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 Enveloped, dsDNA Viruses
 Replication in nucleus of host cell
 Have a similar morphology (Icosahedral).
 Causes primary and latent infection
 Reactivation occurs during
immunosuppressive condition.
 Alpha herpesvirus
 Herpes simplex virus type 1 HSV-1
 Herpes simplex virus type 2 HSV-2
 Varicella-zoster virus VZV
 Beta herpesvirus
 cytomegalovirus CMV
 Human herpesvirus type 6 HHV-6
 Gamma herpesvirus
 Epstein-Barr
virus EBV
 Human herpesvirus type 8 HHV- 8
Herpes simplex virus
 HSV-1 infect the upper part of the body.
 HSV-2 infect the lower part of the body -
genital infections
 There is little cross protection.
 HSV-1 and HSV-2 can be differentiated by
DNA sequencing and type specific antisera.
Herpes simplex virus
 Transmission:
 HSV-1 is transmitted primarily by saliva and
HSV-2 by sexual contact.
 Vice versa can occur due abnormal sexual
 Neonates can be infected during passing
through the infected birth canal.
Entry by skin or mucous membranes

viral multiplication sensory nerve

lysis of cells root ganglia

HSV-1 → Trigeminal ganglia &
HSV-2 → Lumbosacralganglia

vesicles latency

ulcers Reactivation Cold, Fever, Surgery

 Reactivation:
 Many factors can provoke a recurrence
 These include: physical or psychological
stress, infection, fever, irradiation, sunlight,
and menstruation.
Clinical condition
HSV is involved in a variety of clinical manifestations
which includes:
1. Acute gingivostomatitis
2. Herpes Labialis (cold sore)
3. Ocular Herpes
4. Herpes Genitalis
5. Other forms of cutaneous herpes
7. Meningitis
8. Encephalitis
9. Neonatal herpes
Clinical condition
 Gingivostomatitis:
 Characterized by
fever, irritability and
vesicular lesion in
 Usually a self
limiting disease
which lasts around
2-3 weeks.
Clinical condition
Herpes labialis (cold sore)
 Characterized by
cops of vesicles at
junction of the lips
or nose.
Clinical condition
 Ophthalmic:
 Keratoconjunctivitis
 Corneal ulcers
 Repeated attacks can lead to blindness
Clinical condition
 Cutaneous lesions
 Among the health care
 Painful lesions no pus
 Eczema herpeticum
occurs in patients with
 Herpetic whitlow
typically affect the
Clinical condition
 Genital lesion:
 Painful vesicular
lesions ingenital area.
 Sites: penis, vulva,
vagina, cervix, anus,
urethra, prostate etc.
 May be asymptomatic
Clinical condition
 Neonatal herpes:
 Both HSV-1 & HSV-2 can cause severe
infection acquired
 Infection may be milder form like: lesions in
the skin, mouth & eyes or severe
disseminated infection (encephalitis).
 Severe infection occurs if mother suffers
from primary infection.
 Can be prevented by cesarean section.
Clinical condition
 Encephalitis:
 Caused by HSV-1 & is characterized by
fever, headache, vomitting & neurological
Lab. diagnosis:
 Specimens: aspirate from vesicle, scraping from
base of ulcer & serum / CSF for antibody.
 Virus can be isolated by cell culture & confirmed by
detecting cytopathic effect.
 Detection of multinucleated giant cell.
 Viral DNA can be dtected by PCR.
 Electron microscopy of vesicle fluid - rapid result
but cannot distinguish between HSV and VZV
 Immunofluorescence of skin scrappings - can
distinguish between HSV and VZV
Thank You
Varicella zoster
Varicella zoster
 Double stranded DNA, enveloped virus
 One antigenic serotype only.
 Humans are natural Host.
 Transmission:
 Highly contagious disease.
 Transmitted through respiratory droplet &
direct contact.
Pathogenesis of Varicella
Entry & replicate in mucosa of upper
respiratory tract
Primary viremiaspread to skin

skin rash: macule > papule > vesicle > crust

Virus latent in sensory (Dorsal)


Later life virus reactivate & causes

Varicella; skin rash
■Incubation period 14-
21 days.
■ Mild prodrome: fever,
■ Rash appears on
trunk & spread to head
& extremities
■Itching is prominent
during rash.
Varicella; skin rash
Herpes Zoster (Shingles)
 Reactivation of varicella zoster virus can
occur years or even decades after illness
with chickenpox.
 Painful vesicles along the course of a
sensory nerve.
 Generally associated with anything that
causes reduced immunocompetence.
Congenital Varicella Syndrome

 Greater risk usually occur in the 1st trimester

of pregnancy with primary infection of VZV
 Varicella syndrome;
 low birth weight,
 atrophy of extremity with skin scarring,
 brain and eye defects
 deafness
Varicella zoster
 Complications
 Bacterial infection of skin lesions

 Pneumonia (viral or bacterial)

 Central nervous system manifestations
 Reye syndrome
 post-infetion encephalitis
 congenital and neonatal varicella
Pain and hyperaesthesia
Pain and hyperaesthesia
Laboratory Diagnosis of VZV
 Detection of multinucleated giant cell.
 Direct detection
electron microscopy; vesicle fluid
immunofluorescence; skin scrapping
 Serology
IgG -> past infection
IgM -> recent primary infection
 Definitive diagnosis by isolation of virus by
 Rapid varicella virus identification using PCR
 Varicella vaccine contains live, attenuated
virus approved for persons 1-2 years of
 Measles-mumps-rubella-varicella vaccine
approved for children 12 months through 12
 Vaccine prevents vericella but not zoster.

 Morphologically identical but

antigenically different to other herpes
 Humans are the natural host.
 Primary infection & latency occurs in B

 Transmission: Occurs
by kissing & exchange
of saliva.
 Affects adolescents
and young adults
 worldwide distribution.

 EBV causes:
Infectious mononucleosis,
Burkits lymphoma,
Other B cell lymphoma,
Nasopharyngeal carcinoma &
Hairy leukoplakia in AIDS patients.
The classic triad of
mononucleosis is:
 sore throat,
 Fever
 Lymphadenopathy
(usually in the neck, groin
or under the arms)
Other symptoms include:
 Fatigue and malaise
 Rash
 Enlargement of the spleen
and liver
 Hepatitis & encephalitis
can develop.
Hairy Leukoplakia
 Oral Hairy Leukoplakia
 Nonmalignant
hyperplastic lesion of
epithelial cells
Burkitts lymphoma

 It usually occurs in children aged 3-14 years.

 BL cells show translocation of c-myc
oncogene between the long arm of
chromosome 8 and chromosomes 14.
Lab. diagnosis
 Hematological: Atypical lypmhocytosis.
 Immunolobical:
 Monospot test, agglutination test to detect
hetarophil antibody (Monospot test relies on
the agglutination of horse RBCs by
heterophile antibodies in patient's serum).
 EBV specific IgM & IgG detection.
 Paul-Bunnell test: Determination of the
highest dilution of the patient's serum
(heterophile antibodies) will agglutinate
sheep erythrocytes.
 Cytomegalovirus or Human Herpesvirus 5
 Single serotype.
 Forms giant cell hence called
 Transmission:
 Fetus: from mother via placenta
 Infant: during birth or breast feeding.
 From person to person through saliva, urine,
or other bodily fluids.
 Can be transmitted by sexual intercourse
 Also transmitted by transplanted organs,
and rarely from blood transfusions.
Clinical finding
 CMV infection of newborn: When infection
occurs in 1st trimester, neonate suffers from an
asymptomatic infection to a disease with fever,
hepatosplenomegaly, mental or motor retardation
and sometimes death.
 In immunocompetent adult: causes heterophil-
negative infectious mononucleosis without sore
Clinical finding

 In immunocompromised persons: It may include

CMV retinitis, diarrhea , respiratory infection, and
Lab. diagnosis
 Isolation of virus.
 Detectionof nucleic acid by PCR.
 Fluorescence microscopy.
 Antibody titre.
 Microscopic detection of giant cell.
 HHV8
 Transmitted sexually or by organ
 Causes kaposis sarcoma in AIDS