The influence of Th17-dominant conditions (autoimmune diseases) or Th1 deficient ones (HIV infection) on disease outcome should also be explored. Furthermore, the impact of other regulatory cytokines elevated in severe disease (IL-10, IL-13) on the evolution of host immune choose size responses to nvH1N1 infections may represent alternative therapeutics for controlling severe illness.Key messages? The great majority of infections caused by the new influenza pandemic virus are mild and self-limiting in nature. Nevertheless, a small percentage of the patients develop severe respiratory disease. Analysis of the immune mediators involved in host responses to the virus along with the evaluation of the humoral responses in mild and severe cases may help understand the pathogenic events leading to poor outcomes.
? Early response to the virus in both hospitalized and outpatients was characterized by expression of chemokines (CXCL10, CCL2 and CCL4), also observed in the response to SARS CoV, H5N1 and RSV, which previous literature describes to correspond to innate antiviral responses.? Patients who develop respiratory compromise in the first days following infection with nvH1N typically showed Th1 and Th17 hyper-cytokinemia, compared to mild patients and healthy controls. These cytokine profiles have been previously reported to participate in both antiviral and pro-inflammatory responses.? Increased systemic levels of IL-15, IL-12p70, IL-6 constituted a hallmark of critical illness. These mediators are known to promote the development of adaptive responses and also pro-inflammatory ones in other viral infections.
? Our findings constitute a major avenue to guide the design of further works studying the beneficial or detrimental role of Th1 and Th17 responses in this disease.AbbreviationsFGF-b: Human Fibroblast Growth Factor-basic; G-CSF: granulocyte colony-stimulating factor; GM-CSF: granulocyte macrophage colony-stimulating factor; IFN-��: interferon alpha; IFN-��: interferon ��; IL-1RA: Interleukin 1 receptor antagonist; IP-10: Interferon-inducible protein-10; MCP-1: monocyte chemoattractant protein-1; MIP-1��: macrophage inflammatory protein-1��; MIP-1��: macrophage inflammatory protein-1��; nvH1N1; new variant of H1N1 influenza virus; PDGF-BB: platelet-derived growth factor; TNF-��: tumour necrosis factor ��; VEGF: vascular endothelial growth factor.
Competing interestsThe authors declare that they have no competing interests.Authors’ contributionsTP, JR and IML assisted in the design of the study, Brefeldin_A coordinated patient recruitment, analysed and interpreted the data, and assisted in writing the paper. PR, MCG, CS, DM, JMG, SH, ES, MG, AC, BV, CJL, JAD, CH, IG and PC supervised clinical aspects, participated in patient recruitment, assisted in the analysis, interpretation of data, and writing the report.