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High-fat diet exacerbates SIV pathogenesis and accelerates disease progression
Tianyu He, … , Cristian Apetrei, Ivona Pandrea
Tianyu He, … , Cristian Apetrei, Ivona Pandrea
Published November 11, 2019
Citation Information: J Clin Invest. 2019;129(12):5474-5488. https://doi.org/10.1172/JCI121208.
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Research Article AIDS/HIV Article has an altmetric score of 3

High-fat diet exacerbates SIV pathogenesis and accelerates disease progression

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Abstract

Consuming a high-fat diet (HFD) is a risk factor for obesity and diabetes; both of these diseases are also associated with systemic inflammation, similar to HIV infection. A HFD induces intestinal dysbiosis and impairs liver function and coagulation, with a potential negative impact on HIV/SIV pathogenesis. We administered a HFD rich in saturated fats and cholesterol to nonpathogenic (African green monkeys) and pathogenic (pigtailed macaques) SIV hosts. The HFD had a negative impact on SIV disease progression in both species. Thus, increased cell-associated SIV DNA and RNA occurred in the HFD-receiving nonhuman primates, indicating a potential reservoir expansion. The HFD induced prominent immune cell infiltration in the adipose tissue, an important SIV reservoir, and heightened systemic immune activation and inflammation, altering the intestinal immune environment and triggering gut damage and microbial translocation. Furthermore, HFD altered lipid metabolism and HDL oxidation and also induced liver steatosis and fibrosis. These metabolic disturbances triggered incipient atherosclerosis and heightened cardiovascular risk in the SIV-infected HFD-receiving nonhuman primates. Our study demonstrates that dietary intake has a discernable impact on the natural history of HIV/SIV infections and suggests that dietary changes can be used as adjuvant approaches for HIV-infected subjects, to reduce inflammation and the risk of non-AIDS comorbidities and possibly other infectious diseases.

Authors

Tianyu He, Cuiling Xu, Noah Krampe, Stephanie M. Dillon, Paola Sette, Elizabeth Falwell, George S. Haret-Richter, Tiffany Butterfield, Tammy L. Dunsmore, William M. McFadden Jr., Kathryn J. Martin, Benjamin B. Policicchio, Kevin D. Raehtz, Ellen P. Penn, Russell P. Tracy, Ruy M. Ribeiro, Daniel N. Frank, Cara C. Wilson, Alan L. Landay, Cristian Apetrei, Ivona Pandrea

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Figure 10

HFD increases severity of CV lesions in SIV-infected PTMs.

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HFD increases severity of CV lesions in SIV-infected PTMs.
Representativ...
Representative H&E images of (A) myocardial and (B) epicardial immune infiltration, (C) lymphoid aggregates in epicardium, (D) myocardial cytolysis, (E) myocardial fatty infiltration (arrows), (F) microthrombi (arrows), (G) aortic dissection, (H) myocardial and (I) pericardial fibrosis in HFD-receiving PTMs. (J) Representative trichrome-stained images of cardiac fibrosis observed in HFD-receiving infected PTMs compared with control-infected and SIV– PTMs. Quantification of the percent area of collagen is shown in (K). Data were compared with Kruskal-Wallis test corrected for multiple comparisons and are presented as individual values with median. Sample size (n) and P values are presented on graphs. SIV–, preinfection pre-HFD; SIV+, chronic infection without HFD; HFD SIV+, chronic infection with HFD. (L) Representative H&E images of signs of evolving atherosclerosis with organized thrombus in HFD-receiving PTMs. Original magnifications: ×200.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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