ALCOHOL AND AIDS-A MURINE MODEL

酒精和艾滋病——小鼠模型

• 批准号: 3028478
• 负责人: ELIZABETH ANN FITZPATRICK
• 金额: $ 2.86万
• 依托单位: UNIVERSITY OF KENTUCKY
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-08-29 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3028478
• 关键词: AIDS; B lymphocyte; HIV infections; T cell receptor; T lymphocyte; alcoholic beverage consumption; alcoholism /alcohol abuse; cytokine; disease /disorder model; drug abuse; flow cytometry; human immunodeficiency virus; immunosuppression; laboratory mouse; leukocyte activation /transformation; model design /development; pathogenic diet; polymerase chain reaction; virus replication

The acquired immunodeficiency syndrome (AIDS) has become a critical health problem in the United States. Infection with the disease-causing lentivirus-HIV-results in a progressive and debilitating immunosuppression. Because of the period between initial infection with HIV and onset of AIDS is quite variable among individuals, it is important to determine the role of co-factors, such as alcohol abuse, in the development of the disease. It has been reported that ethanol consumption has a detrimental effect on the ability of the host to generate humoral and cellular immune responses. Chronic alcohol abuse is common among drug users, a group at high risk for AIDS, and ethanol associated immunosuppression may act synergistically with HIV-induced immunosuppression to shorten the onset of disease and/or increase the severity of disease. We will use the retroviral-induce murine acquired immunodeficiency syndrome (MAIDS) model to determine the effect of acute and chronic ethanol consumption on the development of HIV-associated immunosuppression. Experiments are designed to determine the effect of ethanol on the replication of the MAIDS virus mixture in infected animals. We will also examine the effect of ethanol on the percentage of T and B cells which are activated by virus infection as well as the subsets of T and B cells responsible for the lymphoproliferation. Finally we will examine the mechanisms of retroviral-induce immunosuppression and the effect of ethanol consumption on generation of these mechanisms.

获得性免疫缺陷综合症（艾滋病）已成为一个关键的 美国的健康问题。感染致病菌 慢病毒-艾滋病毒-结果在一个渐进的和衰弱的 免疫抑制由于初次感染与 艾滋病毒和艾滋病的发病在个体之间有很大的差异， 重要的是要确定辅助因素的作用，如酗酒， 疾病的发展。据报道，乙醇 消费对宿主的能力有不利影响， 产生体液和细胞免疫反应。长期酗酒是 在吸毒者中很常见，这是一个艾滋病高危人群， 相关的免疫抑制可能与HIV诱导的 免疫抑制以缩短疾病发作和/或增加 疾病的严重程度。我们将使用逆转录病毒诱导小鼠获得性 免疫缺陷综合征（MAIDS）模型，以确定急性 和慢性酒精消费对HIV相关性 免疫抑制设计实验以确定 乙醇对感染的MAIDS病毒混合物复制的影响 动物我们还将研究乙醇对 T和B细胞，它们被病毒感染激活， T和B细胞亚群负责淋巴细胞增殖。 最后，我们将研究逆转录病毒诱导的机制。 免疫抑制和乙醇消耗对产生的影响 这些机制。

项目成果

Activation-dependent apoptosis in CD4+ T cells during murine AIDS.

小鼠艾滋病期间 CD4 T 细胞的激活依赖性凋亡。

• DOI: 10.1006/cimm.1993.1248
• 发表时间: 1993
• 期刊: Cellular immunology
• 影响因子: 4.3
• 作者: Cohen,DA;Fitzpatrick,EA;Barve,SS;Guthridge,JM;Jacob,RJ;Simmerman,L;Kaplan,AM
• 通讯作者: Kaplan,AM

Ethanol as a possible cofactor in the development of murine AIDS.

乙醇作为小鼠艾滋病发展的可能辅助因子。

• DOI: 10.1111/j.1530-0277.1995.tb00967.x
• 发表时间: 1995
• 期刊: Alcoholism, clinical and experimental research
• 作者: Fitzpatrick,EA;Rhoads,CA;Espandiari,P;Kaplan,AM;Cohen,DA
• 通讯作者: Cohen,DA