We identified higher plasma levels of IL1RA, IL2, IL6, CCL3, CCL4 and IL10 as markers of severity. Of these, IL6 is a known marker of influenza disease severity with probable involvement in tissue damage [12, 14] . CCL3 and CCL4 are important mediators of virus induced inflammation. IL10 is recognized as a regulatory (anti-inflammatory) cytokine and can act on multiple cell types to regulate immune and inflammatory responses [15] . IL6 is known to be responsible for regulating plasma levels of IL1RA and IL10 [16] . Among Spanish patients, serum IL15, IL12p70 and IL6 were recognized as the hallmark of severity [10] . Significant increases in TLR levels without corresponding rise in cytokines suggest aberrant immune response in critically ill patients. The possibility of viral proteins diminishing cytokine production cannot be ruled out. Similar to in-vitro studies [17, 18] , cytokine storm associated with pathogenesis of H5N1 infection [12] was not the feature of p-H1N1-09 infection. The observations of no increase in the levels of plasma IFNG in both patient categories when compared to controls as well as basal gene expression in the lungs of critically ill patients point out lack of co-ordination in the modulation of innate and adaptive immune responses.