The document discusses several human herpes viruses: - Herpes simplex virus types 1 and 2 cause oral/facial and genital lesions, respectively. - Varicella zoster virus causes chickenpox initially and shingles upon reactivation. - These viruses establish latency in neuronal or lymphoid tissues after primary infection. - They are enveloped DNA viruses that infect via fusion with host cells and replicate in the nucleus before assembling and budding from the nuclear membrane.

1. MEDICAL VIROLOGY
HERPES VIRUS
KMVSOHMM

2. SCOOPE
• INTRODUCTION
• CLASSIFICATION
• HSV-1 & HSV-2
• VZV

3. INTRODUCTION
• Herpesvirus family consists six important
human viruses:
Herpes simplex virus (HSV) type1 and 2.
Varicella zoster virus(VZV).
Cytomegalovirus (CMV).
Epstein-Barr virus (EBV).
Human herpes virus-8.

4. IMPORTANT FEATURES
• All are structurally similar:
Each has icosahedral protein core surrounded by
a lipoprotein envelope.
Tegument joins capsid to the envelope.
Genome is linear ds-DNA in the capsid.
Virion does not contain polymerase.
They are large 120-200nm diameter next to
poxvirus.
Noted for their latent infection.

5. IMPORTANT FEATURES
HSV-1 STRUCTURE VIRAL- STRUCTURE

6. CLASSIFICATION
• Three categories basing on the site of primary
infection and latent infection:
Alpha herpes virus; infect epithelial cells and
cause latent infection in the neuronal cells.
HSV&VZV.
Beta herpes virus; infect and cause latent
infection in variety of tissues. CMV&HHV-6.
Gamma herpes virus; infect and cause
infection in lymphoid tissue. HHV&EBV-8.

7. CLASSIFICATION

8. HSV-1 & HSV-2
• Distinguishable by;
Antigenicity and location of lesion.
HSV-1 lesions are above the waist, HSV-2 lesions
are below the waist. Human are the host.
• Diseases:
Gingivostomatitis, encephalitis, keratitis, herpes
labialis. In HSV-1 infection.
Genital herpes, neonatal herpes and aseptic
meningitis. In HSV-2.

9. SUMMARY OF REPLICATION OF HSV

10. SUMMARY OF REPLICATION
Attachment: glycoproteins on the surface of
enveloped virus bind to their transmembrane
receptors on the host cell.
Fusion: envelope fuses with cell membrane
creating a pore through which contents enter
the host cell.
Entry into nucleus: virion uncoates; genome
DNA enters the nucleus; becomes circular

11. SUMMARY OF REPLICATION
Early mRNA is transcribed from by the host cell
RNA polymerase; then translated into early non-
structural proteins.
Viral DNA polymerase, replicates genome DNA,
initiating synthesis of late structural proteins; are
transported into nucleus for virion assembly
Virion acquires its membrane by budding off
nuclear membrane and leaves the cell by
exocytosis.

12. TRANSMISSION & EPIDE
• HSV-1; through saliva, infections occur around
the face.
• HSV-2; through sexual contact, infections
occur around the genital area.
o Roughly, 80% of US-population have HSV-1
and 40% have recurrent labialis.
o Most HSV-1 infection occur in children. HSV-2
infection don't occur until age of sexual
activity.

13. PATHOGENESIS
Viral replication occurs in skin and mucous
membrane at initial site of infection.
 Migration up the neuron; becomes latent in
sensory ganglion cells. HSV-1 in the trigeminal
and HSV-2 in lumbar & sacral ganglia.

14. PATHOGENESIS
Reactivation can be induced by sunlight,
hormonal changes, trauma, stress and fever;
then moved down the neuron, replicates in
the skin.
Causing skin leisions;-i.e. vesicle; filled with
serum, virus particle & debris, which becomes
infectious upon rapture.
Multinucleated giant cells are found at the
base of the lesion, its diagnostic.

15. CLINICAL FINDINGS IN HSV-1
 Gingivosomatitis; fever, irritability and
vesicular lesions around the mouth.
 Herpes labialis; crops of vesicles around the
mucocutaneous junction of the nose or lips.
 Keratoconjuctivitis; corneal ulcerations and
epithelial conjuctival lesions.
 Encephalitis; temporal lobe necrotic lesion,
fever, headache, vomiting, seizures and
altered mental state

16. CLINICAL FINDINGS IN HSV-2
 Genital herpes; painful vesicular lesions of
male and female genital area. Primary
infection is associated with fever and inguinal
adenopathy.
 Neonatal herpes; encephalitis in disseminated
infection and lesions around eyes, mouth,
skin.
 Aseptic meningitis; usually self limiting.

17. LAB-DIAGNOSIS
• Test samples;
CSF
Fluid from lesion.
• Methods
Tzanck smear.
PCR.
Serologic test, e.g. neutralization test.
Cell culture, ELISA.

18. VARICELLA-ZOSTER
• Disease;
chicken pox (varicella), primary disease,
 and zoster (shingles), the recurrent form.
• Epide; >90% of US-populations have antibody
by 10thyear of age, more in children (varicella)
and herpes zoster in older population. VSV
occurs worldwide.

19. TRANSMISSION
 Respiratory droplet
 Direct contact with lesions
 Through placenta.

20. PATHOGENESIS
VZV infects the mucosa of the upper
respiratory tract, spreads hematogenously to
the skin, were it causes vesicular rash.
Multinucleated giant cells are seen at the base
of the lesion.

21. PATHOGENESIS
 Suppression of the cell-
mediated immunity
results in viral activation
causing vesicular skin
lesions and nerve pain.

22. PATHOGENESIS
After recovery of the host cell, virus becomes
latent in dorsal root ganglia.
IgG, IgM and IgA are produced following
infection. IgM persists for life to confer
protection.

23. CLINICAL FINDINGS

24. CLINICAL FINDINGS
• Varicella;
Incubation period is 14-21 days, brief prodromal
symptoms of malaise and fever.
Papulovesicular rash in crops on the trunk
spreads to head and extremities.
Pruritis
Reye’s syndrome; encephalopathy and liver
degeneration.

25. CLINICAL FINDINGS
• Zoster;
Painful vesicles along course of sensory nerve.
In immunosupressed pts, severe disseminated
infection such as pneumonia.

27. LAB-DIAGNOSIS
• Most diagnoses are made clinically.
• Tzanck smear.
• Cell culture.
• Serology.
Prevention: Varivax vaccine for varicella
zostavax vaccine for zoster and varicella zoster
immunoglobulin (VZIG) for prophylaxis.