Experimental microbial dysbiosis does not promote disease progression in SIV-infected macaques

被引：0

作者：

Alexandra M. Ortiz

Jacob K. Flynn

Sarah R. DiNapoli

Ivan Vujkovic-Cvijin

Carly E. Starke

Stephen H. Lai

MacKenzie E. Long

Ornella Sortino

Carol L. Vinton

Joseph C. Mudd

Leslie Johnston

Kathleen Busman-Sahay

Yasmine Belkaid

Jacob D. Estes

Jason M. Brenchley

机构：

[1] Barrier Immunity Section,Vaccine and Gene Therapy Institute

[2] Laboratory of Viral Diseases,Oregon National Primate Research Center

[3] National Institutes of Allergy and Infectious Diseases (NIAID),undefined

[4] National Institutes of Health (NIH),undefined

[5] Mucosal Immunology Section,undefined

[6] Laboratory of Parasitic Diseases,undefined

[7] NIAID,undefined

[8] NIH,undefined

[9] AIDS and Cancer Virus Program,undefined

[10] Frederick National Laboratory for Cancer Research,undefined

[11] Leidos Biomedical Research,undefined

[12] Inc.,undefined

[13] Oregon Health and Science University,undefined

[14] NIAID Microbiome Program,undefined

[15] NIH,undefined

[16] Oregon Health and Science University,undefined

来源：

Nature Medicine | 2018年 / 24卷

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摘要：

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.

引用

页码：1313 / 1316

页数：3

共 32 条

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