关键词: cardiovascular diseases cytopathogenic effect, viral noncommunicable diseases quality of life sodium chloride, dietary

Mesh : Humans HIV Infections / drug therapy epidemiology complications Hypertension / drug therapy epidemiology Risk Factors HIV-1 / pathogenicity Animals

来  源:   DOI:10.1161/CIRCRESAHA.124.323979   PDF(Pubmed)

Abstract:
HIV type 1 (HIV-1) is the causative agent of AIDS. Since the start of the epidemic, HIV/AIDS has been responsible for ≈40 million deaths. Additionally, an estimated 39 million people are currently infected with the virus. HIV-1 primarily infects immune cells, such as CD4+ (cluster of differentiation 4+) T lymphocytes (T cells), and as a consequence, the number of CD4+ T cells progressively declines in people living with HIV. Within a span of ≈10 years, HIV-1 infection leads to the systemic failure of the immune system and progression to AIDS. Fortunately, potent antiviral therapy effectively controls HIV-1 infection and prevents AIDS-related deaths. The efficacy of the current antiviral therapy regimens has transformed the outcome of HIV/AIDS from a death sentence to a chronic disease with a prolonged lifespan of people living with HIV. However, antiviral therapy is not curative, is challenged by virus resistance, can be toxic, and, most importantly, requires lifelong adherence. Furthermore, the improved lifespan has resulted in an increased incidence of non-AIDS-related morbidities in people living with HIV including cardiovascular diseases, renal disease, liver disease, bone disease, cancer, and neurological conditions. In this review, we summarize the current state of knowledge of the cardiovascular comorbidities associated with HIV-1 infection, with a particular focus on hypertension. We also discuss the potential mechanisms known to drive HIV-1-associated hypertension and the knowledge gaps in our understanding of this comorbid condition. Finally, we suggest several directions of future research to better understand the factors, pathways, and mechanisms underlying HIV-1-associated hypertension in the post-antiviral therapy era.
摘要:
HIV1型(HIV-1)是AIDS的病原体。自从疫情开始以来,艾滋病毒/艾滋病已导致约4000万人死亡。此外,目前估计有3900万人感染了这种病毒。HIV-1主要感染免疫细胞,如CD4+(分化簇4+)T淋巴细胞(T细胞),因此,HIV感染者的CD4+T细胞数量逐渐下降.在约10年内,HIV-1感染导致免疫系统的系统性衰竭和发展为AIDS。幸运的是,有效的抗病毒治疗可有效控制HIV-1感染并预防与AIDS相关的死亡。当前抗病毒治疗方案的功效已将HIV/AIDS的结果从死刑转变为具有HIV感染者寿命延长的慢性疾病。然而,抗病毒治疗不能治愈,受到病毒抗性的挑战,可能是有毒的,and,最重要的是,需要终身坚持。此外,寿命的改善导致艾滋病毒感染者中与艾滋病无关的发病率增加,包括心血管疾病,肾脏疾病,肝病,骨病,癌症,和神经疾病。在这次审查中,我们总结了与HIV-1感染相关的心血管合并症的知识现状,特别关注高血压。我们还讨论了已知的导致HIV-1相关高血压的潜在机制,以及我们对这种合并症的理解中的知识差距。最后,我们提出了几个未来研究的方向,以更好地理解这些因素,通路,以及抗病毒治疗后时期HIV-1相关高血压的潜在机制。
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