Herpes simplex virus

Herpes Simplex Virus

1. Herpes S implex Virus

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

3. 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

4. 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

5. Classification of human herpesviruses Biologic properties Examples Subfamily(“ herpesvirinae ) 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. epidemiology 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 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. sTRUCTURE Virions are spherical, 150-200nm in diameter HSV-1 and HSV-2 contains an envelope- derived from the nuclear membrane of the infected cell; contains viral glycoproteins a tegument—an amorphous layer of proteins that surround the capsid an icosahedral capsid Genome (linear, a large double-stranded viral DNA; encoding 70-200 proteins)

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

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

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

12. 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)

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

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

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

16. Clinical significance 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. 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

18. 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

19. TREatment and prevention 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. references Harvey RA, Champe PC, Fischer BD. Lippincott’s I llustrated Reviews: Microbiology. 2 nd 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

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