Selected article for: "infection initial stage and initial stage"

Author: Matsuda, Shunji; Kiyota, Naoko; Yoshizumi, Masakazu; Noda, Masahiro
Title: Alteration in serum levels of inflammatory cytokines during parainfluenza virus type 1 infection in patients with severe multiple disabilities.
  • Cord-id: 7fv1o3pc
  • Document date: 2014_1_1
  • ID: 7fv1o3pc
    Snippet: An epidemic of parainfluenza virus type 1 (PIV1) infection occurred in a hospital ward housing patients with severe motor and intellectual disabilities. Twenty-three infected patients exhibited persistent high fever for 4-16 days and decreased lymphocyte counts. One-half of the symptomatic patients had increased blood monocyte counts and the other half progressed to bronchitis or pneumonia. We also compared levels of 27 cytokines in the sera of 21 patients during the acute and normal phases of i
    Document: An epidemic of parainfluenza virus type 1 (PIV1) infection occurred in a hospital ward housing patients with severe motor and intellectual disabilities. Twenty-three infected patients exhibited persistent high fever for 4-16 days and decreased lymphocyte counts. One-half of the symptomatic patients had increased blood monocyte counts and the other half progressed to bronchitis or pneumonia. We also compared levels of 27 cytokines in the sera of 21 patients during the acute and normal phases of infection. Cytokine levels were measured with a bead immunoassay performed using the Luminex Multiplex System. Serum levels of interleukin (IL)-1Ra, C-C-motif chemokine (CCL) 2, and C-X-C-motif chemokine (CXCL) 10 significantly increased during the acute phase. In contrast, the serum level of CXCL8 decreased slightly. These results suggest the involvement of monocytes/macrophages and respiratory epithelial cells in the initial stage of PIV1 infection. A previous report using nasal wash samples also found a significant increase in levels of CXCL10 during the acute phase. Hence, CXCL10 may be a useful marker of a cytokine storm produced upon viral infection. However, alterations in levels of IL-1Ra, CCL2, and other cytokines differed between the 2 studies, suggesting that the cytokine profile produced systemically at viral infection is different from that produced at mucosal sites. Further analysis is required to clarify the mechanisms underlying cytokine production during PIV1 infections.

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