title: Human herpesvirus 7 in patients with pityriasis rosea. Electron microscopy investigations and polymerase chain reaction in mononuclear cells, plasma and skin.
abstract: BACKGROUND
  Clinical evidence suggests a viral etiology for pityriasis rosea (PR).
  
  
  OBJECTIVE
  To evaluate human herpesvirus (HHV)-6 and HHV-7 as candidates for the etiology of PR.
  
  
  METHODS
  Blood and skin tissue from 12 patients with acute PR, and 12 patients with other dermatoses were studied, as well as blood samples from 25 healthy persons. Serum interferon (IFN)-alpha and IFN-gamma were analyzed by ELISA. Analysis of morphological changes in cocultured peripheral blood mononuclear cells (PBMC) and electron microscopy (EM) to identify viral particles were performed. Polymerase chain reaction (PCR) with specific primers for HHV-6 and HHV-7 DNA sequences was performed on the plasma and PBMC of patients and healthy controls and on the skin of patients with PR and other skin diseases.
  
  
  RESULTS
  PR plasma contained detectable IFN-alpha and IFN-gamma, whereas plasma from controls did not. PBMC from PR patients showed ballooning cells and syncytia after 7 days in culture whereas PBMC from controls and recovered PR patients did not. This cytopathic effect was also documented in a PR patient who relapsed and in Sup-T1 cell cultures inoculated with the cell-free supernatant from centrifuged cultured PBMC; in this supernatant, herpesvirus, virions were detected by EM, PCR identified HHV-7 DNA in PBMC, plasma and skin from all patients with active PR and in the PBMC only of 5 patients tested 10-14 months later. Weaker signals of HHV-7 DNA were detected in PBMC of 11 controls, but not in their plasma. Skin was negative for HHV-7 in all control specimens.
  
  
  CONCLUSIONS
  Although the detection of HHV-7 DNA in PBMC and tissues does not prove directly a causal role, HHV-7 DNA in cell-free plasma corresponds to active replication which supports a causal relationship. We propose that PR is a clinical presentation of HHV-7 reactivation.
authors.affiliation: Institute of Dermatology, University of Genoa, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Drago
authors.forename: E
authors.initials: E
authors.lastname: Ranieri
authors.forename: F
authors.initials: F
authors.lastname: Malaguti
authors.forename: M L
authors.initials: ML
authors.lastname: Battifoglio
authors.forename: E
authors.initials: E
authors.lastname: Losi
authors.forename: A
authors.initials: A
authors.lastname: Rebora
mesh_terms: D002478:Cells, Cultured; D017077:Culture Media, Conditioned; D017931:DNA Primers; D004279:DNA, Viral / Q000032:analysis / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D005500:Follow-Up Studies; D015726:Giant Cells / Q000473:pathology; D006566:Herpesviridae Infections / Q000097:blood / Q000473:pathology; D015654:Herpesvirus 6, Human / Q000235:genetics / Q000302:isolation & purification; D016199:Herpesvirus 7, Human / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D016898:Interferon-alpha / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000473:pathology; D008854:Microscopy, Electron; D017515:Pityriasis Rosea / Q000097:blood / Q000473:pathology / Q000821:virology*; D016133:Polymerase Chain Reaction; D012008:Recurrence; D012867:Skin / Q000473:pathology / Q000821:virology; D012871:Skin Diseases / Q000097:blood / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000473:pathology; D014766:Viremia / Q000821:virology; D014771:Virion / Q000648:ultrastructure; D014775:Virus Activation; D014779:Virus Replication
chemical_list: D017077:Culture Media, Conditioned; D017931:DNA Primers; D004279:DNA, Viral; D016898:Interferon-alpha; D007371:Interferon-gamma