Herpes virruses

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.