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Editorials |

Another Piece of the Community-Acquired Pneumonia Puzzle

Richard G. Wunderink, MD, FCCP
Author and Funding Information

Correspondence to: Richard G. Wunderink, MD, FCCP, Northwestern University Feinberg School of Medicine, 676 North St. Clair St, Suite 14-044, Chicago, IL 60611; e-mail: r-wunderink@northwestern.edu

Dr. Wunderink is Professor of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.


The author has no conflict of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(6):1112-1114. doi:10.1378/chest.08-1832
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The risk of death from infection clearly has a genetic component.1 The risk of death from infection when a parent dies of infection before 50 years of age exceeds the risk of cardiovascular death if a parent dies of the same before age 50. However, the exact genetic risks are unknown. The deaths attributable to classic primary immunodeficiency diseases (PIDs), such as common variable immunodeficiency syndrome, only explain a small fraction of these excess deaths. However, the definition of PID is changing with a greater appreciation of nonleukocyte and adult-onset diseases, and recognition that forms of PID only lead to susceptibility to specific unusual infections.2 Increasingly, the ancestral genotype rather than the mutation is being recognized the at-risk genotype,3 such as the Duffy antigen and malaria risk and the β-chemokine receptor-5 and HIV.

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