ArticleAIDS (London, England)2019
Elevated indoleamine-2,3-dioxygenase enzyme activity in a novel mouse model of HIV-associated atherosclerosis.
Article in AIDS (London, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Gut-heart immuno-metabolic disruption associated with inflammaging and subclinical coronary artery disease in people with HIV on antiretroviral therapy.Immunity & ageing : I & A · 2026Article
- Exercise-induced effects on atherogenesis and tryptophan catabolism via the kynurenine pathway in an HIV-associated atherosclerosis mouse model.Experimental physiology · 2026Article
- Persistent activation of monocytes/macrophages and cell senescence in SIV-infected macaques on ART.Frontiers in immunology · 2026Article
- Persistent Activation of Monocytes/Macrophages and Cell Senescence in SIV-Infected Macaques on ART.bioRxiv : the preprint server for biology · 2025Article
- Increased Atherosclerosis in HIV-Infected Humanized Mice Is Caused by a Single Viral Protein, Nef.The Journal of infectious diseases · 2025Article
- Mouse Models of HIV-Associated Atherosclerosis.International journal of molecular sciences · 2025Review
- Deficiency of Caspase-1 Attenuates HIV-1-Associated Atherogenesis in Mice.International journal of molecular sciences · 2023Article
- SARS-CoV-2 infection dysregulates NAD metabolism.Frontiers in immunology · 2023Article
- HIV Protein Tat Induces Macrophage Dysfunction and Atherosclerosis Development in Low-Density Lipoprotein Receptor-Deficient Mice.Cardiovascular drugs and therapy · 2022Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveHIV atherosclerosis and cardiovascular disease (CVD) represent a significant human health burden in the era of combination antiretroviral therapy (cART). The pathogenesis of HIV atherosclerosis is still poorly understood, due, in part, to the lack of a suitable small animal model. Indoleamine-2,3-dioxygenase (IDO) enzyme activity is the first and rate-limiting step in tryptophan catabolism and is measured by the kynurenine to tryptophan ratio (KTR). The serum KTR is a biomarker of inflammation and has recently been implicated as an important risk factor for CVD in patients living with HIV (PLWH) who are virologically suppressed under cART. However, IDO activity in HIV-associated CVD has not been studied in mouse model before.
designA novel mouse model of HIV atherosclerosis (Tg26/ApoE) was generated and examined for IDO activity and atherogenesis throughout 8 weeks on a high-fat diet. Tg26/ApoE mice were compared with Tg26 and ApoE single transgenic mice, before and during a high-fat diet.
methodSerum kynurenine, tryptophan and percentage of aortic plaque formation were measured. Additionally, levels of relevant cytokines were investigated in Tg26/ApoE and ApoE.
resultsTg26/ApoE developed an accelerated atherosclerosis with increasing levels of KTR that were associated with plaque progression. This accelerated plaque was potentially driven by elevated levels of circulating IL-6.
conclusionThese results indicate that Tg26/ApoE serve as a new mouse model for HIV-induced atherogenesis, and aid in understanding the role of tryptophan catabolism in the pathogenesis of HIV atherosclerosis/CVD.
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