FRI-431 Bacterial Burden and Seminal HIV-1 RNA Shedding in Kenyan Men

Friday, October 12, 2012: 7:00 PM
Hall 4E/F (WSCC)
Dandi Huang , Vaccine and Infectious Disease, Fred Hutchinson Cancer Research Center, Seattle, WA
Daisy Ko , Vaccine and Infectious Disease, Fred Hutchinson Cancer Research Center, Seattle, WA
Snow Hou , Vaccine and Infectious Disease, Fred Hutchinson Cancer Research Center, Seattle, WA
Robert Coombs , Medicine, University of Washington, Seattle, WA
John Krieger , Urology, University of Washington, Seattle, WA
Eduard Sanders , Kenya Medical Research Institute, Kilifi, Kenya
Norbert Peshu , Kenya Medical Research Institute, Kilifi, Kenya
David Fredricks , Medicine, University of Washington, Seattle, WA
Susan Graham , Kenya Medical Research Institute, Kilifi, Kenya
Genitourinary tract (GT) infections are known to increase sexual transmission of HIV-1, but no published studies have characterized the GT bacterial biota of HIV-1 infected men and its association with seminal HIV-1 RNA shedding. A prior study identified distal genitourinary structures such as the seminal vesicles and prostate as important sources of seminal HIV-1 RNA in males. The current study investigates how the seminal bacterial burden and composition correlate with the HIV-1 viral load. The sample population of 42 HIV-1 positive Kenyan men includes high-risk individuals such as transactional sex workers and men who have sex with men (MSM). Study participants screened negative for gonorrhea and chlamydia (Aptima GC/CT Detection System®) and trichomonas (In-Pouch TV®) at all included visits. Quantitative broad-range 16S rRNA gene polymerase chain reaction (qPCR) and reverse transcriptase qPCR (RT-qPCR) were performed on DNA extracted from semen samples to measure the total bacterial burden and HIV load. Samples were also subjected to genus and species specific qPCRs targeting Atopobium, Gardnerella vaginalis, Leptotrichia, Sneathia, Megasphaera, and Bacterial Vaginosis Associated Bacteria (BVAB) 1, 2 and 3. Our results show that higher total bacterial burden correlates with higher HIV-1 viral load in semen (Spearman’s rho =0.309, p=0.003). The semen samples contained low levels of bacterial DNA from Atopobium, G. vaginalis, Leptotrichia and Sneathia, Megasphaera, and no detectable BVAB 1. These results show that total seminal bacterial burden predicts HIV-1 shedding, and this may create an opportunity to interrupt the transmission of HIV-1 by reducing GT bacterial burden.