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首页> 外文期刊>AIDS Research and Human Retroviruses >Cryptosporidiosis in rhesus macaques challenged during acute and chronic phases of SIV infection.
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Cryptosporidiosis in rhesus macaques challenged during acute and chronic phases of SIV infection.

机译：在恒河猴的急性和慢性阶段，恒河猴的隐孢子虫病受到了挑战。

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The intestinal immune dysfunction due to loss of mucosal and peripheral CD4(+) T cells in individuals with HIV/AIDS is presumably responsible for the establishment of persistent cryptosporidiosis. Simian immunodeficiency virus (SIV)-infected macaques were used to investigate the phase/timing in SIV infection, which permits a self-limiting Cryptosporidium parvum infection to become persistent in immunodeficient hosts because of significant mucosal immune defects. Two groups of SIV-infected macaques were challenged with C. parvum; one was challenged during the acute SIV infection phase (2 weeks post-SIV infection) and the second was challenged during the chronic SIV phase (CD4 counts 200-500 cells/mul of blood). Samples (fecal, blood, biopsy, and necropsy) were collected at different time points after infection to correlate the progression of disease with the immune status of the animals. All seven SIV-infected macaques challenged during the acute phase of SIV infection became persistently infected and excreted oocysts for 1-4 months. However, four of the six in the chronic SIV phase became infected with cryptosporidiosis, of which one survived 2 weeks and one became naturally infected. Sequential analysis of CD4(+) in blood and intestines of coinfected macaques exhibited pronounced losses of CD4 T cells during the first 2 weeks after SIV infection, followed by transient rebound of CD4 T cells in the gut after C. parvum infection, and then a gradual loss over subsequent months. Persistent cryptosporidiosis was more consistently induced during the acute SIV phase indicating that profound viral damage to gut lymphoid tissue during the acute phase was more conducive, compared with the chronic phase, to establishing persistent cryptosporidiosis than low circulating CD4 T cells.
机译：在艾滋病毒/艾滋病患者中，由于粘膜和外周CD4（+）T细胞的丧失而导致的肠道免疫功能异常可能是造成持续性隐孢子虫病的原因。使用猿猴免疫缺陷病毒（SIV）感染的猕猴来研究SIV感染的阶段/时间，由于自身的粘膜免疫缺陷，使得自限性隐孢子虫感染可以在免疫缺陷宿主中持续存在。两组被SIV感染的猕猴用小球藻攻击。一种在急性SIV感染阶段（SIV感染后2周）受到攻击，第二种在慢性SIV感染阶段（CD4计数200-500细胞/多血）受到攻击。在感染后的不同时间点采集样本（粪便，血液，活检和尸检），以将疾病的进展与动物的免疫状况相关联。在SIV感染的急性期受到攻击的所有7只SIV感染的猕猴都被持续感染并排出卵囊，持续1-4个月。但是，在慢性SIV期的6例中有4例感染了隐孢子虫病，其中1例存活了2周，而1例自然感染。在SIV感染后的最初2周内，对合并感染的猕猴的血液和肠道中的CD4（+）进行顺序分析，显示CD4 T细胞明显丢失，随后小肠衣原体感染后肠道中CD4 T细胞短暂反弹。在随后的几个月中逐渐损失。持续性隐孢子虫病在急性SIV阶段被更一致地诱导，这表明与慢性期相比，在急性期对肠道淋巴组织的严重病毒损害比低循环CD4 T细胞更有利于建立持续性隐孢子虫病。

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