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Although most cases of influenza A 2009 H1N1 were mild and self-limited, many
cases developed severe pneumonia leading to acute respiratory distress syndrome (ARDS)
and death. It is not clear what determined the disease severity in these cases. Host factors
including pregnancy, obesity, and chronic illnesses are certainly contributing factors, but
other unknown host and viral factors may also play pivotal roles. The pandemic influenza A
2009 H1N1 virus has been shown to induce more severe lung pathology in ferrets and
monkeys than seasonal influenza viruses. This may be a result of receptor-binding property
of the virus, as the pandemic virus binds not only to α2,6-linked sialic acid, expressed mainly
in upper airway, but also with a lower affinity to α2,3-linked sialic acid, expressed in alveoli.
The ability of this virus to infect alveolar epithelial cells may play a crucial role in
pneumonia and ARDS. On the other hand, evidences are pointing to host innate responses as
major determinants of disease outcome. Therapeutic approaches aiming at modifying innate
inflammatory responses have been proposed but not yet fully explored. Both mechanistic
studies and clinical trials addressing these alternative treatments are needed for a better
pandemic influenza preparedness.
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