FOCUS ISSUE ON HIV AND THE CARDIOMETABOLIC SYNDROME

关注艾滋病毒和心脏代谢综合征

• 批准号: 7721563
• 负责人: TODD CADE
• 金额: $ 0.24万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-02-01 至 2009-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7721563
• 关键词: Adult; Age; Aging; Anti-Retroviral Agents; Antineoplastic Agents; Area; Behavioral; Cardiovascular Diseases; Cardiovascular system; Cause of Death; Centers for Disease Control and Prevention (U.S.); Cessation of life; Child; Chronic; Complex; Computer Retrieval of Information on Scientific Projects Database; Condition; Data; Developed Countries; Developing Countries; Development; Diabetes Mellitus; Drug abuse; Dyslipidemias; Eating Behavior; Epidemic; Funding; Future; General Population; Genetic; Genetic Predisposition to Disease; Grant; HIV; HIV-2; Habits; Health Services Accessibility; Heart Diseases; Human; Iceberg; Image; Immune; Infection; Inflammation; Institution; Insulin Resistance; Journals; Knowledge; Learning; Left; Life; Life Style; Link; Low income; Lung diseases; Malignant Neoplasms; Metabolic; Minority; Monitor; Numbers; Obesity; Pathogenesis; Pharmaceutical Preparations; Pharmacotherapy; Process; Provider; RNA; Research; Research Personnel; Resources; Risk; Risk Factors; Scientist; Screening procedure; Source; Stroke; Syndrome; Testing; Therapeutic; Therapeutic Intervention; Toxic effect; United States National Institutes of Health; Virus Diseases; Virus Replication; Visceral; Woman; biomedical scientist; experience; men; multidisciplinary; novel therapeutics; peer; socioeconomics; virus related cancer

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Infection with human immunodeficiency virus (HIV), use of highly active antiretroviral drug therapies (HAART), undesirable lifestyle/behavioral choices, genetic background, and other factors all contribute to adverse metabolic and morphometric changes in appreciable numbers of adults and children living with HIV. At least in the developed world, HIV/AIDS has transitioned from certain death to a chronic, manageable condition with the potential for long-term salubrious survival, due to therapeutic advances made over the past 10yrs. But many challenges remain, as outlined by the articles in this volume of the Journal of the CardioMetabolic Syndrome. With longer-term survival, will HIV-infected people succumb to the causes of death that are most common among aging humans in the industrialized world, especially components of the cardiometabolic syndrome (heart disease, stroke, lung disease, diabetes), but at an earlier age? Does HIV-infection and the accompanying chronic proinflammatory processes, impart increased risk for these most common causes of death? Are there HIV-specific risk factors for the cardiometabolic syndrome? Recent observational data indicate that deaths from cardiovascular disease, diabetes, non-HIV-related cancer, and drug abuse may be increasing among HIV-infected people (4-8). In addition, socioeconomic and demographic data from the CDC suggest that low-income, poorly educated, young minority men and women with poor access to health care constitute a disproportionate percentage of people newly infected with HIV (2, 3). Are these not the same groups in the general population that are at greater risk for developing diabetes, obesity, heart disease, and cancer? Likewise, the HIV epidemic is most serious in resource-limited areas of the world. As these regions become more developed and industrialized, we anticipate a "collision of epidemics"; HIV and the cardiometabolic syndrome, and recent analyses support this notion (1). The issues are complex and will require multidisciplinary teams and approaches to resolve. The more fundamental questions are left to be resolved by the biomedical scientists (i.e., the contributing authors to this volume and their peers) and include: Are we being alarmist? After all, we only have 10yrs of experience with antiretroviral medications. Maybe newer medications and treatment paradigms will have fewer toxicities. What are the underlying mechanisms that link HIV, HAART, lifestyle habits, and genetic predisposition to the development of cardiometabolic syndromes? Do these mechanisms point us to established or novel therapeutic interventions for the cardiometabolic syndrome in HIV? By studying cardiometabolic syndrome in HIV, can we learn more about the pathogenesis of cardiometabolic syndrome in the general population? Are there interactions between the immune and cardiovascular systems that we are overlooking? Can technological and analytical advances (e.g., imaging, "omics", RNA knockdown) help us identify, characterize, or treat the evolving cardiometabolic syndrome in HIV? How can we develop, test, and implement better screening, monitoring, and treatments for the cardiometabolic syndrome in HIV in all parts of the world? Does the research and knowledge gained about HIV and HAART in the developed countries, properly inform providers about how to treat and manage HIV-infected people in resource limited regions of the world? These are all difficult questions. They strongly suggest that research on HIV and the cardiometabolic syndrome must continue to receive support. We propose that research efforts have only scraped the "tip of the iceberg". Given our limited experience with HAART and the complexities of HIV-replication, combined with our extensive knowledge of the proatherogenic disposition of dyslipidemia, inflammation, visceral adiposity, insulin resistance, poor eating behaviors and physical inactivity, one can only envision that this is the "tip of the iceberg" for a future epidemic of cardiometabolic syndrome in people living with HIV. We hope that scientists and clinicians continue to seek unbiased knowledge and the truth about these issues, and that granting agencies and policymakers respond to this knowledge appropriately.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 人类免疫缺陷病毒（HIV）感染、高活性抗逆转录病毒药物疗法（HAART）的使用、不良生活方式/行为选择、遗传背景和其他因素都会导致大量艾滋病毒感染者的代谢和形态变化。 至少在发达国家，由于过去十年治疗方法的进步，艾滋病毒/艾滋病已经从必死无疑转变为一种慢性、可控制的疾病，并有可能长期健康生存。 但正如《心脏代谢综合征杂志》本卷中的文章所概述的那样，许多挑战仍然存在。 随着生存时间的延长，艾滋病毒感染者是否会死于工业化世界老年人中最常见的死因，尤其是心脏代谢综合征（心脏病、中风、肺病、糖尿病），但年龄较早？ HIV 感染和伴随的慢性促炎症过程是否会增加这些最常见死因的风险？心脏代谢综合征是否存在 HIV 特异性危险因素？最近的观察数据表明，艾滋病毒感染者中死于心血管疾病、糖尿病、非艾滋病毒相关癌症和药物滥用的人数可能正在增加 (4-8)。 此外，疾病预防控制中心的社会经济和人口数据表明，低收入、教育程度低、难以获得医疗保健的年轻少数族裔男女在新感染艾滋病毒的人中所占比例过高 (2, 3)。 这些人不正是普通人群中患糖尿病、肥胖症、心脏病和癌症的高风险人群吗？ 同样，艾滋病毒流行在世界上资源有限的地区最为严重。 随着这些地区变得更加发达和工业化，我们预计会出现“流行病碰撞”； HIV 和心脏代谢综合征以及最近的分析支持了这一观点 (1)。 这些问题很复杂，需要多学科团队和方法来解决。 更基本的问题有待生物医学科学家（即本书的撰稿人及其同行）​​解决，包括：我们是否危言耸听？毕竟，我们在抗逆转录病毒药物方面只有 10 年的经验。也许更新的药物和治疗模式的毒性会更少。 HIV、HAART、生活习惯和遗传倾向与心脏代谢综合征的发生相关的潜在机制是什么？ 这些机制是否为我们指明了针对艾滋病毒心脏代谢综合征的既定或新颖的治疗干预措施？通过研究艾滋病毒心脏代谢综合征，我们能否更多地了解普通人群心脏代谢综合征的发病机制？免疫系统和心血管系统之间是否存在我们忽视的相互作用？技术和分析进步（例如成像、“组学”、RNA 敲低）能否帮助我们识别、表征或治疗 HIV 中不断演变的心脏代谢综合征？ 我们如何在世界各地开发、测试和实施更好的针对艾滋病毒心脏代谢综合征的筛查、监测和治疗？发达国家关于艾滋病毒和高效抗逆转录病毒疗法（HAART）的研究和知识是否能够正确告知医疗服务提供者如何治疗和管理世界资源有限地区的艾滋病毒感染者？ 这些都是难题。他们强烈建议有关艾滋病毒和心脏代谢综合征的研究必须继续得到支持。我们认为研究工作只是刮开了“冰山一角”。鉴于我们在HAART方面的经验有限以及HIV复制的复杂性，再加上我们对血脂异常、炎症、内脏肥胖、胰岛素抵抗、不良饮食行为和缺乏身体活动等促动脉粥样硬化的广泛了解，人们只能想象，这只是未来艾滋病毒感染者中流行的心脏代谢综合征的“冰山一角”。我们希望科学家和临床医生继续寻求有关这些问题的公正知识和真相，并希望资助机构和政策制定者对这些知识做出适当的反应。