Social and psychological risk for infectious illness

传染病的社会和心理风险

• 批准号: 7233570
• 负责人: SHELDON A COHEN
• 金额: $ 55.23万
• 依托单位: CARNEGIE-MELLON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-07-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7233570
• 关键词: Address; Adrenal hormone preparation; Adult; Affect; Alcohol consumption; Anti-Inflammatory Agents; Anti-inflammatory; Antibodies; Attention; Autonomic nervous system; Behavior; Behavioral; Behavioral inhibition; Biochemical; Biological; Biological Assay; Blood Pressure; Body Temperature; Cellular Immunity; Characteristics; Chemicals; Clinical; Communicable Diseases; Conflict (Psychology); Cotinine; Daily; Data; Delayed Hypersensitivity; Demographic Factors; Diet; Disease; Disease Resistance; Disease susceptibility; Drops; Electronics; Emotional; Emotions; Environment; Environmental Risk Factor; Equilibrium; Event; Goals; Health; Heart Rate; Host resistance; Hostility; Hydrocortisone; Hypothalamic structure; Immune; Immune response; Immunity; Individual; Individual Differences; Infection; Inflammation; Inflammatory; Inflammatory Response; Intake; Intervention; Interview; Life; Link; Measurement; Measures; Mediating; Mediator of activation protein; Mitogens; Modeling; Molds; Monitor; Mucociliary Clearance; Neurosecretory Systems; Nicotine; Nose; Outcome; Parasympathetic Nervous System; Pathway interactions; Peripheral Blood Mononuclear Cell; Personality; Persons; Pharmacologic Substance; Physical activity; Physiological; Pituitary Gland; Play; Predisposition; Procedures; Process; Production; Psychosocial Factor; Quarantine; Range; Rate; Recovery; Regulation; Reporting; Resistance to infection; Resolution; Rest; Rhinovirus; Risk; Role; Saliva; Sampling; Severity of illness; Shyness; Skin; Sleep; Smoking; Social Characteristics; Social Environment; Social Network; Social support; Stream; Stress; Symptoms; System; Techniques; Technology; Testing; Time; Upper Respiratory Infections; Viral; Virus; Virus Diseases; Virus Shedding; Work; behavior influence; clinical Diagnosis; cytokine; day; design; desire; diaries; disorder risk; environmental intervention; extravert; immune function; improved; innovation; interest; interpersonal conflict; introvert; member; novel; pill; prospective; psychologic; psychosocial; respiratory; respiratory infection virus; response; social; trait

DESCRIPTION (provided by applicant): Our primary goals are to assess the influence of the social environment on susceptibility to upper respiratory illness and to identify the pathways through which environmental factors "get under the skin" to influence disease expression. We hypothesize that the social environment influences behavior, hypothalamic-pituitary-adrenocortical (HPA) and autonomic nervous system (ANS) responses which in turn influence the regulation of both cellular and humoral immune response to the virus. We use a unique prospective design. We first assess characteristics of the social environment and the status of behavioral and physiological systems we predict to link these characteristics to host resistance in 260 healthy adults who are seronegative for antibodies to the challenge virus. Subsequently, we expose each subject by intranasal drops to one of two strains of rhinovirus and monitor them closely for evidence of infection and illness in a cloistered environment. Measures of illness collected immediately before and daily during the cloister include virus shedding and titer, nasal pro-inflammatory, anti-inflammatory and anti-viral cytokine production, nasal and general symptoms, body temperature, nasal secretion production and nasal mucociliary clearance function. Using these data, we will determine if the social environment influences illness expression by altering baseline cellular immune status (delayed type hypersensitivity), Th-1/Th-2 cytokine balance, and the ability to produce pro-inflammatory cytokines (from mitogen stimulated peripheral blood mononuclear cells); whether it influences the regulation of cytokine production in response to the infection; and whether the association between the social environment and immunity are mediated by the ANS (separating sympathetic and parasympathetic contributions) and/or HPA systems. All analyses will control for demographic factors and will focus on whether the social environment predicts clinical illness (verified infection + clinical diagnosis). The results of this study will define the pathways by which one's social environment influences their susceptibility to upper respiratory virus infection and may identify potential targets for behavioral or pharmaceutical interventions to restore disease resistance in persons most at risk because of their social environments.

描述（由申请人提供）：我们的主要目标是评估社会环境对上呼吸道疾病易感性的影响，并确定环境因素“进入皮肤”影响疾病表达的途径。我们假设，社会环境影响行为，下丘脑-垂体-肾上腺皮质（HPA）和自主神经系统（ANS）的反应，这反过来又影响调节细胞和体液免疫反应的病毒。我们采用独特的前瞻性设计。我们首先评估社会环境的特征和行为和生理系统的状态，我们预测这些特征与260名健康成年人的宿主抗性有关，这些健康成年人对挑战病毒的抗体呈阴性。随后，我们通过鼻内滴注将每个受试者暴露于两种鼻病毒株中的一种，并密切监测他们在封闭环境中的感染和疾病证据。在修道院之前立即和每天收集的疾病测量包括病毒脱落和滴度，鼻促炎、抗炎和抗病毒细胞因子产生，鼻和全身症状，体温，鼻分泌物产生和鼻粘膜纤毛清除功能。利用这些数据，我们将确定社会环境是否通过改变基线细胞免疫状态来影响疾病表达（迟发型超敏反应）、Th-1/Th-2细胞因子平衡和产生促炎细胞因子的能力（来自有丝分裂原刺激的外周血单核细胞）;它是否影响响应于感染的细胞因子产生的调节;以及社会环境和免疫之间的关联是否由ANS（分离交感神经和副交感神经贡献）和/或HPA系统介导。所有分析将控制人口统计学因素，并将重点关注社会环境是否预测临床疾病（经证实的感染+临床诊断）。这项研究的结果将确定一个人的社会环境影响他们对上呼吸道病毒感染的易感性的途径，并可能确定行为或药物干预的潜在目标，以恢复由于社会环境而处于最高风险的人的疾病抵抗力。