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Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
Herpes Simplex I and II
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Herpes Simplex I and II

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Herpes Simplex I and II

Herpes Simplex I and II

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  • 1. Herpes Simplex I and II Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  • 2. Herpesviridae • The Herpesviridae are a large family of DNA viruses that cause diseases in animals, including humans The family name is derived from the Greek word herpein ("to creep"), referring to the latent, re-occurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections. Dr.T.V.Rao MD 2
  • 3. Herpes Viruses DNA group • Most important Human Pathogens • Wide Host cell range • Life Long Infection – Periodic reactivation • Immunocompromised • Large number of genes, • Some viruses susceptible to treatment. Dr.T.V.Rao MD 3
  • 4. • Alphaherpesvirinae – Herpes simplex virus type 1 HSV-1 – Herpes simplex virus type 2 HSV-2 – Varicella-zoster virus VZV • Betaherpesvirinae – cytomegalovirus CMV – Human herpesvirus type 6 HHV-6 – Human herpesvirus type 7 HHV-7 • Gammaherpesvirinae – Epstein-Barr virus EBV CLASSIFICATION (Human pathogens) Dr.T.V.Rao MD 4
  • 5. Infecting Humans. Herpes Simplex virus 1 and 2 Varicella Zoster Viruses Cytomegalovirus virus Epstein Barr virus Human Herpes viruses 6, 7. Kaposi's Sarcoma associated Viruses Dr.T.V.Rao MD 5
  • 6. Properties of Herpes Viruses. • Spherical in Shape • Icosahedral 150 to 200 nm in size • Genome – Double stranded DNA Linear • Envelope contains Glycoprotein's Dr.T.V.Rao MD 6
  • 7. Out Standing Characteristics • Encode many enzymes. • Cause Latent Infections. • Indefinite persistence. • Relation in Immunocompromised • Relation to Cancers. Dr.T.V.Rao MD 7
  • 8. Herpes Virus Dr.T.V.Rao MD 8
  • 9. Classification of Human Herpes virus • Subfamily – Alpha Neurons Herpes simplex 1,2 Dr.T.V.Rao MD 9
  • 10. Subfamily Beta Glands and Kidney Cytomegalovir us Lymphoid tissues Herpes 6,7 Dr.T.V.Rao MD 10
  • 11. Subfamily - Gamma • Lymphoid tissue ( Herpes 5 ) Epstein Barr virus Kaposi Sarcoma (Virus Herpes 8) Dr.T.V.Rao MD 11
  • 12. Intranuclear infection of infected cells Dr.T.V.Rao MD 12
  • 13. Herpes Virus Replication Replicates in Host Cell Nucleus Form Cow dry A Type inclusion bodies. More than 50 different types proteins in infected cell. Large number of enzymes in DNA synthesis Dr.T.V.Rao MD 13
  • 14. Herpes Simplex 1 and 2 Dr.T.V.Rao MD 14
  • 15. Human Herpes Virus 1 and 2 • They are also called Human Herpes Virus 1 and 2 (HHV-1 and HHV-2) and are neurotropic and neuroinvasive viruses; they enter and hide in the human nervous system, accounting for their durability in the human body. HSV-1 is commonly associated with herpes outbreaks of the face known as cold sores or fever blisters, whereas HSV-2 is more often associated with genital herpes. Dr.T.V.Rao MD 15
  • 16. Herpes 1and 2 • HSV-1 is commonly associated with herpes outbreaks of the face known as cold sores or fever blisters, whereas HSV-2 is more often associated with genital herpes. Dr.T.V.Rao MD 16
  • 17. Infections in Humans.( Herpes Simplex 1 and 2 ) • Wide spread in Humans • Broad Host Ranges. • Replicate in Many types of Cells. • Produce cytolytic effects • Most Common Diseases. • Gingival stomatitis, Keratoconjunctivitis • Encephalitis Genital diseases, • New Born Infections, Latent Infections in Nerve Cells, • Recurrence. Dr.T.V.Rao MD 17
  • 18. HERPES SIMPLEX VIRUS (HSV) • HSV 1 infect the upper part of the body - mouth and the face • HSV 2 infect the lower part of the body - genital infections • There is little cross protection • Therefore, one can get both the infections Dr.T.V.Rao MD 18
  • 19. Properties of Herpes Simplex VirusesProperties of Herpes Simplex Viruses Type 1 andType 1 and 22 • Similar in Organization • Restriction Enzyme Differentiates • H S V 1 contact with Saliva. • H S V 2 Sexual • Maternal infection ( Genital Infection spreads to New Born ) • Replicates in 8-16 hours. Dr.T.V.Rao MD 19
  • 20. Out characters of Herpes group of viruses • Out standing characters • 1 Encode many enzymes • Latent infections are common • Persist indefinitely in infected hosts. • Frequent reactivation in infected hosts • Some care cancer causing. Dr.T.V.Rao MD 20
  • 21. HSV 1 differs from HSV 2 • HSV 1 • Monoclonals differs • On CAM HSV 2 larger pocks • Replicate well on Chick embryo fibroblast • More neurovirulent • Type 2 strains are more antiviral resistant • Restriction endonulease analysis diffentiates • HSV 2 • Monoclonal's differentiate • Smaller • No • Lesser • Lesser Dr.T.V.Rao MD 21
  • 22. Virus Grows in the following. • Primary and Continues Cell lines. • Monkey and Rabbit Kidney, • Human Amnion • Syncytial formation and Giant cell formations • Multiplies in Chorio Allontoic membrane • Monoclonal Antibodies differentiates Type 1 and 2 types. Dr.T.V.Rao MD 22
  • 23. Sources of infection - Saliva - Skin lesions -Oropharyngeal lesions - Carriers Dr.T.V.Rao MD 23
  • 24. Pathogenesis. • Most Common Human Viral Infection • Causes catalytic effect causes the necrosis of cells. • Infects Skin and Mucous membrane • Cowdry type A inclusions are produced • Multinucleated Giant cells are demonstrated Dr.T.V.Rao MD 24
  • 25. Pathogenesis Entry by skin or mucous membranes viral multiplication sensory nerve lysis of cells root ganglia vesicles latency ulcers REACTIVATION COLD FEVER SURGERY UNKNOWN Dr.T.V.Rao MD 25
  • 26. TransmissionTransmission • Close contact • Skin and epithelial contact, • Defects in Mucosal membrane • Multiples Locally, • Enters through cutaneous nervefibers • Intraaxonally to Ganglion • Centrifugal Migration • Recurrent manifestation in Skin and Mucosa. Dr.T.V.Rao MD 26
  • 27. Predisposition of Latent Infection in • Ganglion • Trigeminal HSV 1 • Sacral HSV 2 • Immunity. • Cell Mediated ( CMI ) • Predisposing Factors Axonal Injury Physical and Emotional stress U V light 80% Adults harbour Antibodies to HSV Dr.T.V.Rao MD 27
  • 28. Dr.T.V.Rao MD 28
  • 29. Dr.T.V.Rao MD 29
  • 30. Clinical Manifestations • Oropharyngeal Disease Buccal Gingival Mucosa Incubation 3 to 5 days • May last for 2-3 weeks • Gingvo stomatitis Sub mandibular lymphadenopathy • Present with painful ulcers. Dr.T.V.Rao MD 30
  • 31. Recurrent Blisters in Herpes simplex 1 Dr.T.V.Rao MD 31
  • 32. Herpes lesions in the oral cavity Dr.T.V.Rao MD 32
  • 33. Eye Infections and Genital Infections. • Corneal ulcerations pacifications • Blindness • Vesiculo ulcerative Lesions penis, Cervix, Vulva and Vagina. Manifest with Painful lesions. Dr.T.V.Rao MD 33
  • 34. Herpes simplex 1 infecting eye Dr.T.V.Rao MD 34
  • 35. Herpes 2 producing Genital Lesions Dr.T.V.Rao MD 35
  • 36. Skin InfectionsSkin Infections • Infect abrasions • Dentists, ( Herpetic Whitlow) Health care workers, • Eczema , Burns Dr.T.V.Rao MD 36
  • 37. Neonatal Herpes. • In Uterus • At Birth • After Birth. • Delivery By Caesarean Section Reduces the Infection Dr.T.V.Rao MD 37
  • 38. Neonatal Infection – Normal delivery Dr.T.V.Rao MD 38
  • 39. OtherManifestations. • Meningitis, • Encephalitis • Multi organ Involvement • Increased incidence in Immune compromised AIDS, • Haematological Malignancies. Dr.T.V.Rao MD 39
  • 40. Recurrent infections in HSV 1 andRecurrent infections in HSV 1 and 22 Dr.T.V.Rao MD 40
  • 41. Immunity • Mothers Ig G protects for 6 months. • Primarily Ig M Later Ig g produced. Main Participants in Immunity. C M I and Killer Cells and Interferon play major role in immunity Dr.T.V.Rao MD 41
  • 42. Laboratory Diagnosis • Microscopy, • Antigen Detection • DNA detection PCR. • Viral Isolation. • Serology Dr.T.V.Rao MD 42
  • 43. Dr.T.V.Rao MD 43
  • 44. Microscopy, • Tzanck Smear • Intranuclear Type A Inclusion Bodies • Electron Microscopy • Fluorescent Antibody Dr.T.V.Rao MD 44
  • 45. Specimens for Diagnosis. •Saliva. •CSF •Vesicle fluid. Dr.T.V.Rao MD 45
  • 46. Viral Isolation • Chick embryo • In Tissue Cultures Primary Embryonic Kidney Human Amnion Dr.T.V.Rao MD 46
  • 47. Serology, •ELISA Test • Neutralization Tests • Complement Fixation Tests Dr.T.V.Rao MD 47
  • 48. Chemotherapy • Idoxuridine used topically in eye and skin infections – first successful antiviral agent. • Acyclovir and vidarabine helps in systemic infections • Other Drugs – Valaciclovir, Famiciclovir, • Orally effective • Foscarnet. Dr.T.V.Rao MD 48
  • 49. Epidemiology. • World Wide Distribution • HSV 1 early in life 6 months to 3 years. • 70% to 90% Adults have Antibodies • Poor Living Conditions • HSV 2 Sexually transmitted. • Risk to mother and foetus • Abortions < 20 weeks gestation • HSV 2 increases predisposition to HIV infection Dr.T.V.Rao MD 49
  • 50. • Programme Created by Dr.T.V.Rao MD for Medical and Paramedical Students for Global education on Infectious Diseases • Email • doctortvrao@gmail.com Dr.T.V.Rao MD 50

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