HERPES SIMPLEX VIRUS PPT

1. HERPES
SIMPLEX
VIRUS
MMITTAL PULKIT
IM565

2. INTRODUCTION
● Herpes (Greek: creep or crawl)
● Herpes simplex viruses belong to the ubiquitous
Herpesviridae family
● Human herpes simplex virus (HSV) causes contagious
infection with a large reservoir in the general population
● Herpesviruses are able to establish lifelong persistent
infections in their hosts and undergo periodic reactivation ;
incurable
● HSV has a potential for significant complications in the
immunocompromised host

3. INTRODUCTION
● HSV-1 is normally associated with orofacial
infections and encephalitis
● HSV-2 usually causes genital infections and can be
transmitted from infected mothers to neonates
● Both viruses establish latent infections in sensory
neurons and, upon reactivation, cause lesions at or
near point of entry into the body

4. CLASSIFICATION OF HUMAN
HERPESVIRUSES
Biologic properties Examples
Subfamily(
“herpesviri
nae)
Growth cycle and
cytopathology
Latent
infections
Genus
(“virus)
Official name
(“Human
herpesvirus”)
Common name
Alpha Short, cytolytic Neurons Simplex 1 Herpes simplex virus type
1
2 Herpes simplex virus type
2
Varicello 3 Varicella-zoster virus
Beta Long, cytomegalic Glands,
kidneys
Cytomegalo 5 Cytomegalovirus
Long,
lymphoproliferative
Lymphoid
tissue
Roselo 6 Human herpesvirus 6
7 Human herpesvirus 7
Gamma Variable,
lymphoproliferative
Lymphoid
tissue
Lymphocrypto 4 Epstein-Barr virus
Rhadino 8 Kaposi's sarcoma-
associated herpesvirus

5. TRANSMISSION
● Transmission of both HSV types is by
direct contact with virus-containing
secretions or with lesions on mucosal
or cutaneous surfaces
● HSV-1 is spread by contact, usually by infected saliva
● HSV-1 primarily infects skin above the waist
● HSV-2 is transmitted sexually or from a maternal genital
infection to a newborn
● HSV-2 primarily infects skin below the waist

6. REPLICATION
i. Virus adsorption and penetration
i. Viral DNA replication and
nucleocapsid assembly
i. Acquisition of the viral envelope
i. Latency

7. PATHOGENESIS
● Ballooning of infected cells
● Production of Cowdry type
A intranuclear (Lipschutz)
inclusion bodies
● Margination of chromatin
● Formation of
multinucleated giant cells

8. CLINICAL SIGNIFICANCE
● HSV-1
▪ Acute gingivostomatitis
▪ Recurrent herpes labialis (cold
sores)
▪ Herpetic whitlow
▪ Keratoconjunctivitis
▪ Encephalitis
● HSV-2
▪ Genital herpes
▪ Neonatal herpes
(may be by HSV-1 as
well)

9. CLINICAL SIGNIFICANCE
● Primary infections of the upper body
Fig. Herpes simplex gingivostomatitis
Fig. Herpetic whitlow
Fig. Recurrent herpes labialis
(cold sores) Fig. Keratoconjunctivitis

10. CLINICAL SIGNIFICANCE
● Primary infections of the genital tract
Fig. Genital herpes simplex infections

11. CLINICAL SIGNIFICANCE
● Latency
▪ HSV-1: Trigeminal ganglia
▪ HSV-2: Sacral ganglia
Fig. Primary and recurrent herpes simplex
infections

12. LABORATORY DIAGNOSIS
A. Cytopathology:
▪ A rapid cytologic method
▪ Scrapings obtained from the base
of a vesicle is stained with 1% aq.
solution of toluidine blue ‘0’ for
15 seconds
▪ Presence of multinucleated giant
cells or ‘Tzanck cells’ = + HSV
▪ Intranuclear inclusion bodies with
Giemsa-stained smears

13. LABORATORY DIAGNOSIS
B. Isolation and identification:
▪ Inoculation of tissue cultures in human diploid
fibroblasts is preferred for viral isolation
▪ Typical cytopathic changes may be seen in 24-48 hrs
C. Polymerase chain reaction:
D. Serology:
▪ Antibodies appear in 4–7 days after infection; reach a
peak in 2–4 weeks
▪ Rise in Ab titre may be demonstrated by ELISA or
complement fixation tests

14. TREATMENT

15. PREVENTION
currently there are no licensed
vaccines against either HSV type.
● Transmission can be reduced
by:
▪ avoidance of contact with
potential virus-shedding lesions
▪ safe sexual practice
▪ antiviral therapy

16. THANK YOU