesviridae family members encode a large array of enzymes involved in:

nucleic acid metabolism (thymidine kinase)
DNA synthesis (DNA polymerase)
Protein processing (protein kinases)

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The nucleic acid metabolism enzymes produced by herpesviridae family members include:

Thymidine kinase

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Human herpes viruses can broadly be categorized as:

Alpha herpesviruses
Beta herpesviruses
Gamma herpesviruses

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Alpha herpesviruses include:

HSV-1 (HHV-1)
HSV-2 (HHV-2)
VZV (HHV-3)

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Herpes virus responsible for fever blisters:

HSV-1 (alpha)

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Herpes virus responsible for sexually transmitted genital lesions:

HSV-2 (alpha)

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Herpes virus responsible for chicken pox & shingles:

VSV (alpha)

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Herpes virus responsible for roseola:

HHV-6 & HHV-7 (beta)

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List the beta herpesviruses:

Cytomegalovirus (CMV)
HHV-6
HHV-7

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List the gamma herpesviruses:

Epstein-Barr virus (EBV) (HHV-4)
Kaposi’s sarcoma (HHV-8)

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Herpes virus responsible for infectious mononucleosis:

Epstein-Barr virus (EBV) (HHV-4)

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Herpes virus responsible for infectious mono

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Transmission of HSV-1 & HSV-2 occur through:

Direct contact

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Transmission of VSV occurs through:

Inhalation & direct contact

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Transmission CMV & EBV occur through:

Saliva & blood

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The portal of entry for HSV-1 & HSV-2 is:

Mucous membranes & skin

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Th portal of entry for VZV is:

Respiratory tract & mucous membranes

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The portal of entry for CMV & EBV is:

Bloodstream & mucous membranes

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Herpes viruses are fragile, susceptible to heat, detergent & drying due to:

Envelope

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To become infected with a herpes virus, it generally requires:

Direct inoculation

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_____ is more susceptible to herpesvirus infection than ____

Mucous membranes; skin

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CMV & 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 results in a local spread of herpes virus?

Budding directly onto & into adjacent cells

Budding onto & into adherent cells results in the local spread of herpes virus, as well as:

Syncytia formation (characteristic of herpes virus)

Herpes viruses replicates & assemble in the:

Cell nucleus

Because the herpes virus replicates & assembles in the nucleus this causes some very severe changes in nuclear structure including:

1. Chromatin shifted to margins of nucleus 2. Cowry type A acidophilic intranuclear inclusion bodies

Under a microscope, stained cells infected with herpes virus show _______ formation

Syncytia

The multinucleate cells seen when viewing stained herpes virus under microscope:

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 a ______ in recovery form primary disease & 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 herpes virus infections?

Cell-mediated immune mechanisms

In the immune response to an alpha herpes infection, MHC class I & II proteins displaying viral antigens on surface of infected cell activate:

T lymphocytes

The T lymphocytes activated by MHC class I & II proteins displaying viral antigen on surface of infected cell ultimately function to:

1. Directly kill the infected cell 2. Secrete cytokines & chemokine to attract macrophages

The cell-mediated response to alpha-herpes virus infection varies:

With age

Who is at most risk for problems associated with HSV infections? Who is at most risk for problems associated with VZV infections?

Neonates (HSVs) Elderly (VZVs)

HSV-1, HSV-2 & VSZ evade the host immune response through:

Envelope glycoproteins bind Fc domain of antibodies & complement components

HSV-1, HSV-2 & VSZ evade the host immune response through envelope glycoproteins bind Fc domain of antibodies & complement components:

Blocking their ability to promote an antiviral response

In order to evade the immune response, HSV proteins reduce _____ production & its downstream signaling pathway

Type I interferon

In order to evade the immune response, HSV can prevent ______ from being expressed on the surface of infected cells

MHC class I & II proteins

Results no expression of viral & therefore no peptides for MHC proteins to display:

Latency of Herpesviruses

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 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 & ganglia

-Herpes virus that is acquired very early in life -2/3 of adults are Ab+

HSV-1

-Herpes virus that is mostly transmitted by genital contact -uncommon before adolescence -1/5 of adults are Ab+

HSV-2

Most HSV-1 and HSV-2 infections are:

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 & 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 in neurons

The usual course of herpes simplex virus infection and disease includes:

1. acute disease 2. recovery 3. latency 4. 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 herpesviruses can be induced by:

1. local trauma 2. mental tension (stress) 3. fatigue 4. menstruation 5. exposure to bright light 6. aging effects

Infections associated with herpes simplex viruses include:

1. Ocular herpes 2. Oral herpes 3. 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 for oral herpes:

HSV-1 (sometimes HSV-2) Very common All Resolution Yes

Describe the predominant virus type, frequency, age group, usual outcome and recurrence for genital herpes:

HSV-2 (sometimes HSV-1) Common Adolescence & adults Resolution 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 orla mucosa, tongue or gingivae

Herpetic stomatitis can often be confused with:

Acute necrotizing ulcerative gingivitis (ANUG) when gingivae is inflamed

Herpes labials (cold sore) is a result of:

Reactivation of latent HSV-1 or HSV-2

Herpetic dermatitis & herpetic whitlow is HSV-1 or HSV-2 infection that appears on the:

Skin & fingers

Varicella-zoster virus (VZV) (HHV-3) is the causative agent of:

Chicken pox & shingles

Transmission of VZV:

Aerosol (inhalation) & 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 occurs in the respiratory tract and the virus then progresses to:

Phagocytic cells via the bloodstream & lymphatic system

Following VZV progressing to phagocytic cells via the bloodstream & lymphatic system, _____ occurs, spreading the virus throughout the body

Secondary viremia

Secondary viremia follow VZV infection spreads the virus throughout the body, including the:

Skin

When does secondary viremia following VZV infections 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 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 from cell-to-cell except for:

Epithelial cells of lung keratinocytes & skin lesions, which can release virus

VZV replication is similar to HSVs but:

Slower

The smallest genome of HHVs is:

VZV (around 125,000 bp)

Where does the latent infection of VZV establish itself?

1. Neurons 2. Dorsal root ganglia 3. Cranial nerve ganglia

VZV is often reactivate in older adults, why?

Impaired cell-mediated immunity

When VZV is reactivated in older adults the virus is release 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 at:

Vesicular rash along the entire dermatome

VZV reactivation produces a vesicular rash along the entire dermatome=

Herpes zoster or shingles

Postherpetic neuralgia occurs in 30% of older patients and causes:

Pain for month to years after zoster

Why is the entire dermatome affected by VZV reactivation?

Because the dermatome is an area of skin innervate 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 & on recurrent disease, however anti-VZV antibodies can help:

minor role; precent primary disease

Is there a VZV vaccine?

Yes & its effective

Anti-VZV antibodies limit:

Viremic spread of virus

What play the major role in recovery of VZV as they do for HSVs?

Cell-mediated immune mechanisms

Childhood infection of VZV=

Chicken pox

Primary infection of VZV for adults is ___ and can cause _____ in 30% of adults and may be fatal

more severe; interstitial pneumonia

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

B lymphocytes & epithelial cells

EBV has a tropism for:

B lymphocytes & epithelial cells

Cytomegalovirus (CMV; HHV-5) infects:

A wide variety of cells

EBV & 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 in EBB occurs in:

Memory B cells

The EBV viral proteins produced during latency promote:

B cell proliferation

CMV and EBV infection 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 & 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 with EBV

When EBV is acquired after childhood it results in:

Infectious mononucleosis (symptomatic)

Most common viral infection of the fetus in humans:

Congenital CMV

Congenital CMV leads to ____ & _____ including ____ & ____

Severe disease; permanent neurological damage; hearing loss; learning disabilities

Persistent CMV & EBV infections are associated with:

Chronic inflammatory diseases & cancer

Persistent EBV is particularly associated with:

1. Hodgkins disease 2. African Burkitt lymphoma 3. Nasopharyngeal carcinoma

CMV has very characteristic cellular 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 other species called _____

RBC antigens; heterophiles antibodies

Agglutination of horse RBCs by heterophiles antibody in patient's 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 with Herpesvirus type 7 include:

Roseola

The syndrome associated with Kaposi's sarcoma associated virus (HHV-8) include:

Kaposi's sarcoma

The oral manifestation of ______ includes lesions that may be found in mouth before skin rash develops:

Chickenpox (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 divisions

With _____ oral pain often precedes rash & mimics toothache pain

Shingles

The most common intraoral sites affected by shingles include:

1. anterior half of tongue 2. soft palate 3. cheek

The cause of infectious mononucleosis:

Epstein-Barr virus (EBV)

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

Infectious mononucleosis (EBV)

Describe the oral manifestations of Kaposi's sarcoma associated virus:

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: 1. Viruses may cause DIRECT _____ 2. Gingival viruses may promote ______ 3. CMV & EBV can infect ______, ______, & ______ in lesions & impair cell function 4. Viruses can induce a pro-inflammatory response that can result in _____ 5. Viruses can suppress host defenses _____ & _____

1. cytopathic effects 2. attachment/colonization 3. monocytes, macrophages, & lymphocytes 4. tissue destruction 5. locally & systemically