This document discusses several herpesviruses including herpes simplex virus types 1 and 2, varicella zoster virus, and human herpesvirus 6. It provides details on their classification, associated diseases, transmission, pathogenesis, diagnosis and treatment. Herpes simplex virus types 1 and 2 cause oral and genital herpes respectively. Varicella zoster virus causes chickenpox and shingles. Human herpesvirus 6 is associated with roseola infantum and certain neurological conditions. The viruses establish latency after primary infection and can reactivate periodically. Antiviral therapy includes acyclovir for treatment of active infections.

3. 0 Finger printing w/in herpesviruses: restriction
endonuclease and genome sequence analysis
0 Thermo-labile and inactivate by lipid solvents such
as alcohol and detergents

4. 0 Herpes viridae (ABG-HH)
0 Results are confidential hence enveloped
0 Affect’s skin w/c envelope’s our entire body
1. Alpha-herpesvirinae
1. HSV-1
2. HSV-2
3. VariCella zoSter
1. Varicella- chickenpox
2. Zoster-shingles
Herpes’
Habitat is
Vagina

5. 2. Beta-herpesvirinae
2. Cytomegalovirus
-cell abnormally large
-Decrease Immune system & Infectious mononucleosis
(B-lymphocytes)
3. Gamma-herpesvirinae
3. Epstein Barr Virus (EBV)
GENITAL HERPES

6. 1
2
3
4
• Virus fuses viral envelope with plasma membrane following attachment to
the cell surface
• Fusion of membranes releases two proteins from the virion
• VHS shuts off protein synthesis; -trans-inducing factor (-TIF or VP16) is
transported to the nucleus
• Viral DNA is released from the capsid at the nuclear pore into the nucleus
and immediately circularizes
• Transcription of genes by cellular enzymes is induced by -TIF.

7. 5
6
7
8
9
• The five mRNAs are transported into the cytoplasm and translated (filled
polyribosome)
• The proteins are transported into the nucleus
• New round of transcription results in synthesis of proteins.
• Chromatin is degraded and displaced toward the nuclear membrane;
nucleoli (round hatched structures) become disaggregated.
• Viral DNA is replicated by a rolling circle mechanism, which yields
concatemers of viral DNA.
• New round of transcription-translation yields the proteins, consisting
primarily of structural proteins of the virus.

8. 10
11
12
13
14
• The capsid proteins form empty capsids
• Unit-length viral DNA is cleaved from concatemers and packaged into
the preformed capsids
• Capsids containing viral DNA acquire a new protein.
• Viral glycoproteins and tegument proteins accumulate and form
patches in cellular membranes. Capsids attach to the underside of
membrane patches containing viral proteins and are enveloped
• Enveloped particles accumulate in the endoplasmic reticulum and are
transported into the extracellular space.

9. 0HERPES SIMPLEX VIRUS
0Can grow easily in cells
0Has TWO distinct types:
1. HSV type 1
Associated primarily with the MOUTH, EYE
and CNS
2. HSV type 2
Found most often in the GENITAL tract.

10. 0 For both type primarily is sexual and oral
contact.
0 To infect people, the herpes simplex viruses (both
HSV-1 and HSV-2) must get into the body through
tiny injuries in the skin or through a mucous
membrane, such as inside the mouth or on the
genital area.
0 Both viruses can be carried in bodily fluids (such as
saliva, semen, or fluid in the female genital tract) or
in fluid from herpes sores.

11. 0 The envelope of HSV contains
at least 11 glycoproteins.
0 Three of the glycoproteins (g)
are essential for production
of infectious virus:
0 gB and gD(common to both
type)
Involved in adsorption to and
penetration into cells
0 gH together w/ gL
involved in fusion at entry and
in release of virus
VIRULENCE FACTOR

12. 0 PRIMARY INFECTION
0 Complement fixation tests (CFTs) are useful in diagnosis
0 Vesicle- typical lesion
0 A ballooning degenaration of intra-epithelial cells which
contain nfectious fluid.
0 The base of the vesicle contains multinucleated cells (Tzanck
cells) and infected nuclei contain eosinophilic inclusion bodies.

13. 0 Latency reflects persistent infection (as manifest by the
presence of the viral genome) during which no infectious
virus is produced, except during intermittent episodes of
reactivation.
HSV 1
• Trigeminal ganglion
• Other sensory and
autonomic ganglia
• Adrenal tissue and
brain
HSV 2
• Sacral ganglia

14. 0 When reactivated virus produces clinically apparent disease.
0 Experience paresthesiae (tingling, warmth, itch) on the
site followed by erythema and a papule usually with in 24
hours.
0 Most common site are at the mucocutaneous junction of the
lip, on the chin or inside the nose.
0 Lesions are popularly known as “cold sores” or “fever
blisters”
First time
recurrence

16. Eye infection
Oral infection
Eczema herpeticum
HSV encephalitis
with meningitis
Neonatal herpes simplex

17. 0 Through sexual contact
0 SITES:
0 In male: the glans and shaft of the penis are the most
frequent
0 In female: the labia and vagina, or cervix may be
involved

18. Culture-Using diploid
fibroblast cells
(+) ballooned cells in foci
Swab-method
of choice
Serology-PCR
DNA detection- most
sensitive and specific test
Electron microscopy
Immunostainingprovides rapid diagnosis on
cells scraped from the base of lesions

19. 0 ANTIVIRAL THERAPY
0 ACYLCLOVIR-most widely used; excellent safety record; can be
used in pregnancy;for acute HSV
0 Long-term suppressive therapy- for frequently recurring genital
herpes
0 Ointment- for mild lesions
CONTROL
 Alleviating over crowding
 Good hygiene
 Education regarding the infectious stages
 Use of condoms
0 Use a dental dam for oral sex
0 Limit your number of sexual partners
0 Be aware that nonoxynol-9, the chemical spermicide used in gel
and foam contraceptive products and some lubricated condoms,
does not protect against any sexually transmitted disease

20. 0 Genus: Varicellovirus
0 2 clinical manifestation
0 Varicella (chickenpox)
0 Zoster (shingles)
0 Primary infection is
highly contagious
0 90% adults have
antibody
0 Appears in
childhood
0 Symptoms:
0 Febrile illness
0 Rash
0 Vesicular lesion

22. Herpes Zoster
0 Clinical manifestation of reactivated VZV
0 Occurs in adults
0 Virus remains in dorsal root of the cranial
nerve ganglia

23. 0Commonly presents with rash
0Followed by vesicular lesion in unilateral
dermatome pattern

24. Varicella zoster
Diagnosis
0 Use of Fluorescentlabeled monoclonal
antibody against
VZV
0 Culture of VZV in
human embryonic
lung cells
Prevention
0 Attenuated vaccine,
single dose gives
lifetime immunity.

26. 0 Genus: Roseolovirus
0 2 variants, indistinguishable serologically
0 Variant A
0 Variant B
0Cause of disease
0 95% young adults are serologically
positive (+)

27. 0Found in salivary glands and stool
0Saliva is the route of transmission
0Childhood disease associated,
known as “roseola infantum” or
“sixth disease”
0Children get protection from
maternal antibody until 2years and
6 months of age

28. 0 Maculopapular rash appears after fever
0 30% of children to acquire the virus will
experience seizures with symptoms
0 The virus is involved in progressive
multifocal leukoencelopathy and multiple
sclerosis

29. 0Lymphocyte cell culture
0Polymerase Chain Reaction
(PCR)