Editors' ChoiceObesity

The heavy toll of influenza

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Science Translational Medicine  30 Sep 2015:
Vol. 7, Issue 307, pp. 307ec167
DOI: 10.1126/scitranslmed.aad3613

Influenza is unpleasant but usually self-limiting. After a few miserable days of fever, body aches, cough, and runny nose, most people are back on their feet. Certain people, however—pregnant and post-partum women, the elderly, and those with cancer, diabetes, or chronic lung and cardiovascular diseases—are at higher risk of hospital admission, acute respiratory failure, and death.

Epidemiological studies, derived largely from the 2009 influenza pandemic, have linked a new risk factor—obesity—with severe influenza complications. Although the reasons behind this association are not entirely clear, obesity is thought to impair cellular immune function and, in animal models, promotes a dysregulated immune response to flu virus infection. Excess weight also strains respiratory function and predisposes to other high-risk comorbidities. Now, Travanty et al. suggest that the pandemic flu strain itself may be contributing to poor influenza outcomes by being more infectious in obese people than in those of normal weight.

By using lungs donated but unsuitable for transplantation, Travanty et al. assessed the infectivity of primary alveolar epithelial cells (AECs) with strains of the influenza A(H1N1pdm09) virus. They found that AECs from obese donors (BMI ≥ 30) were, on average, significantly more susceptible to infection than AECs from nonobese (BMI 18 to 30) persons. Enhanced infectivity in obese persons, the authors suggest, might give rise to a higher viral burden and predispose to influenza-related complications.

There are caveats to this study. Two pandemic flu strains were used to infect AECs from only 15 nonobese and 9 obese lung donors, with data from only one strain shown. Other host characteristics are clearly at play; indeed, the AECs most susceptible to infection were derived from an overweight but not obese woman (BMI 28). And the cellular mechanism of susceptibility remains to be elucidated. Still, these data suggest that part of the enhanced susceptibility to severe influenza disease in the obese may occur at a cellular level, independent of systemic factors like impaired immunity or respiratory physiology.

E. Travanty et al., Differential susceptibility of human lung primary cells to H1N1 influenza viruses. J. Virol. 10.1128/JVI.01792-15 (2015). [Abstract]

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