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Impact of a fat-rich diet on the pathogenesis of SIV infection in the African green monkey host - "induced microbial translocation and elevated immune activation and inflammation/ impacted survival/ altered metabolism profile and liver "
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Reported by jules Levin
Durban 2016 July 18-22
Presenter
Cuiling Xu
Authors
C. Xu1, T. He1, G. Haret-Richter1, D. Franck2, B. Policicchio1, E. Brocca-Cofano1, D. Ma1, J. Stock1, R. Tracy3, A. Landay4, C. Wilson2, C. Apetrei1, I. Pandrea1
Institutions
1University of Pittsburgh, Center for Vaccine Research, Pittsburgh, United States, 2University of Colorado, Denver, United States, 3University of Vermont, Burlington, United States, 4Rush University, Chicago, United States
Abstract
Background: High dietary fats were reported to induce intestinal dysbiosis, drive gut inflammation and breakdown the intestinal epithelial barrier, granting intestinal flora access to the bloodstream. As microbial translocation is a major determinant of the chronic immune activation and HIV/SIV disease progression, we investigated whether fat diet impacts HIV/SIV pathogenesis.
Methods: The nonprogressive African green monkey (AGM) model of SIV is an ideal system to assess the role of fat diet on disease progression, because they do not develop SIV-related intestinal dysfunction. We included 4 AGMs that received a fat diet prior and after SIVsab infection, and 5 controls in which the impact on key parameters of SIV infection such as: viral loads, CD4+ T cell counts, microbial translocation, immune activation and inflammation were compared and contrasted.
Results: LPS levels increased in the AGMs receiving fat diet prior and after SIV infection. Fat-rich diet also resulted in increases of immune activation (HLA-DR CD38, CD69 and Ki-67) and inflammation (inflammatory cytokines-IL-6, IL-17 and C reactive protein), leading to a prolonged depletion of CD4+ T cells compared to controls. However, these significant alterations of key parameters that are associated with the lack of disease progression in natural hosts of SIVs did not reach the levels described during progressive HIV/SIV infection. Furthermore, these changes did not result in significant increases in the levels of viral replication in the AGMs receiving a fat diet.
Conclusions: Administration of fat-rich diet resulted in alterations of markers of pathogenicity in the nonprogressive SIV infection of AGMs. Although not major, these changes were significant, suggesting that a diet very rich in fats may negatively impact HIV pathogenesis, especially if combined with other behavioral risk factors reported to impact gut integrity or systemic inflammation, such as alcohol consumption, drug usage and smoking. Detailed studies on the correlations between fat diet, alterations in the intestinal microbiota, metabolic markers, liver function and SIV progression to AIDS are in progress.
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