Patients with previously diagnosed respiratory disease such as COPD and asthma were well controlled on their treatment. H1N1 induced inflammation and was the factor that dysregulated their condition. WBC count and CRP were elevated in patients with suspected bacterial infection. Hypoxemia was more severe in patients with opacities on chest x-rays. The mean values in 7/44 patients with abnormal liver functions did not exceed 138 IU/L for ALT and 125 IU/L for AST. These patients did not present jaundice or other clinical signs of liver dysfunction. Patients with BMI ≥ 30 kg/m 2 were 20/44, implicating a mild clinical course overall, since BMI ≥ 30 is considered an adverse prognostic factor. The laboratory findings were not correlated with the respiratory functions, based on the fact that patients upon exacerbation or with opacities on chest x-ray would present a severe deterioration of their respiratory capacity. None of the patients had been previously vaccinated, but all patients received oseltamivir immediately on hospitalization and antibiotics upon suspicion of bacterial respiratory infection preventing an escalation of the inflammation and infection. The mechanisms of H1N1-induced respiratory effects have received considerable attention [39] [40] [41] [42] [43] [44] . Recent studies have shown that the high mortality rate of avian influenza virus infections is a consequence of an overactive inflammatory response and the severity of infection is closely related with virus-induced cytokine dysregulation. The most important feature of influenza A immune-pathogenesis is the appearance of "cytokine storm", which is characterized by the extreme production and secretion of numerous pro-inflammatory cytokines. This is responsible for the development of lethal clinical symptoms, such as massive pulmonary edema, acute bronchopneumonia, alveolar hemorrhage, reactive hemophagocytosis, and acute respiratory distress syndrome, associated with necrosis and tissue destruction. and IFN-gamma. It has been detected that mutations of some viral genes (NS1, PB2, HA and NA) are responsible for the "cytokine storm", by increasing the viral replication rate, expending the tissue tropism, as well as facilitating the systemic invasion and the development of resistance against the host antiviral response. Glu92 and Ala149 mutations and carboxyl-terminal ESEV/ EPEV motif of NS1 protein have been implicated as determinants of virulence for A/H5N1 strains. In addition, Lys627 mutation in PB2 protein, polybasic aminoacid mutations in the cleavage region of hemagglutinin (HA) polyprotein, and glycosylation and sialyzation mutations in HA and neuraminidase (NA) proteins were found to enhance the immune-mediated pathology of highly virulent A strains [40] [41] [42] [43] [44] [45] . Furthermore, in a preliminary analysis of macrophage gene expression data based on published studies, 64 genes in H1N1-infected cells showed at least 1.5-fold difference in expression level compared to mock infected cells in at least one time point [43] . Impressively, as many as 60 genes were thereby upregulated [43] .