Disrupted human-pathogen co-evolution: a model for disease.

Citation data:

Frontiers in genetics, ISSN: 1664-8021, Vol: 5, Issue: AUG, Page: 290

Publication Year:
2014
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Repository URL:
https://digitalcommons.dartmouth.edu/facoa/1306
PMID:
25202324
DOI:
10.3389/fgene.2014.00290
PMCID:
PMC4142859
Author(s):
Kodaman, Nuri; Sobota, Rafal S.; Mera, Robertino; Schneider, Barbara G.; Williams, Scott M.
Publisher(s):
Frontiers Media SA
Tags:
Biochemistry, Genetics and Molecular Biology; Medicine; host-pathogen coevolution; human disease; helicobacter pylori; mycobacterium tuberculosis; human papillomavirus; genome-genome interactions; Diseases; Infectious Disease; Medical Genetics; Medical Sciences; Medicine and Health Sciences
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article description
A major goal in infectious disease research is to identify the human and pathogenic genetic variants that explain differences in microbial pathogenesis. However, neither pathogenic strain nor human genetic variation in isolation has proven adequate to explain the heterogeneity of disease pathology. We suggest that disrupted co-evolution between a pathogen and its human host can explain variation in disease outcomes, and that genome-by-genome interactions should therefore be incorporated into genetic models of disease caused by infectious agents. Genetic epidemiological studies that fail to take both the pathogen and host into account can lead to false and misleading conclusions about disease etiology. We discuss our model in the context of three pathogens, Helicobacter pylori, Mycobacterium tuberculosis and human papillomavirus, and generalize the conditions under which it may be applicable.