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猫免疫缺陷病毒使猫易患急性全身性弓形虫病。

Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis.

作者信息

Davidson M G, Rottman J B, English R V, Lappin M R, Tompkins M B

机构信息

Department of Companion Animal and Special Species Medicine, North Carolina State University, Raleigh.

出版信息

Am J Pathol. 1993 Nov;143(5):1486-97.

Abstract

This study was designed to examine the effects of a pre-existing, clinically asymptomatic feline immunodeficiency virus (FIV) infection on a primary challenge with Toxoplasma gondii. Parenteral challenge of FIV-infected cats with tachyzoites of the ME49 strain of T. gondii caused a precipitous drop in all lymphocytes (CD4+, CD8+, and B cells) and generalized severe toxoplasmosis. The predominant postmortem lesions included acute and often fatal interstitial pneumonia, dominated histologically by macrophages, and multifocal to coalescing hepatic necrosis. Immunohistochemistry revealed numerous T. gondii antigen and tachyzoites in macrophages and other cell types in the lung lesions. The proliferative response of peripheral blood mononuclear cells to specific (T. gondii antigen) and nonspecific (Concanavalin A) mitogens was defective in the dually infected cats, suggesting marked immunosuppression. In contrast to the dually infected cats, cats infected only with T. gondii developed a transient, mild clinical disease characterized by anorexia, lethargy, and multifocal chorioretinitis. Lymphocyte changes in T. gondii-infected cats included an early pan-lymphopenia followed by reestablishment of all lymphocyte subset profiles. These cats also showed a reduced proliferative response to Concanavalin A at 1 week after challenge, but a measurable in vivo response to T. gondii antigens, as evidenced by in vitro lymphocyte proliferation in the absence of a mitogenic stimulus. These results show that infection of cats with FIV-NCSU, markedly enhances their susceptibility to a primary T. gondii infection and provides a model to study the mechanisms of the underlying immunological defect(s) occurring early after HIV infection that may predispose individuals to development of acquired immunodeficiency syndrome and associated diseases.

摘要

本研究旨在检测预先存在的、临床上无症状的猫免疫缺陷病毒(FIV)感染对初次感染刚地弓形虫的影响。用刚地弓形虫ME49株速殖子对感染FIV的猫进行肠胃外攻击,导致所有淋巴细胞(CD4 +、CD8 +和B细胞)急剧减少,并引发全身性严重弓形虫病。主要的死后病变包括急性且常致命的间质性肺炎,组织学上以巨噬细胞为主,以及多灶性至融合性肝坏死。免疫组织化学显示,肺部病变中的巨噬细胞和其他细胞类型中有大量刚地弓形虫抗原和速殖子。双重感染猫的外周血单核细胞对特异性(刚地弓形虫抗原)和非特异性(刀豆球蛋白A)有丝分裂原的增殖反应存在缺陷,提示明显的免疫抑制。与双重感染的猫不同,仅感染刚地弓形虫的猫会出现短暂的轻度临床疾病,其特征为厌食、嗜睡和多灶性脉络膜视网膜炎。感染刚地弓形虫的猫的淋巴细胞变化包括早期全淋巴细胞减少,随后所有淋巴细胞亚群谱重新建立。这些猫在攻击后1周对刀豆球蛋白A的增殖反应也降低,但对刚地弓形虫抗原有可测量的体内反应,体外淋巴细胞在无促有丝分裂刺激的情况下增殖即可证明。这些结果表明,用FIV - NCSU感染猫会显著增强它们对初次刚地弓形虫感染的易感性,并提供了一个模型来研究HIV感染后早期发生的潜在免疫缺陷机制,这些机制可能使个体易患获得性免疫缺陷综合征及相关疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb8/1887187/6144830127af/amjpathol00071-0261-a.jpg

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