ena-STUDY-UNIVERSITY OF NEBRASKA LINCOLN-03-12-2015-17:05:21:565-113
Microbial Dysbiosis in gut of Acutely and Chronically SIV Infected macaques
Microbial dysbiosis has been linked to systemic immune activation and accelerated disease progression from acute HIV-1 infection to the end stage disease AIDS.  HIV-1 infection leads to a massive depletion of CD4 T cells within the gut associated lymphoid tissue.  As a part of this depletion CD4 Th17 cells are selectively killed and the mechanisms protecting the body against microbial translocation break down.  The loss of immune regulation and systemic immune activation can lead to changes in the gut microbial community.  These changes can manifest themselves as microbial dysbiosis and microbial translocation, which are believed to be key contributors to systemic immune activation and chronic inflammation.  Chronic inflammation persists in patients treated for HIV-1 and likely contributes to the high incidence of age-related diseases seen in these patients.  Using SIV as a model for HIV-1 transmission and pathogenesis; a study was conducted to determine the changes in the gut microbiota composition through cross-sectional samples of infected individuals. Rhesus Macaque fecal samples were collected from the Jejunum and Rectum and characterized by 16S rRNA Illumina Mi-Seq paired-end sequencing.  A longitudinal study was then performed using 6 infected individuals sampled across different time points of infection.  We were able to  draw important conclusions about how SIV induced changes in the immune system can impact the make-up of gut microbiota, and how the changes in microbiota could possibly impact microbial translocation and chronic inflammation.  Specifically we were able to observe increases in inflammation tolerant taxa, increases in motile taxa, and the loss of taxa important for metabolism related to immune regulation.  The data obtained could be beneficial in providing alternative or complementary treatment options and a better understanding of HIV-1 transmission and pathogenesis.
Microbial dysbiosis has been linked to systemic immune activation and accelerated disease progression from acute HIV-1 infection to the end stage disease AIDS.  HIV-1 infection leads to a massive depletion of CD4 T cells within the gut associated lymphoid tissue.  As a part of this depletion CD4 Th17 cells are selectively killed and the mechanisms protecting the body against microbial translocation break down.  The loss of immune regulation and systemic immune activation can lead to changes in the gut microbial community.  These changes can manifest themselves as microbial dysbiosis and microbial translocation, which are believed to be key contributors to systemic immune activation and chronic inflammation.  Chronic inflammation persists in patients treated for HIV-1 and likely contributes to the high incidence of age-related diseases seen in these patients.  Using SIV as a model for HIV-1 transmission and pathogenesis; a study was conducted to determine the changes in the gut microbiota composition through cross-sectional samples of infected individuals. Rhesus Macaque fecal samples were collected from the Jejunum and Rectum and characterized by 16S rRNA Illumina Mi-Seq paired-end sequencing.  A longitudinal study was then performed using 6 infected individuals sampled across different time points of infection.  We were able to  draw important conclusions about how SIV induced changes in the immune system can impact the make-up of gut microbiota, and how the changes in microbiota could possibly impact microbial translocation and chronic inflammation.  Specifically we were able to observe increases in inflammation tolerant taxa, increases in motile taxa, and the loss of taxa important for metabolism related to immune regulation.  The data obtained could be beneficial in providing alternative or complementary treatment options and a better understanding of HIV-1 transmission and pathogenesis.