FOCUS ISSUE ON HIV AND THE CARDIOMETABOLIC SYNDROME

关注艾滋病毒和心脏代谢综合征

基本信息

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
项目类别：
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

项目摘要

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.

该副本是利用众多研究子项目之一由NIH/NCRR资助的中心赠款提供的资源。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此，可以在其他清晰的条目中表示。列出的机构是对于中心，这不一定是调查员的机构。感染人类免疫缺陷病毒（HIV），使用高度活跃的抗逆转录病毒药物疗法（HAART），不良的生活方式/行为选择，遗传背景和其他因素，都导致不良代谢和形态计数器，患有艾滋病毒的成人和儿童的不良代谢和形态变化。至少在发达国家，由于过去10年中的治疗性进步，艾滋病毒/艾滋病已经从某些死亡转变为长期可管理的，有可能出现长期生存的状况。但是，如《心脏代谢综合征杂志》杂志中的文章所概述的那样，仍然存在许多挑战。具有长期的生存，将艾滋病毒感染的人屈服于工业化世界中衰老的人类中最常见的死亡原因，尤其是心脏代谢综合征的成分（心脏病，中风，肺部疾病，糖尿病），但在年龄？艾滋病毒感染和随附的慢性促炎过程是否会增加对这些最常见的死亡原因的风险？心脏代谢综合征是否有HIV特异性危险因素？最近的观察数据表明，心血管疾病，糖尿病，非HIV相关癌症和药物滥用的死亡可能正在增加HIV感染者（4-8）。此外，来自CDC的社会经济和人口统计数据表明，获得医疗保健的低收入，受过良好教育的年轻男性和不良的男女占新感染艾滋病毒的人中的比例不成比例（2，3）。这些在普通人群中与患糖尿病，肥胖，心脏病和癌症的风险更大的群体是否相同？同样，艾滋病毒流行病在世界上有限的领域中最严重。随着这些地区变得越来越发达和工业化，我们预计会有“流行病的碰撞”。 HIV和心脏代谢综合征，最近的分析支持了这一概念（1）。这些问题很复杂，需要多学科的团队和方法才能解决。生物医学科学家（即，对本卷及其同行的作者的贡献者）要解决的更根本的问题要解决：我们是警报者吗？毕竟，我们只有10年的抗逆转录病毒药物经验。也许较新的药物和治疗范例将减少毒性。将HIV，HAART，生活方式习惯和遗传易感性与心脏代谢综合征的发展联系起来的基本机制是什么？这些机制是否指向HIV中心脏代谢综合征的确定或新颖的治疗干预措施？通过研究HIV中的心脏代谢综合征，我们可以更多地了解一般人群中心脏代谢综合征的发病机理吗？我们忽略的免疫和心血管系统之间是否存在相互作用？技术和分析的进步（例如成像，“ OMICS”，RNA敲低）可以帮助我们在HIV中识别，表征或治疗不断发展的心脏代谢综合征？我们如何在世界各地开发，测试和实施对艾滋病毒中心脏代谢综合征的更好的筛查，监测和治疗？关于发达国家的艾滋病毒和哈特的研究和知识是否适当地告知提供者如何治疗和管理世界有限地区的艾滋病毒感染者？这些都是困难的问题。他们强烈建议对HIV和心脏代谢综合征的研究必须继续得到支持。我们建议研究工作只刮了“冰山一角”。考虑到我们在HAART方面的有限经验以及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，不良饮食行为和身体不活动的广泛了解，只能设想这就是“这就是”冰山一角“对于艾滋病毒患者的心脏代谢综合征的未来流行。我们希望科学家和临床医生继续寻求公正的知识和有关这些问题的真相，并授予机构和政策制定者对这一知识做出适当回应。