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GENERAL PROPERTIES
human herpes virus
DNA virus
STRUCTURAL ELEMENTS
STRUCTURE
REPLICATON
Continued virion assembly and maturation → secondary envelopment → released from the cell
Budding from nuclear membrane → provides primary (temporary) envelopment
Viral transcription and replication occurs → Assembly
Moves to nuclear pores → DNA released into the nucleus
Fuses with the plasma membrane → Core is released into the cell’s cytoplasm
Virus attaches to receptors on host cells → endocytosis
PATHOGENESIS
Initially, the infection replicates viruses
in mucoepithelial cells.
The infection spreads throughout the reticuloendothelial
(RE) system and bloodstream, causing flu-like symptoms
and chickenpox.
After resolution of the primary infection, a latency period
occurs and the virus remains dormant in the dorsal root
ganglia.
Reactivation of the infection results in
shingles.
TRANSMISSION
reservoir for VZV
highly contagious
Inhalation of aerosolized
Direct contact
PATHOPHYSIOLOGY
PRIMARY INFECTION (CHICKENPOX):
Transmitted through aerosols→ targets mucoepithelial cells → replication
Viremia → contagious and febrile illness occurs
After resolution, viral particles remain in the dorsal root ganglia or
other sensors ganglia.
Host immune system suppresses replication of the virus → lays dormant
for years to decades (latency period)
HERPES- ZOSTER(SHINGLES)
Host immune system
fails to contain
the virus → VZV
reactivates
Spreads down
the sensory nerve
→ skin → rash
Inflammatory
response in
the sensory ganglia
Involves plasma
cells and T
lymphocytes
Can result in
neuronal damage
→ neuropathic pain
HOST RISK FACTORS
Pregnant
women
Age Factors
• Infants
• Elderly
Immunocompromi
sed patients
• HIV
• /AIDS
• Organ
transplantation
• Chemotherapy
• Chronic steroids
2 distinct
syndromes
Chickenpox
Shingles
CLINICAL SYNDROME
VARICELLA (CHICKEN POX)
vesicular lesions in different stages
14 to 16 days
head, chest, and back spreads
to the rest of the body.
cerebellar ataxia,
encephalitis, viral pneumonia, and hemorrhagic conditions
Full recovery weeks to months.
HERPES- ZOSTER(SHINGLES)
Reactivation of endogenous latent sensory
ganglia.
painful, itchy or tingly
headache, photophobia and malaise in the
prodromal phase.
clusters of vesicles
three to five days
pigmentation changes and scarring on the skin.
bacterial super
infection of the lesions, cranial and visceral involvement
EPIDEMIOLOGY
CHICKENPOX
95% of people age of 20 years
100 deaths
hospitalization and deaths
SHINGLES
30% of the population
previously affected with
chickenpox
LAB DIAGONOSIS
1. MICROSCOPY
2. CYTOLOGY base of the lesions
3. ELECTRON MICROSCOPY
vesicles of either varicella or
zoster.
4. IMMUNOFLUORESCENCE CYTOLOGY
more sensitive than EM labor
intensive greater technical expertise
MOLECULAR METHODS
1. PCR assays
human fibroblasts
4. Vesicle fluid and scrapings
5. Immunofluorescence
SEROLOGY
paired acute sera
IF (Immunofluorescence) and RIA or EIA.
Complement fixation test (CFT)
and latex agglutination
PREVENTION
chickenpox vaccine.
live attenuated vaccine administered
subcutaneously.
90% effective
TREATMENT
acyclovir
valacyclovir and famciclovir.
gives passive protection in
immunocompromised children
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