Herpes Simplex Virus

2.  INTRODUCTION
 EPIDEMIOLOGY AND TRANSMISSION
 STRUCTURE
 REPLICATION
 PATHOGENESIS AND CLINICAL SIGNIFICANCE
 LABORATORY DIAGNOSIS
 TREATMENT AND PREVENTION

3.  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

4.  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

5. 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

6.  HSV-associated diseases are among
the most wide-spread infections
affecting nearly 60-95% of human
adults
 No animal reservoirs or vectors
 Highest incidence of HSV-1 infection
occurs among children 6 months to 3
years of age
 70–90% of persons thus acquire type 1
antibodies by adulthood
 Primary infection by HSV-2 is more
common in young adults

7.  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

8.  Virions are spherical, 150-200nm in
diameter
 HSV-1 and HSV-2 contains
i. an envelope- derived from the
nuclear membrane of the
infected cell; contains viral
glycoproteins
ii. a tegument—an amorphous layer
of proteins that surround the capsid
iii. an icosahedral capsid
iv. Genome (linear, a large
double-stranded viral DNA; encoding
70-200 proteins)

9. i. Virus adsorption and penetration
ii. Viral DNA replication and
nucleocapsid assembly
iii. Acquisition of the viral envelope
iv. Latency

10.  HSV causes cytolytic
infections
 Pathologic changes are due to
necrosis of infected cells
together with the inflammatory
response
Viral cytopathy

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

12.  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)

13.  Primary infections of the upper body
Fig. Herpes simplex gingivostomatitis
Fig. Herpetic whitlow
Fig. Recurrent herpes labialis
(cold sores) Fig. Keratoconjunctivitis

14.  Primary infections of the genital tract
Fig. Genital herpes simplex infections

15.  Latency
 HSV-1: Trigeminal ganglia
 HSV-2: Sacral ganglia
Fig. Primary and recurrent herpes simplex
infections

16.  Reactivation
 Hormonal changes, fever, and physical damage
 Severity of any systemic symptoms is considerably
less than that of a primary infection
 Many recurrences are characterized by shedding of
infectious virus in the absence of visible lesions
 HSV-1:
Reactivation frequency- none to several a year
Herpes labialis or cold sores, fever blisters
 HSV-2:
Reactivation frequency- monthly
Asymptomatic; viral shedding

17. 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

18. 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

19.  Aciclovir, Valaciclovir, Famciclovir
 Asymptomatic shedding is
frequent in patients with genital
herpes
 Transmission can be reduced
by:
 avoidance of contact with
potential virus-shedding lesions
 safe sexual practice
 antiviral therapy

20.  Harvey RA, Champe PC, Fischer BD. Lippincott’s
Illustrated Reviews: Microbiology. 2nd edition.
2007.
 Jawetz, Melnick & Adelberg. Medical
Microbiology. The McGraw-Hill Companies. 25th
edition
 Richard J Whitley, Bernard Roizman. Herpes
simplex virus infections. Lancet. 2001; 357: 1513–
18
 Fatahzadeh M & Schwartz RA. Human herpes
simplex virus infections: Epidemiology,
pathogenesis, symptomatology, diagnosis and
management. JAM ACAD DERMATOL. 2007;
737-763