Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Department of Microbiology, Immunology and Tropical Diseases, George Washington University, Washington, DC, United States of America.
PLoS One. 2019 Apr 18;14(4):e0215620. doi: 10.1371/journal.pone.0215620. eCollection 2019.
HIV infection is known to be associated with cardiometabolic abnormalities; here we investigated the progression and causes of these abnormalities. Three groups of participants were recruited: HIV-negative subjects and two groups of treatment-naïve HIV-positive subjects, one group initiating antiretroviral treatment, the other remaining untreated. Intima-media thickness (cIMT) increased in HIV-positive untreated group compared to HIV-negative group, but treatment mitigated the difference. We found no increase in diabetes-related metabolic markers or in the level of inflammation in any of the groups. Total cholesterol, low density lipoprotein cholesterol and apoB levels were lower in HIV-positive groups, while triglyceride and Lp(a) levels did not differ between the groups. We found a statistically significant negative association between viral load and plasma levels of total cholesterol, LDL cholesterol, HDL cholesterol, apoA-I and apoB. HIV-positive patients had hypoalphalipoproteinemia at baseline, and we found a redistribution of sub-populations of high density lipoprotein (HDL) particles with increased proportion of smaller HDL in HIV-positive untreated patients, which may result from increased levels of plasma cholesteryl ester transfer protein in this group. HDL functionality declined in the HIV-negative and HIV-positive untreated groups, but not in HIV-positive treated group. We also found differences between HIV-positive and negative groups in plasma abundance of several microRNAs involved in lipid metabolism. Our data support a hypothesis that cardiometabolic abnormalities in HIV infection are caused by HIV and that antiretroviral treatment itself does not influence key cardiometabolic parameters, but mitigates those affected by HIV.
HIV 感染与心血管代谢异常有关；在这里，我们研究了这些异常的进展和原因。我们招募了三组参与者：HIV 阴性受试者和两组未经治疗的 HIV 阳性受试者，一组开始接受抗逆转录病毒治疗，另一组未接受治疗。与 HIV 阴性组相比，未经治疗的 HIV 阳性组的内-中膜厚度（cIMT）增加，但治疗减轻了这种差异。我们没有发现任何一组的糖尿病相关代谢标志物或炎症水平增加。在 HIV 阳性组中，总胆固醇、低密度脂蛋白胆固醇和载脂蛋白 B 水平较低，而甘油三酯和 Lp(a)水平在各组之间没有差异。我们发现病毒载量与总胆固醇、LDL 胆固醇、HDL 胆固醇、载脂蛋白 A-I 和载脂蛋白 B 的血浆水平之间存在统计学上显著的负相关。HIV 阳性患者在基线时有低α脂蛋白血症，我们发现 HIV 未经治疗的患者中高密度脂蛋白（HDL）颗粒的亚群分布发生了重新分布，小 HDL 的比例增加，这可能是由于该组中血浆胆固醇酯转移蛋白水平增加所致。在 HIV 阴性和 HIV 未经治疗的患者组中，HDL 功能下降，但在 HIV 经治疗的患者组中没有下降。我们还发现 HIV 阳性和阴性组之间几种参与脂质代谢的 microRNA 的血浆丰度存在差异。我们的数据支持这样一种假设，即 HIV 感染中的心血管代谢异常是由 HIV 引起的，抗逆转录病毒治疗本身不会影响关键的心血管代谢参数，但可以减轻 HIV 影响的参数。
