TY - JOUR
T1 - Metagenomics and personalized medicine
AU - Virgin, Herbert W.
AU - Todd, John A.
N1 - Funding Information:
The authors would like to acknowledge helpful conversations with Thad Stappenbeck, Ramnik Xavier, Emil Unanue, Jeff Gordon, Balfour Sartor, Adolfo Garcia-Sastre, and Dermot McGovern. We thank Tom Smith for providing the images of noroviruses used in Figure 4. H.W.V. is supported by the NCI, NIAID, NCRR, the Crohn's and Colitis Foundation of America, and the Broad Medical Foundation. J.A.T. is supported by the NIDDK, NIHR, the Wellcome Trust, the Juvenile Diabetes Research Foundation International, and the European Union.
PY - 2011/9/30
Y1 - 2011/9/30
N2 - The microbiome is a complex community of Bacteria, Archaea, Eukarya, and viruses that infect humans and live in our tissues. It contributes the majority of genetic information to our metagenome and, consequently, influences our resistance and susceptibility to diseases, especially common inflammatory diseases, such as type 1 diabetes, ulcerative colitis, and Crohn's disease. Here we discuss how host-gene-microbial interactions are major determinants for the development of these multifactorial chronic disorders and, thus, for the relationship between genotype and phenotype. We also explore how genome-wide association studies (GWAS) on autoimmune and inflammatory diseases are uncovering mechanism-based subtypes for these disorders. Applying these emerging concepts will permit a more complete understanding of the etiologies of complex diseases and underpin the development of both next-generation animal models and new therapeutic strategies for targeting personalized disease phenotypes.
AB - The microbiome is a complex community of Bacteria, Archaea, Eukarya, and viruses that infect humans and live in our tissues. It contributes the majority of genetic information to our metagenome and, consequently, influences our resistance and susceptibility to diseases, especially common inflammatory diseases, such as type 1 diabetes, ulcerative colitis, and Crohn's disease. Here we discuss how host-gene-microbial interactions are major determinants for the development of these multifactorial chronic disorders and, thus, for the relationship between genotype and phenotype. We also explore how genome-wide association studies (GWAS) on autoimmune and inflammatory diseases are uncovering mechanism-based subtypes for these disorders. Applying these emerging concepts will permit a more complete understanding of the etiologies of complex diseases and underpin the development of both next-generation animal models and new therapeutic strategies for targeting personalized disease phenotypes.
UR - http://www.scopus.com/inward/record.url?scp=80053462850&partnerID=8YFLogxK
U2 - 10.1016/j.cell.2011.09.009
DO - 10.1016/j.cell.2011.09.009
M3 - Review article
C2 - 21962506
AN - SCOPUS:80053462850
VL - 147
SP - 44
EP - 56
JO - Cell
JF - Cell
SN - 0092-8674
IS - 1
ER -