によって R G 15年前.
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Organic solvent
Thermolabile
Where does replication occur?
Nucleus
Lipid envelope
Icosahedral
Linear dsDNA
For Ag detection
Most common transplacentally transmitted infection in the U.S.
No heterophile Ab
Enlargement of infected cells with pronuclear inclusions
leads to..
Benign disease
Heterophile antibodies
Cross-react w/ sheep, goat RBCs
Heterophile Ab
All of these may serve as buzzwords
Oral Hairy leukoplakia
B cell lymphoma
Where would you find a high incidence of African Burkitt's lymphoma?
Regions w/ high incidence of malaria
Where is it endemic?
China
Atypical lymphocytes
When resistant to acyclovir
Valacyclovir or "Valtrex" is a prodrug of...
Acyclovir
SES
Immuno. status
Humans only reservoir
Asymptomatic shedding
Direct contact w/ infected secretions
Only for primary infection
Antigen detection
Scrape the lesion
Most definitive
Clinical manifestations of HSV-2 infection
1. Primary infection presents as papules progressing to vesicles and pustules,
lymphadenopathy and tenderness, 3-4 weeks duration
2. Recurrent infection characterized by prodrome followed by groups of vesicles on external genitalia, 1-2 weeks duration
3. Neonatal herpes usually due to HSV-2 acquired by passage through infected birth
canal; 60% mortality with survivors suffering neurologic sequelae; disseminated vesicular lesions with internal organ involvement
Neonatal herpes
Clinical manifestations of HSV-1 infection
1. Primary infection often asymptomatic; 50-90% of population is seropositive
2. Primary gingivostomatitis—fever, irritability, painful vesicular lesions on buccal
mucosa, tongue, gums, throat, 1-2 weeks duration
3. Recurrent infection characterized by prodrome, followed by unilateral vesicles of 1
week duration
4. Ocular lesions can lead to permanent corneal scarring
5. Causes 10% of viral encephalitis with 70% mortality if untreated
Genital herpes
Encephalitis
Ocular herpes
Herpetic whitlow
Fever blisters
Gingivostomatitis
Pathophysiology of infection
1. Acute infection results in multinucleated cells (syncytia), ballooning degeneration of epithelial cells, necrosis, inclusion bodies, inflammatory response, cell to cell spread, latent infection of ganglia
2. Latent infection does not destroy ganglia; viral genome persists as circular DNA; reactivation of virus replication leads to recurrent disease
3. Recurrence triggered by stress, ultraviolet light, hormonal flux
4. Spreads from cell to cell in presence of antibody
5. Cell-mediated immunity contributes to symptoms and resolution
Triggers for recurrence
Hormonal flux
UV light
Stress
Syncytia
