Microbial Translocation from the Vaginal Microbiome and GI tract during Hyperacute SIVmac239 infection


Identification: Bussan, Hailey


Description

Microbial Translocation from the Vaginal Microbiome and GI tract during Hyperacute SIVmac239 infection
 
Hailey Bussan1,3, Adam Ericsen4,5, Eric Peterson2, Laurel Stewart1, Matt Semler1, Gabrielle Barry2, Jens Eickhoff6, Dawn Dudley1, and David O'Connor1,2
1Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison; 2Wisconsin National Primate Research Center, University of Wisconsin-Madison; 3Medical Scientist Training Program, University of Wisconsin-Madison School of Medicine and Public Health; 4Yerkes National Primate Research Center; 5Emory University; 6Department of Biostatistics and Medical Informatics, University of Wisconsin-Madison
 
Movement of microbial products from the GI tract is known to cause systemic immune activation during chronic human-immunodeficiency virus (HIV) and simian-immunodeficiency virus infection (SIV). Recently, we showed that microbial translocation occurs in the first days following intrarectal SIV infection. Previously, the origin of microbial translocation has only been tested and described from the GI tract. We hypothesized that since the vaginal microbiome has been implicated in risk acquisition of HIV and related inflammation, vaginal microbial products could also be implicated in hyperacute translocation. We sequenced and described microbial communities in plasma, stool, and vaginal swabs from eight MCM treated with dextran sodium sulfate, a chemical colitogen that causes intestinal epithelial damage, and infected with SIVmac239 intrarectally. Using 16S Illumina-based sequencing, we found plasma microbial diversity increased within two days of SIV infection with contributions of unique taxa from the stool and vaginal microbiome. We are in the process of repeating this study with DSS-naive macaques challenged intrarectally and intravaginally. This study suggests that the vaginal microbiome also contributes to acute translocation and immune activation even when individuals are infected intrarectally. Therapeutic methods aimed at preventing microbial translocation to reduce immune activation may need to target potential translocation from both the GI tract and vagina.
 

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