title: Severe and persistent depletion of circulating plasmacytoid dendritic cells in patients with 2009 pandemic H1N1 infection.
abstract: BACKGROUND
  Dysregulation of host immune responses plays a critical role in the pathogenesis of severe 2009 pandemic H1N1 infection. Whether H1N1 virus could escape innate immune defense in vivo remains to be investigated. The aim of this study was to evaluate the pattern of innate immune response during human 2009 H1N1 infection. We performed the enumeration of circulating myeloid dendritic cells (mDC) and plasmacytoid DC (pDC) in blood from patients with H1N1 pneumonia shortly after the onset of symptoms and during follow-up at different intervals of time. The analysis of CD4 and CD8 count, CD38 T-cell activation marker and serum cytokine/chemokine plasma levels was also done.
  
  
  RESULTS
  Blood samples were collected from 13 hospitalized patients with confirmed H1N1-related pneumonia at time of admission and at weeks 1, 4, and 16 of follow-up. 13 healthy donors were enrolled as controls. In the acute phase of the disease, H1N1-infected patients exhibited a significant depletion in both circulating pDC and mDC in conjunction with a decrease of CD4 and CD8 T cell count. In addition, we found plasmatic hyperproduction of IP-10 and RANTES, whereas increase in T-cell immune activation was found at all time points. When we assessed the changes in DC count over time, we observed a progressive normalization of mDC number. On the contrary, H1N1-infected patients did not achieve a complete recovery of pDC count as values remained lower than healthy controls even after 16 weeks of follow-up.
  
  
  CONCLUSIONS
  H1N1 disease is associated with a profound depletion of DC subsets. The persistence of pDC deficit for several weeks after disease recovery could be due to H1N1 virus itself or to a preexisting impairment of innate immunity.
authors.affiliation: Infectious Diseases Unit, Sapienza University, Polo Pontino, SM Goretti Hospital, Latina, Italy.
authors.forename: Miriam
authors.initials: M
authors.lastname: Lichtner
authors.forename: Claudio M
authors.initials: CM
authors.lastname: Mastroianni
authors.forename: Raffaella
authors.initials: R
authors.lastname: Rossi
authors.forename: Gianluca
authors.initials: G
authors.lastname: Russo
authors.forename: Valeria
authors.initials: V
authors.lastname: Belvisi
authors.forename: Raffaella
authors.initials: R
authors.lastname: Marocco
authors.forename: Claudia
authors.initials: C
authors.lastname: Mascia
authors.forename: Cosmo
authors.initials: C
authors.lastname: Del Borgo
authors.forename: Fabio
authors.initials: F
authors.lastname: Mengoni
authors.forename: Ilaria
authors.initials: I
authors.lastname: Sauzullo
authors.forename: Gabriella
authors.initials: G
authors.lastname: d'Ettorre
authors.forename: Claudia
authors.initials: C
authors.lastname: D'Agostino
authors.forename: Anna P
authors.initials: AP
authors.lastname: Massetti
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Vullo
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology / Q000821:virology; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology*; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D022423:Myeloid Cells / Q000276:immunology / Q000473:pathology / Q000821:virology; D009976:Orthomyxoviridae Infections / Q000453:epidemiology* / Q000276:immunology / Q000821:virology; D058873:Pandemics; D012720:Severity of Illness Index
chemical_list: D018925:Chemokines; D016207:Cytokines