Department of Biology, Carleton University, Ottawa, Ontario, Canada.
Department of Health Sciences, Carleton University, Ottawa, Ontario, Canada.
Mediators Inflamm. 2018 Sep 27;2018:6238978. doi: 10.1155/2018/6238978. eCollection 2018.
With the advent of antiretroviral therapy (ART), HIV-infected individuals are now living longer and healthier lives. However, ART does not completely restore health and treated individuals are experiencing increased rates of noncommunicable diseases such as dyslipidemia, insulin resistance, type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease. While it is well known that persistent immune activation and inflammation contribute to the development of these comorbid diseases, the mechanisms underlying this chronic activation remain incompletely understood. In this review, we will discuss emerging evidence that suggests that alterations in cellular metabolism may play a central role in driving this immune dysfunction in HIV patients on ART.
随着抗逆转录病毒疗法（ART）的出现，HIV 感染者现在能够活得更长久、更健康。然而，ART 并不能完全恢复健康，接受治疗的个体患非传染性疾病的比率在不断上升，如血脂异常、胰岛素抵抗、2 型糖尿病、心血管疾病和非酒精性脂肪肝疾病等。虽然众所周知，持续的免疫激活和炎症会导致这些合并症的发生，但这种慢性激活的机制仍不完全清楚。在这篇综述中，我们将讨论新出现的证据，表明细胞代谢的改变可能在驱动接受 ART 的 HIV 患者免疫功能障碍中起核心作用。
