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Herpesviruses Herpes simplex I & II (cold sores, genital herpes) Varicella zoster (chicken pox, shingles) Cytomegalovirus (microcephaly, infectious mono)

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Presentation on theme: "Herpesviruses Herpes simplex I & II (cold sores, genital herpes) Varicella zoster (chicken pox, shingles) Cytomegalovirus (microcephaly, infectious mono)"— Presentation transcript:

1 Herpesviruses Herpes simplex I & II (cold sores, genital herpes) Varicella zoster (chicken pox, shingles) Cytomegalovirus (microcephaly, infectious mono) Epstein-Barr virus (mononucleosis, Burkitt’s lymphoma) Human herpesvirus 6 & 7 (Roseola) Human herpesvirus 8 (Kaposi’s sarcoma) D- virology

2 Cold Sores

3 Zoster

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6 Roseola

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8 Virus Subfamily Disease Site of Latency Herpes Simplex Virus I α Orofacial lesions Sensory Nerve Ganglia Herpes Simplex Virus IIα Genital lesions Sensory Nerve Ganglia Varicella Zoster Virusα Chicken Pox Sensory Nerve Ganglia Recurs as Shingles Cytomegalovirusβ Microcephaly/Mono Lymphocytes Human Herpesvirus 6β Roseola Infantum CD4 T cells Human Herpesvirus 7β Roseola Infantum CD4T cells Epstein-Barr Virusγ Infectious Mono B lymphocytes, salivary Human Herpesvirus 8γ Kaposi’s Sarcoma Kaposi’s Sarcoma Tissue Human Herpesviruses

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10 Herpes Simplex Virus Prototype of group

11 Virion stabiliy Enveloped virus Sensitive to dessication Easily inactivated by detergents and lipid solvents

12 Virion structure Enveloped, spherical virion Icsoahedral capsid nm >12 virally encoded glycoproteins Tegument proteins

13 Genome structure Linear double-stranded DNA kb Genetic complexity -- isomers

14 Genome structure Linear double-stranded DNA kb Genetic complexity # of genes

15 Replication Penetration by fusion with plasma membrane Nuclear site of replication 80 or so viral proteins are expressed in regulated fashion: IE - immediate early E - Early L - Late Capsids assemble in nucleus and bud through nuclear membrame

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17 Life-long Latency

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20 Three manifestations of HSV latency Key Feature: there is a wide spectrum of clinical presentations Some individuals (5 - 10%) have frequent clinical reactivation Most individuals reactivation is clinically asymptomatic In ALL cases, virus is shed

21 Transmission of HSV-1 and HSV-2 Skin to skin contact The virus does not penetrate intact skin Mild abrasion or chapping of skin can allow infection

22 Tissue tropism of HSV-1 and HSV-2 HSV-1: Causes 95% of orofacial herpes (remainder caused by HSV-2) Causes % of primary genital herpes (but seldom recurs there) HSV-2: Causes primary and recurrent genital herpes infections May cause primary oral herpes but, like HSV-1 in genital area, it seldom recurs there

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28 Eczema/Herpes

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31 Herpes Simplex Virus type 2 Infects the genital tract Is sexually transmitted Complicates childbirth

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34 Diagnosis of Herpes Simplex Virus Infections: Viral Culture Tzanck prep Culture with monoclonal antibody staining Serology Polymerase chain reaction (PCR)

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36 Spectrum of HSV recurrence Asymptomatic shedding Shedding with clinically apparent lesions

37 A study of HSV-2 recurrence in women

38 Asymptomatic Shedding of HSV Occurs in both HSV-1 and HSV-2 The only form of shedding in 1/2 to 2/3 of infected patients Involves low amounts of virus Accounts for most transmissions to infected contacts and neonates Is not completely suppressed by acyclovir

39 2/3

40 of the acquisitions of genital herpes come from clinically asymptomatic partners

41 Alpha HerpesvirusesSite of Latency Herpes Simplex Virus type 1Sensory neurons Herpes Simplex Virus type 2Sensory neurons Varicella Zoster VirusSensory neurons Beta Herpesviruses CytomegalovirusLymphocytes Human Herpesvirus 6CD4 T cells Human Herpesvirus 7CD4 T cells Gamma Herpesviruses Epstein-Barr VirusB lymphocytes Human Herpesvirus 8Sarcoma tissue

42 Two Unique Features of VZV: Airborne spread or skin to skin contact More severe infection if primary infection occurs as an adult

43 Complications of Varicella Reye’s Syndrome Bacterial Superinfection of lesions (more common in younger patients) Varicella pneumonia Neonatal varicella -- disseminated, 30% mortality

44 Varicella Pneumonia AgeFatalities per 100,000 <

45 Varicella patients at risk ADULTS PREGNANCY (3rd trimester) IMMUNOCOMPROMISED The mortality rate for varicella pneumonia in leukemic children receiving chemotherapy is 1,000 times higher than in healthy children. Note: Children with isolated agammaglobulinemia are not at risk!

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48 Neonatal Varicella

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51 Zoster

52 Varicella Vaccine Prevents % of chickenpox occurrence Greatly reduces the severity in the rest Attenuated virus Can still establish latency and reactivate Question: How long will immunity last?

53 Complications of Zoster Postherpetic Neuraligia Affects % of zoster patients over 50 Pain may persist for months or even years

54 Alpha HerpesvirusesSite of Latency Herpes Simplex Virus type 1Sensory neurons Herpes Simplex Virus type 2Sensory neurons Varicella Zoster VirusSensory neurons Beta Herpesviruses CytomegalovirusLymphocytes Human Herpesvirus 6CD4 T cells Human Herpesvirus 7CD4 T cells Gamma Herpesviruses Epstein-Barr VirusB lymphocytes Human Herpesvirus 8Sarcoma tissue

55 In utero Early childhood (saliva, etc.) Venereal in young adults Blood transfusion Organ transplantation Transmission of CMV

56 Clinical Manifestations of CMV Normal Host: Asymptomatic in the majority of cases Infectious mononucleosis Congenital CMV: Primary CMV infection in 3rd trimester of pregnancy of a seronegative mother Immunocompromised: Pneumonitis in bone marrow transplants Retinitis in AIDS patients

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60 Alpha HerpesvirusesSite of Latency Herpes Simplex Virus type 1Sensory neurons Herpes Simplex Virus type 2Sensory neurons Varicella Zoster VirusSensory neurons Beta Herpesviruses CytomegalovirusLymphocytes Human Herpesvirus 6CD4 T cells Human Herpesvirus 7CD4 T cells Gamma Herpesviruses Epstein-Barr VirusB lymphocytes Human Herpesvirus 8Sarcoma tissue

61 EBV Mono

62 EBV mononucleosis

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65 Heterophile Antibody (IM) EBV induces many cellular proteins An antibody against one of these new celular proteins is able to agglutinate sheep red blood cells EBV monucleosis is heterophile antibody positive CMV mono is heterophile antibody negative

66 IM Serology VCA IgM rises and falls early in infection VCA IgG antibodies persist EBV mononucleosis is heterophile antibody positive CMV mononucleosis is heterophile antibody negative; no antibodies to VCA of EBV

67 Antiviral therapy

68 Deoxyguanosine AcyclovirGanciclovir RibavirinVidarabineDeoxyadenosine

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