Castel, P. Kok, G.L.A. Reijnierse, G.A.E Ponjee, M. Herruer, R.C. Eijkman-Rotteveel, P.W. Schenk and their personnel for their help in achievement and storage of the plasma samples. These data were presented in part at the 47th Annual Meeting of the Infectious sellekchem Diseases Society of America 2009, October 29 to November 1, Philadelphia, PA, Abstract LB-26. This study was partly supported by an unrestricted grant of the Bronovo Hospital Research Foundation.
Originating from Mexico and spreading initially in the United States and Canada, a novel influenza A(H1N1) virus infection (nvA(H1N1)) of swine origin spread globally during spring 2009 to mid-February 2010. Rates of hospitalization and death have varied widely according to country [1].
Among hospitalized patients 9 to 31% have been admitted to intensive care units (ICUs) where the rate of death was 14 to 46%[2-6].In Romania the pandemic wave lasted from September 2009 to February 2010, reaching a peak in December. The Romanian Ministry of Health reported 7,008 confirmed cases of nvA(H1N1) influenza, the death rate being 1.9%.Primary influenza pneumonia had a high mortality rate during pandemics not only in immune-compromised individuals and patients with underlying co-morbid conditions, but also in young healthy adults [7].During nvA(H1N1) virus infection, experimental and clinical studies have identified dysregulated systemic inflammation as an important pathogenetic mechanism correlating with severity and progression of the disease [8,9]. The role of most immune responses in controlling and clearance of H1N1 influenza A or its contribution to severe respiratory compromise is not well known.
To and colleagues found higher plasma levels of proinflammatory cytokines and chemokine in the group of patients with acute respiratory distress syndrome (ARDS) caused by viral A(H1N1) influenza, throughout the initial 10 days after symptom onset [8]. Bermejo-Martin and colleagues found that mediators involved in the development of Th17 cells (IL-6, IL-8, IL-9, IL-17), Th1 cells (TNF��, IL-15, IL-12p70) and type II interferon (IFN��) had high systemic levels in hospitalized patients with nvA(H1N1) influenza [9]. The detrimental or beneficial role of these cytokines in severe illness is not known.
The aim of our study was to further investigate the profile of Th1 and Th17 mediators and interferon-inductible protein-10 (IP-10), an innate-immunity mediator, as early host response in a group of critical and noncritical hospitalized patients with nvA(H1N1) from Cluj-Napoca, Romania, and to correlate them with the clinical aspects.Materials and methodsPatients Carfilzomib and controlsThe study was performed between October 2009 and February 2010 in the ICUs of the Emergency County Clinical Hospital and of the Teaching Hospital of Infectious Diseases, Cluj-Napoca, Romania.