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⦿INTRODUCTION
⦿EPIDEMIOLOGYAND TRANSMISSION
⦿STRUCTURE
⦿REPLICATION
⦿ PATHOGENESIS AND CLINICAL SIGNIFICANCE
⦿LABORATORY DIAGNOSIS
⦿TREATMENTAND PREVENTION
CONTENT
⦿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
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
INTRODUCTION
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
CLASSIFICATION OF HSV
⦿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
EPIDEMIOLOGY
⦿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 infectio
to a newborn
⦿HSV-2 primarily infects skin below the waist
TRANSMISSION
⦿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)
STRUCTURE
i. Virus adsorption and penetration
ii. Viral DNA replication and
nucleocapsid assembly
iii. Acquisition of the viral envelope
iv. Latency
REPLICATION
⦿HSV causes cytolytic
infections
⦿Pathologic changes are due to
necrosis of infected cells
together with the inflammatory
response
Viral cytopathy
PATHOGENESIS
⦿ Ballooning of infected cells
⦿Production of Cowdry type
A intranuclear (Lipschutz)
inclusion bodies
⦿Margination of chromatin
⦿Formation of
multinucleated giant cells
PATHOGENESIS
⦿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)
CLINICAL SIGNIFICANCE
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
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
LABORATORY DIAGNOSIS
⦿ 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
TREATMENT AND PREVENTION
⦿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
REFERENCE
herpes simplex virus- ppt.pptx

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herpes simplex virus- ppt.pptx

  • 1. ⦿INTRODUCTION ⦿EPIDEMIOLOGYAND TRANSMISSION ⦿STRUCTURE ⦿REPLICATION ⦿ PATHOGENESIS AND CLINICAL SIGNIFICANCE ⦿LABORATORY DIAGNOSIS ⦿TREATMENTAND PREVENTION CONTENT
  • 2. ⦿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 INTRODUCTION
  • 3. ⦿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 INTRODUCTION
  • 4. 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 CLASSIFICATION OF HSV
  • 5. ⦿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 EPIDEMIOLOGY
  • 6. ⦿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 infectio to a newborn ⦿HSV-2 primarily infects skin below the waist TRANSMISSION
  • 7. ⦿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) STRUCTURE
  • 8. i. Virus adsorption and penetration ii. Viral DNA replication and nucleocapsid assembly iii. Acquisition of the viral envelope iv. Latency REPLICATION
  • 9. ⦿HSV causes cytolytic infections ⦿Pathologic changes are due to necrosis of infected cells together with the inflammatory response Viral cytopathy PATHOGENESIS
  • 10. ⦿ Ballooning of infected cells ⦿Production of Cowdry type A intranuclear (Lipschutz) inclusion bodies ⦿Margination of chromatin ⦿Formation of multinucleated giant cells PATHOGENESIS
  • 11. ⦿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) CLINICAL SIGNIFICANCE
  • 12. 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 LABORATORY DIAGNOSIS
  • 13. 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 LABORATORY DIAGNOSIS
  • 14. ⦿ 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 TREATMENT AND PREVENTION
  • 15. ⦿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 REFERENCE