The two patients who died showed a higher degree of pathological commitment of the disease at the OLB. Most of our patients were young to middle-aged and had previously been healthy. Increased risk for severe S-OIV illness is found in young children, 10-19 age groups, patients older than 65 years, pregnant women, obese people and those with comorbidities. 1, 7, 20 Fifteen to thirty per cent of patients with H1N1 infection required ICU admission. Mortality among the patients who required mechanical ventilation was around 58%. 7 In our case series the OLB findings showed that the lung damage was most likely due to infection by the influenza virus. The main pathological finding revealed necrotizing bronchiolitis and DAD, respiratory epithelial cells probably being the primary target of the infection. The extensive destruction of the respiratory and AECs and dysfunction in the immune and adaptative immune response led to DAD. As previously reported, possible mechanisms of damage include direct injury to the respiratory and alveolar epithelium exposing the basement membrane and leading to alveolar collapse by loss of surfactant, 13,14,21 with a secondary cytokine storm. 22 This is followed by exudation of macromolecules from the circulation, which finally form hyaline membranes. Activation of the cytokines is part of the immune reaction aiming to eradicate the virus. In this study, the systemic IFNc and TNFa cytokine activation probably resulted in reactive hemophagocytic syndrome in the bronchiole-associated lymphoid tissue and possibly also mediated the epithelial necrosis. 23 A mild inflammatory infiltration is most often seen in viral pneumonias; this has been explained by a cytokine-mediated blockade of lymphocytopoiesis and also by blockade of release from the bone marrow. 24 In our cases, expression in the lung of IFNc by small mononucleated cells and TNFa by macrophages and AECs was low. This finding may be supported by Kim and colleagues, 25 Conversely, we found a very strong expression of IL-4, IL-10 and iNOS by macrophages. The sparse inflammatory and immune reaction found in our samples, which involves targetting of the virus by NK cells, lymphocytes T and B cells, CD8+ cytotoxic T-lymphocyte cells, as well as CD1a and S100 cells, may be due to a combination of lymphoid tissue necrosis and apoptosis and exhaustion of lymphoid proliferation in response to the cytokine overdrive. In addition, the high IL-10 expression associated with its anti-inflammatory action may explain the low degree of inflammation observed in our cases. Taken together, our results suggest that in S-OIV infection, altered innate and adaptative immune responses may lead to incomplete virus eradication in the primary target of the infection and, consequently, imbalance between inflammation and reparation, resulting in bronchiolar obliteration and DAD.