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模拟人类嗜T淋巴细胞病毒I型感染的T细胞动态变化及发病机制。

Modeling the T-cell dynamics and pathogenesis of HTLV-I infection.

作者信息

Stilianakis N I, Seydel J

机构信息

Department of Medical Biometry, University of Tübingen, Westbahnhofstrasse 55, 72070 Tübingen, Germany.

出版信息

Bull Math Biol. 1999 Sep;61(5):935-47. doi: 10.1006/bulm.1999.0117.

Abstract

Human T-cell lymphotropic virus type I (HTLV-I) infection in humans causes a chronic infection of CD4+ T cells, and is associated with various disease outcomes, among them with the development of adult T-cell leukemia (ATL). The T-cell dynamics after HTLV-I infection can be described in a mathematical model with coupled differential equations. The infection process is modeled assuming cell-to-cell infection of CD4+ T cells. The model allows for CD4+ T cell subsets of susceptible, latently infected and actively infected cells as well as for leukemia cells. Latently infected T cells may harbor the virus for several years until they become activated and able to infect susceptible T cells. Uncontrolled proliferation of CD4+ T cells with monoclonal DNA-integration of HTLV-I results in the development of ATL. The model describes basic features that characterize HTLV-I infection; the chronic infection of CD4+ T cells, the increasing number of abnormal cells and the possible progression to ATL.

摘要

人类I型嗜T细胞病毒(HTLV-I)感染人体会导致CD4+ T细胞的慢性感染,并与多种疾病结局相关,其中包括成人T细胞白血病(ATL)的发生。HTLV-I感染后的T细胞动态可以用一个耦合微分方程的数学模型来描述。感染过程是在假设CD4+ T细胞进行细胞间感染的情况下建模的。该模型考虑了易感、潜伏感染和活跃感染的CD4+ T细胞亚群以及白血病细胞。潜伏感染的T细胞可能携带病毒数年,直到它们被激活并能够感染易感T细胞。HTLV-I单克隆DNA整合导致CD4+ T细胞不受控制地增殖,从而引发ATL。该模型描述了HTLV-I感染的基本特征;CD4+ T细胞的慢性感染、异常细胞数量的增加以及可能发展为ATL的过程。

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