Jiabing Chen

Publications (2)6.22 Total impact

• Source

  Available from: Kevin C Kain

  Article: Dynamic changes in clinical features and cytokine/chemokine responses in SARS patients treated with interferon alfacon-1 plus corticosteroids.

  Sarah E Ward, Mona R Loutfy, Lawrence M Blatt, Katharine A Siminovitch, Jiabing Chen, Anna Hinek, Bryan Wolff, Dieu H Pham, Hassan Deif, Elizabeth A LaMere, Kevin C Kain, Gabriella A Farcas, Patti Ferguson, Mary Latchford, Gary Levy, Liasum Fung, James W Dennis, Enoch K Y Lai, Eleanor N Fish
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  ABSTRACT: Severe acute respiratory syndrome (SARS), caused by a novel coronavirus, emerged in early 2003 as a major international health crisis. We report on serum cytokine levels, viral load and clinical parameters over the course of the disease in a cohort of nine adult SARS patients treated with steroids and interferon alfacon-1 at North York General Hospital in Toronto, Ontario. Considerable variation among SARS patients with respect to circulating viral load and patterns of SARS-CoV-evoked cytokine responses was recorded. No single cytokine profile was observed in all patients, yet serum concentrations of interferon (IFN)-gamma, interleukin (IL)-10, CXCL10, CCL5 and CXCL8 were found to be elevated above normal levels during the course of the disease in all patients. Expression levels for IL-10, IFN-gamma and CXCL10 consistently peaked within 4 days of peak viral load. IL-12p70, IL-4 and tumour necrosis factor-alpha concentrations were consistently highest within 5 days of peak viral load. These results suggest that elevated levels of inflammatory cytokines are sensitive correlates of disease severity, including lung abnormalities and viral load in serum, and may provide a tool for monitoring disease progression in affected individuals.
  Antiviral therapy 02/2005; 10(2):263-75. · 3.16 Impact Factor
• Article: Diversity and relatedness among the type I interferons.

  Jiabing Chen, Ehtesham Baig, Eleanor N Fish
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  ABSTRACT: Type I interferons (IFNs) include the IFN-alpha family of subtypes, IFN-beta, IFN-omega, IFN-tau, IFN-kappa, IFN-lambda, and IFN-zeta. IFN genes lack introns and encode secretory signal peptide sequences that are proteolytically cleaved prior to secretion from the cell. In contrast to the approximately 50% amino acid sequence identity among the human IFN-alpha subtypes, human IFN-alphas share approximately 22% identity with human IFN-beta and 37% identity with human IFN-omega. Many of the conserved residues among the type I IFNs are implicated in receptor recognition and structural integrity. This report provides an update on the gene annotations for the mouse and human IFN gene clusters on chromosome 4 and 9, respectively, with accompanying amino acid sequence alignments. Based on sequence identities, a phylogenic tree analysis for the different mammalian Type I IFNs is also presented, showing the high degree of relatedness among these IFNs. Notably, sequence alignment of the different human and mouse IFN promoter regions reveals different signature patterns for transcription factor binding sites, implying different inducers might differentially activate the transcription of the different IFNs.
  Journal of Interferon & Cytokine Research 01/2005; 24(12):687-98. · 3.06 Impact Factor