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免疫功能低下的恒河猴(猕猴)自然感染和实验感染微小隐孢子虫D基因型。

Natural and experimental infection of immunocompromised rhesus macaques (Macaca mulatta) with the microsporidian Enterocytozoon bieneusi genotype D.

作者信息

Green Linda C, Didier Peter J, Bowers Lisa C, Didier Elizabeth S

机构信息

Department of Biology, Xavier University of Louisiana, 1 Drexel Drive, New Orleans, LA 70125, USA.

出版信息

Microbes Infect. 2004 Sep;6(11):996-1002. doi: 10.1016/j.micinf.2004.05.012.

Abstract

Microsporidia are obligate intracellular parasites that cause opportunistic infections in AIDS and other immunocompromised patients. Eight simian immunodeficiency virus (SIV)-infected rhesus macaque monkeys (Macaca mulatta) were inoculated orally with Enterocytozoon bieneusi spores isolated from intestinal lavage fluid of an AIDS patient (genotype D) to study the natural history of this infection. Four monkeys were already naturally infected with E. bieneusi (also genotype D), and were included to determine if a second inoculum affected the course of illness. Spore shedding was detected in feces of all eight monkeys within the first week of experimental infection. Five monkeys died within 3.5 months of experimental E. bieneusi inoculation. Three of these five monkeys began the study with CD4+CD29+ T cell levels well below 20% of total T lymphocytes. Deaths were due to a variety of AIDS-related manifestations. Microsporidia did not appear to directly contribute to mortality but may have contributed to morbidity. At necropsy, microsporidia were found in bile and tissue sections of the gallbladder but not in the gut, kidneys, or liver. The percent CD4+CD29+ levels of the last three monkeys remained near the level observed at the time of inoculation. These monkeys lived more than 2 years after the end of the study and continued to shed spores. This study corroborates previous reports that E. bieneusi can be reliably transmitted to SIV-infected rhesus monkeys but indicates that the use of SIV-infected monkeys for the study of microsporidiosis is complicated by the confounding effect of other opportunistic or AIDS-related infections.

摘要

微孢子虫是专性细胞内寄生虫,可在艾滋病患者和其他免疫功能低下的患者中引起机会性感染。为了研究这种感染的自然史,给8只感染了猿猴免疫缺陷病毒(SIV)的恒河猴(猕猴)口服从一名艾滋病患者的肠道灌洗液中分离出的比氏肠微孢子虫孢子(基因型D)。4只猴子已经自然感染了比氏肠微孢子虫(也是基因型D),将它们纳入研究以确定第二次接种是否会影响病程。在实验感染的第一周内,在所有8只猴子的粪便中都检测到了孢子排出。5只猴子在实验性接种比氏肠微孢子虫后的3.5个月内死亡。这5只猴子中有3只在开始研究时CD4+CD29+ T细胞水平远低于总T淋巴细胞的20%。死亡原因是各种与艾滋病相关的表现。微孢子虫似乎没有直接导致死亡,但可能导致了发病。尸检时,在胆囊的胆汁和组织切片中发现了微孢子虫,但在肠道、肾脏或肝脏中未发现。最后3只猴子的CD4+CD29+水平百分比仍接近接种时观察到的水平。这些猴子在研究结束后存活了2年多,并继续排出孢子。这项研究证实了之前的报告,即比氏肠微孢子虫可以可靠地传播给感染SIV的恒河猴,但表明使用感染SIV的猴子来研究微孢子虫病会因其他机会性或艾滋病相关感染的混杂效应而变得复杂。

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