HSV-1
Biological properties
1.Morphology and structure
1>120-200 nm
spherical
icosahedral
2>core dsDNA linear (L
segment and S
segment )
3>capsid 162
capsomeres
HSV-1 -capsid from 400kV
Spot-scan Electron Cryomicroscopy
4>envelope
spike-like glycoproteins
such as gB gC gD gE
gG gH gI gL
gM
CULTURE
HSV can replication in many cells
Such as kidney of rabit,
lung of human embryo.
Cells infection by hsv become larger,
round,and has inclusion body in neucleus
(CPE)
PATHOGENESIS
HSV-1 Ocular
HSV-1 Facial
HSV-1 acute
herpetic
gingivostomatitis
HSV Whitlow
HSV-1 Ear
 Process
1. Attachment
gC and/or gB
attach to heparan
sulfate proteoglycan
(HS) on the cell
surface
Herpes Simplex Virus-1
on a blood lymphocyte
2.Penetration
1) gD interact with cellular receptors
2) gC, gB, gD, with gH, and gL trigger
fusion of the viral envelope (nuclear) and the
host cell plasma membrane
a pH-independent
3Retrograde Axonal Capsid Transport
1 )HSV capsid undergoes rapid transport by
retrograde axonal flow to the neuronal
nucleus
2 ) the capsid fuses with the nuclear
membrane and the dsDNA from the virion is
injected into the nucleus via nuclear pores
4 Packaging
empty capsid binds to an initiation
sequence
dsDNA is packaged into the empty
capsid
5 Viron Budding
viral capsids are enveloped at the nuclear
membrane
transport vesicles are transported through
the cytoplasm of the infecte cell(anterograde
transport)
transport vesicles fuse with the plasma
membrane, releasing virions to the extracellular
space
Attachment
Penetration
Retrograde Axonal
Capsid Transport
Viral Production
Latency
Viron Budding
Recurrences
TYPES OF INFECTION




Primary infection
Latent infection
Recurrent infection
Congenital and neonate infection
MECHANISM
 Primary infection
A key factor involved in the intracellular
edema is the keratinocytes of the middle
and basal layers which are infected and
undergo cytolysis, resulting in the formation
of an intraepidermal lesion，which rapidly
evolves into an epidermal lesion, filled with
yellowish fluid, causing displacement of
chromatin
 Secondary infection
gains access to the
distal axonal terminae
of sensory nerves and
travels by retrograde
axonal transport to
neuronal cell bodies in
sensory ganglia,
usually the trigeminal
ganglia, where further
replication or latency
can occur
Trigeminal Nerve
Recurrences can be triggered by
numerous environmental stimuli including a
common cold, fever, severe sunburn,
physical fatigue, emotional disturbance,
trauma, gastrointestinal disturbances,
menstruation, pregnancy, debilitating
illnesses, or food allergy
Immune response
 in primary infections
antibodies to HSV antigens can be
detected within 4 - 8 days (IgM IgG IgA)
viral antigens are presented on dendritic
cells and macrophages to CD4+ Th1 cells
lysis of the Infected cells ----CD4+ T-cells,
CD8 + T-cells, NK cells
 Secondary IR
HSV antigen is taken up by Lagerhan's
cells and presented on MHC II to memory
CD4+ Th cells
The anti-viral functions of T-cells include
cytotoxicity, inhibition of viral growth,
lymphokine secretion, and support of CD8+
and humoral responses
DIAGNOSIS
 Isolation and identification of virus
 Rapid diagnosis
electroscope test
detect HSV antigen
detect DNA -----PCR
TRETMENT
Drug
Mode of Action
Administered
Form
Acyclovir
Disrupts the virusí ability to
reproduce. (replicate)
Capsules or Tablets.
Cream for use in oral
herpes Primary--> for 10
days
Recurrent-> for 5 days
Valacyclovir
Disrupts the virusí ability to
Capsules or Tablets
Primary--> w/in 48 hours
--> for 10 days
Recurrent -> w/in 24 hours
-> for 5 days
Famciclovir
Disrupts the virusí ability to
reproduce. (replicate
reproduce. (replicate
Capsules or Tablets.
Cream for use in oral herpes
Primary --> w/in 6 hours
--> for 5 days
VACCINE
 inactivated virus preparations treated with
formalin
Adjuvanted subunit Vaccine
Skinner Vaccine