At PBMC gene level, down-regulation of a large number of genes was associated with disease severity (Table S1, Figure 3b ). This profile is indicative of massive infiltration of monocyterecruited neutrophils, DCs/macrophages to the target organ for mounting immune response/tissue repair and/or viral proteininduced shut down of the cellular genes, as these cells are known to efficiently replicate the virus [19, 20] . Additional studies are required to examine if the virus specifically down regulates host antiviral genes or dictates generalized shut down of host mRNA synthesis [19, 21] , especially in relation to the disease severity. Paradoxically, constant inflammatory signals provided by the significant increase in several chemokines (CCL2, CCL3, CCL19, CXCL8, CXCL10, CXCL11) and pro-inflammatory cytokines (IL6, IL17, IL1A, IL1B, TNF) in the lung cells may have resulted in massive infiltration of leucocytes and excessive tissue damage. This is to our knowledge the first report on p-H1N1-09-induced gene expression in human lung cells.