Role of Tissue Protection in Lethal Respiratory Viral-Bacterial Coinfection

Author:

Jamieson Amanda M.12,Pasman Lesley1,Yu Shuang1,Gamradt Pia2,Homer Robert J.34,Decker Thomas2,Medzhitov Ruslan1

Affiliation:

1. Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

2. Max F. Perutz Laboratories, University of Vienna, Dr. Bohr Gasse 9/4 A-1030 Vienna, Austria.

3. Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.

4. VA Connecticut Healthcare System Pathology and Laboratory Medicine Service, 950 Campbell Avenue, West Haven, CT 06516, USA.

Abstract

Tolerance Needed It's a common enough occurrence: You're sick as a dog with a cold, but the person in the office next door just has a few sniffles. What accounts for this difference? Most commonly, these sorts of differences are chalked up to differences in resistance—perhaps you have higher viral loads than your office mate. But such differences can also involve differences in the ability to tolerate the same amount of virus. Deciphering the contribution of resistance versus tolerance, however, is difficult. Jamieson et al. (p. 1230 , published online 25 April) studied a mouse model of viral and bacterial co-infection where tolerance and resistance could be separated. Mice infected with influenza virus were more likely to succumb to a secondary infection with Legionella pneumophila as a result of impaired tolerance to tissue damage, rather than because of a difference in bacterial burden.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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