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What is new on HHV 6, 7, 8 infections?

What is new on HHV 6, 7, 8 infections?. Henry J.C. de Vries Dermatology Academic Medical Centre University of Amsterdam The Netherlands. HHV 6 and 7 Acute/primary infection. Until 1986, 5 herpes viruses new human herpes viruses (HHV) HHV-6 and -7

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What is new on HHV 6, 7, 8 infections?

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  1. What is new on HHV 6, 7, 8 infections? Henry J.C. de Vries Dermatology Academic Medical Centre University of Amsterdam The Netherlands

  2. HHV 6 and 7Acute/primary infection • Until 1986, 5 herpes viruses • new human herpes viruses (HHV) • HHV-6 and -7 • both members of the Roseolovirus genus of the β-herpesviruses. • T-lymphotropic but can infect other cell types • primary infections are associated with roseola infantum (a.k.a. exanthem subitum or 6th disease)

  3. HHV 6 and 7Reactivation/endogenous infection • HHV lifetime infection • ubiquitous • reactivation • HHV-7 and HHV-6 reactivation associated with pityriasis rosea (Drago, 1997 and Yasukawa, 1999) • Debated • Innocent bystander? • Multiple agents?

  4. DRESS syndrome C Goldberg, UCSD and Ascend Media Healthcare • Drug Reaction Eosinophilia and Systemic side effect Syndrome (DRESS) • HHV 6 reactivation (Deschamps 2001) • exanthema,hepatitis, colitis lymphadenopathy, eosinophilia, fever • EBV and amoxicillin associated drug rash in mononucleosis infectiosa

  5. Drugs that can cause DRESS Ascend Media Healthcare

  6. Is lichen planus caused by a viral infection? • Highest prevalence in over 50 year olds • Self limiting • Normally one episode • Association with HCV (Mokni 1991) • The epidemiological association is not strong (Imhof, 1997)

  7. Electron microscopy of lichen planus lesional skin lichen planus lichen planus reference herpes virus lichen planus

  8. Study outline • Objective: • To find candidate herpes viruses associated with lichen planus. • Methods: • Lichen planus patients (pathologically confirmed, n=18) • Intra patient comparison of skin biopsies: • lesional vs. non-lesional • before vs. after remission • Inter patient comparison of skin biopsies: • psoriasis patients (lesional, n=11, and non-lesional, n=3) • normal skin (redundant after breast reduction, n=4) • DNA of HSV1 and 2, VZV, CMV, EBV (commercial PCR ) • DNA of HHV 6, -7 and -8 (“in house” nested PCR)

  9. Herpes DNA analysis • All samples were free of HSV-1, HSV-2, VZV, CMV and HHV-8 DNA. • EBV DNA was detected in 2/15 lichen planus lesional samples. * p=0,06, # p=0,05 p values calculated with McNemar test

  10. HHV-7 protein in lesional lichen planus lesional skin non-lesional skin de Vries et al. Br J Dermatol 154: 361, 2006 Immunohistochemical detection viral protein (HHV-7) • tegument protein pp85 (Advanced Biotechnologies) • positive cells/mm2 • (non) lesional lichen planus, psoriasis, normal skin

  11. HHV-7 protein positive cells psoriasis lesional lichen planus normal skin non lesional lichen planus - de Vries et al. Br J Dermatol 154: 361, 2006

  12. plasmacytoiddendritic cells (CD123+) associated with viral infection in lesional lichen planus lesional skin non-lesional skin CD123 positive cells(red), endothelial cells (blue) de Vries et al. Br J Dermatol 154: 361, 2006

  13. HHV-7 replicates in plasmacytoid dendritic (BDCA-2+) cells lesional lichen planus lesional lichen planus HHV-7/BDCA-2 double staining HHV-7/CD-3 double staining de Vries et al. Arch Dermatol Res 299: 213, 2007

  14. HHV-7 DNA and protein positive cellsbefore and after lichen planus remission before treatment after remission de Vries et al. Arch Dermatol Res 299: 213, 2007

  15. Conclusions • herpes virus like particles reside in lesional lichen planus skin • not HSV1, HSV2, CMV, VZV, HHV6 or HHV8 DNA • HHV-7 replicates in lesional lichen planus, not in non-lesional lichen planus, psoriatic or normal skin • HHV-7 replicates in plasmacytoid dendritic cells • HHV-7 replication in lichen planus stops after remission

  16. HHV-7 and lichen planus hypothesis Skin Immune System, Bos JD ed. 3rd edition, 2005 HHV-7 (subclinical) primo infection during childhood HHV-7 reactivation in adult life replication in basal keratinocytes/dermal lymphocytes presentation (plasmacytoid) dendritic cells inflammatory T lymphocytic response destruction of the basal layer

  17. How to prove a causative viral association? viral “innocent bystander” Koch’s postulates geographic variation in viral distribution differences in laboratory protocols virus-virus interactions association with skin diseases? or candidates in search of a disease?

  18. Acknowledgement • Jan van Marle • electronmicroscopy • Jan Weel • virology • Fokla Zorgdrager and Marion Cornelissen • molecular biology • Daisy Picavet and Marcel Teunissen • immunohistochemistry

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