Chapter 41-42 Herpes Viruses Flashcards
what is the genome for herpes virus
double stranded DNA
- enveloped
how big is the genome for herpes virus
125,000-236,000
herpesviridae family members share four significant biological properties:
- encode a large array of enzymes
- synthesis of viral DNAs and capsid assembly occur in the nucleus, while final processing of virions occurs 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 cause disease upon reactivation
what are herpes enzymes involved in
- nucleic acid metabolism: thymidine kinase
- DNA synthesis- DNA polymerase
- protein processing- protein kinase
what are the alpha herpes viruses and what do they cause
- HHV-1: fever blisters
- HHV-2: sexually transmitted genital lesions
- HHV-3: chicken pox and shingles
what are the beta viruses and what do they cause
HHV-5
- HHV-6: roseola
- HHV-7: roseola
what are the gamma herpesviruses and what do they cause
- HHV-4: infectious mononucleosis
- HHV-8
what is the means of transmission and the portal of entry for HSV-1
-direct contact
- mucous membranes, skin
what is the means of transmission and the portal of entry for HSV-2
- direct contact
- mucous membranes, skin
what is the means of transmission and the portal of entry for VZV
-inhalation, direct contact
- respiratory tract, mucous membranes
what is the means of transmission and the portal of entry for CMV
-saliva, blood
- bloodstream, mucous membranes
what is the means of transmission and the portal of entry for EBV
- saliva, blood
- mucous membranes, bloodstream
herpes viruses are ____
fragile, susceptible to heat, detergent, drying
most humans become infected with _____
one or more herpesviruses
herpes viruses generally require______
direct inoculation
which is more suscpetible to herpes virus: mucous membranes or skin
mucous membranes
how are CMV and EBV transmitted
through infected leukocytes
VZV is mostly transmitted by______
aerosols
describe the herpesvirus lytic cycle
-cascade of gene expression
- attach to and infect adjacent cells upon release
- budding directly onto and into adjacent cells
- therefore get a local spread of virus
- syncytia form
virus replicates and assembles in the _____
nucleus
describe how 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 and intranuclear inclusion bodies
anti-herpes virus antibodies play a minor role in_____
recovery from primary disease and recurrent disease
how do cell mediated immune mechanisms play a major role in recovery
-MHC class I and II proeins displaying viral antigens on surface of infected cell
- activate T lymphocytes and directly kill infected cell or secrete cytokines and chemokines to attract macrophages
what herpes virus affects neonates
HSVs
what herpes virus affects elderly
VZV
how do HSV-1, HSV-2, VZV evade immune responses
-envelope glycoproteins bind Fc domain of antibodies and complement components, blocking their ability to promote an antiviral response
-reduce type I interferon production and its downstream signaling pathway
- prevent MHC class I and II proteins from being expressed on the surface of infected cells
what does latency of HSV result in
no expression of viral proteins and therefore no peptides for MHC proteins to display
what is acute herpes simplex disease
- facial or genital herpes, stomatitis or keratitis
- localized
describe the acute disease portion of herpes simplex infections
- 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
when is HSV-1 acquired and how
very early in life- kissing
how many adults are Ab+ for HSV-1
2/3
when is HSV-2 acquired
mostly by genital contact
- uncommon before adolescnece
how many adults are Ab+ for HSV-2
1/5
most HSV-1 and HSV-2 infections are _____
asymptomatic
how many infections have recognizable symptoms
1/3
what are the steps of a herpes simplex virus infection
- acute disease
- recovery
- latency
- recurrent disease
what happens in recovery in herpes infections
healing of lesions and establishment of latent infections in neurons
what happens in latency in herpes infections
maintenance of latent infections in neurons
what is the presentation of recurrent disease in herpes infections
cold sores, fever blisters, keratitis, or genital lesions, localized
describe recurrent herpes disease
reactivation of latent virus and distal spread
- recurrent lesions caused by virus replication in epithelial cells
reactivation of various herpes viruses can be induced by:
- local trauma
- mental tension
- fatigue
- menstruation
- exposure to bright light
- aging effects
what is the virus type, frequency, age group, usual outcome and recurrence of ocular herpes
- type 1
- common
-all - resolution, visual impairment
- recurrent
what is the virus type, frquency, age, usual outcome and recurrence of oral herpes
-1>2
- very common
- all
- resolution
- recurrent
what is the virus type, frequency, age, usual outcome and recurrence of genital herpes
-2>1
- common
-adolescents, adults
-resolution
-yes
what can herpes keratitis lead to
scarring and blindess
what is the most common viral infection of the mouth
herpes stomatitis
what is the primary infection of herpes stomatitis due to
HSV-1 or HSV-2
where are herpes stomatitis vesicles found
oral mucosa, tongue, and gingivae
what is herpes stomatitis confused with
ANUG
what is herpes labialis and what infection is it
- cold sore
- reactivation of latenet HSV-1 or HSV-2
what infection is herpetic dermatitis and herpetic whitlow
HSV-1 or HSV-2
what percentage of adults have VZV antibody
90%
where does VZV replicate
respriatory tract
how does the VZV virus progress
to phagocytic cells via the bloodstream and lymphatic system
describe the spread of secondary VZV 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 virus
VZV virus spreads cell to cell like _____. except _____
HSVs; epithelial cells of lung keratinocytes and skin lesions which can release virus
which replication is faster VZV or HSV
HSV
what neurons are infected by VZVs
dorsal root ganglia or cranial nerve ganglia
describe VZV reactivation in older adults with impaired CMI
- virus release 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
what is a dermatome
an area of skin innervated by fibers from a single dorsal root spinal nerve
what promotes recovery from primary disease
host defenses
what plays a minor role in recovery from primary disease and on recurrent disease in VSZ infections
anti-VZV
what plays a major role in preventing primary disease
VZV vaccine thorugh anti VZV antibodies
what do anti VZV antibodies limit
viremic spread of virus
what play a major role in recovery for HSVs
cell mediated immunity
what is the childhood illness of VZV
chicken pox
what does primary infection of VZV cause in 30% of adults
interstitial pneumonia
what does the epstein barr virus infect
B lymphocytes and epithelial cells
what does cytomegalovirus infect
a wide variety of cells
how do EBV and CMV replicated within host cells
similar to herpes virus
what is the CMV infection
persistent/chronic infection
what is the EBV latent infection
- latent infection in memory B cells
- virus proteins produced during latency promote B cell proliferation
what percentage of adults have CMV and EBV infections
95% in the world
50-60% in the US
- usually asymptomatic when acquired early
how is EBV acquired
similarly to CMV except breast milk is not a route of virus spread
what are sympomatic EBV infections acquired after childhood
infectious mononucleosis
what is the most common viral infection of the fetus in humans
congenital CMV
what does congenital CMV lead to
severe disease and permanent neurological damage including hearing loos and learning disabilities
what cancers and chronic inflammatory diseases are persistent CMV and EBV infections associated with
- Hodgkin disease
- african burkitt lymphoma
- nasopharyngeal carcinoma
how are CMV infections diagnosed histologically
large inclusions in tissue specimens- “owl eye” inclusions
how are EBV infections diagnosed histologically
-PCR
- heterophile antibody or monospot test
- EBV infections induce production of large number of antibodies that recognize RBC antigens of other species
what is a monospot test
agglutination of horse RBCs by heterophile antibody in patients serum
what are the associated syndromes of cytomegalovirus
congenital infection and mononucleosis
what is the associated syndrome of epstein barr virus
mononucleosis
what is the associated syndrome of herpesvirus type 6
roseola
what is the associated syndrome of herpesvirus type 7
roseola
what is the associated syndroms of kapsi’s sarcoma associated virus HHV8
kaposi’s sarcoma
what is the oral manifestation of chickenpox (VZV)
lesions may be found in mouth before skin rash develops
describe the oral manifestations of shingles (VZV reactivation)
- trigeminal nerve affected in 15% of cases
- opthalamic > maxillary > mandibular divisions involved
- oral pain precedes rash and mimics tooth pain
what are the most common oral sites affected in shingles
-anterior half of tongue
- soft palate
- cheek
what are the oral manifestations of epstein barr virus
-painful sore throat at onset of infection
- rash may be present at junction of hard and soft palate - fine petechial hemorrhages
- white psuedomembrane may develop on tonsils and other parts of oral mucosa
what are the oral manifestations of HHV8
kaposi’s sarcoma lesions - endothelial tumor
what herpes viruses are present in majority of advanced periodontal lesions
- EBV and CMV
what are the possible roles of herpesvirus in periodontal disease
- viruses may cause direct cytopathic effects
-gingival viruses may promote bacterial attachment/ colonization - CMV and EBV can infect monocytes, macrophages, and lymphocytes in lesions and impair cell function
- viruses induce a proinflammatory response that can result in tissue destruction
- viruses can suppress host defenses locally and systemically
what can anti herpes virus antibodies prevent
primary disease
describe host response to alpha herpes virus infections
- cell mediated immune mechanisms play the major role in recovery
- cell mediated immune response varies with age
