title: Severe herpes virus (HSV-2) infection in two patients with myelodysplasia and undetectable NK cells and plasmacytoid dendritic cells in the blood.
abstract: BACKGROUND
  How the immune system contains herpes simplex virus (HSV) infections is partly understood. T cells from infected persons proliferate in response to HSV antigens in vitro and may control local relapse rather than primary infection. NK cells have been involved in the control of experimental infections. A potentially important, as yet unexplored, population of interest might be the plasmacytoid dendritic cells (PDC), which contrary to monocytes, produce very high amounts of the major antiviral molecules, type-I interferon (IFN) following interaction with HSV.
  
  
  OBJECTIVE
  Measure type-I IFN production, PDC, and NK cells in patients with unusually severe HSV infections.
  
  
  METHODS
  Two female patients of 33- and 50-year-old, respectively were referred because of severe disseminated HSV2 infection and myelodysplastic marrow. One patient had leukaemia and a primary HSV2 infection whereas the other had systemic lupus erythematosus (SLE) and a chronic HSV2 infection. The following studies were performed at various time points over 18 months: analysis of the lymphocytes and PDC subsets phenotype, lymphocyte proliferation assays to recall antigens; generation of NK cells in cultures, and production of type-I IFN in serum and by HSV-infected and by sendai virus (SV)-infected blood cells.
  
  
  CONCLUSIONS
  PDC and NK cells were undetectable in the blood of both patients and NK cells could not be generated in culture at the time of ongoing infection. PBMC failed to produce IFN after infection with HSV contrasting with a normal T cell proliferation to HSV antigens in patient 1. Our observation suggests that innate immunity, through NK cells and PDC may control HSV infections, and together with IFN-producing capacity, should be investigated in patients with unusually severe HSV infections.
authors.affiliation: Laboratoire d'Imunologie Hôpital de la Pitié, Paris, France. ali.dalloul@inserm.ipsc.u-psud.fr
authors.forename: Ali
authors.initials: A
authors.lastname: Dalloul
authors.forename: Eric
authors.initials: E
authors.lastname: Oksenhendler
authors.forename: Olivier
authors.initials: O
authors.lastname: Chosidow
authors.forename: Patricia
authors.initials: P
authors.lastname: Ribaud
authors.forename: Guylaine
authors.initials: G
authors.lastname: Carcelain
authors.forename: Sylvie
authors.initials: S
authors.lastname: Louvet
authors.forename: Patrice
authors.initials: P
authors.lastname: Massip
authors.forename: Pierre
authors.initials: P
authors.lastname: Lebon
authors.forename: Brigitte
authors.initials: B
authors.lastname: Autran
mesh_terms: D000328:Adult; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology*; D005260:Female; D006561:Herpes Simplex / Q000276:immunology* / Q000503:physiopathology / Q000821:virology; D018258:Herpesvirus 2, Human; D006801:Humans; D016130:Immunophenotyping; D007370:Interferon Type I / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology / Q000473:pathology*; D008213:Lymphocyte Activation; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000150:complications*
chemical_list: D007370:Interferon Type I