1. H S V - 1

3. Biological properties
1.Morphology and structure
1> nm
spherical
icosahedral

4. 2>core dsDNA linear (L segment and S segment )
3>capsid 162 capsomeres
HSV-1 -capsid from 400kV
Spot-scan Electron Cryomicroscopy

5. 4>envelope
spike-like glycoproteins
such as gB gC gD gE
gG gH gI gL gM

6. 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)

7. PATHOGENESIS
HSV-1 Facial
HSV-1 Ocular

8. HSV-1 acute
herpetic
gingivostomatitis

9. HSV Whitlow
HSV-1 Ear

10. 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

11. 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

12. 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

13. 4 Packaging
empty capsid binds to an initiation sequence
dsDNA is packaged into the empty capsid

15. 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

16. Attachment
Penetration
Retrograde Axonal
Capsid Transport
Viral Production
Latency
Viron Budding
Recurrences

17. TYPES OF INFECTION Primary infection Latent infection
Recurrent infection
Congenital and neonate infection

18. 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

19. 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                                                                                               

20. 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

21. Immune response in primary infections
antibodies to HSV antigens can be detected within 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

22. 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

23. DIAGNOSIS Isolation and identification of virus Rapid diagnosis
electroscope test
detect HSV antigen
detect DNA -----PCR

24. TRETMENT Drug Mode of Action Administered Form Acyclovir Valacyclovir
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 reproduce. (replicate
Capsules or Tablets Primary--> w/in 48 hours              --> for 10 days Recurrent -> w/in 24 hours                  -> for 5 days
Famciclovir
Capsules or Tablets. Cream for use in oral herpes Primary --> w/in 6 hours              --> for 5 days

25. VACCINE inactivated virus preparations treated with formalin
Adjuvanted subunit Vaccine
Skinner Vaccine