Abstract
Intestinal microbial dysbiosis has been described in individuals with an HIV-1 infection and may underlie persistent inflammation in chronic infection, thereby contributing to disease progression. Herein, we induced an HIV-1-like intestinal dysbiosis in rhesus macaques (Macaca mulatta) with vancomycin treatment and assessed the contribution of dysbiosis to SIV disease progression. Dysbiotic and control animals had similar disease progression, indicating that intestinal microbial dysbiosis similar to that observed in individuals with HIV is not sufficient to accelerate untreated lentiviral disease progression.
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Acknowledgements
We would like to acknowledge H. Kendall, J. Swerczek, R. Herbert, and all the veterinary staff at the NIH animal center. We would like to thank M. Quiñones, J. Davis, S. Sen and G. Trinchieri, and the NIAID Microbiome Program for technical and analytical assistance. Funding for this study was provided in part by the Division of Intramural Research/NIAID/NIH, by the Oregon National Primate Research Center NIH grant award P51OD011092, and with federal funds from the National Cancer Institute, NIH, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services (DHHS), nor does the mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government.
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J.M.B. conceived the project. A.M.O. and J.M.B. designed the project and wrote the manuscript. A.M.O., J.K.F., S.R.D., C.E.C.S., S.H.L., M.E.L., O.S., C.L.V., J.C.M., L.J., K.B.-S., J.D.E. and J.M.B. performed experiments. A.M.O., J.K.F., S.R.D., I.V.-C., S.H.L., Y.B., J.D.E. and J.M.B. analyzed data.
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Supplementary Figures 1–8 and Supplementary Table 1
Supplementary Dataset 1
LEFSE returned results
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Ortiz, A.M., Flynn, J.K., DiNapoli, S.R. et al. Experimental microbial dysbiosis does not promote disease progression in SIV-infected macaques. Nat Med 24, 1313–1316 (2018). https://doi.org/10.1038/s41591-018-0132-5
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DOI: https://doi.org/10.1038/s41591-018-0132-5
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