Many incurable diseases in humans are related to autoimmunity and are initially induced by a viral infection. Presumably, the virus has antigens with epitopes similar to those found in components of the host's body, thus allowing it to evade immune surveillance. Viral infection activates the immune system, which results in viral clearance. After infection, the enhanced immune system may begin to attack the host's cells, tissues, and organs. In this study, we developed a simple mathematical model in which we identify the conditions needed to trigger an autoimmune response. This model considers the dynamics of T helper (Th) cells, viruses, self-antigens, and memory T cells. Viral infection results in a temporal increase in viral abundance, which is suppressed by an increase in the number of Th cells. For the virus to be eliminated from the body, the level of Th cells must be maintained above a certain threshold to prevent viral replication, even in the absence of virus in the body. This role is realized by memory T cells produced during temporal viral infections. Thus, we investigated the conditions needed for the immune response to be enhanced after viral infection and concluded that cross-immunity must be weak for negative selection and T-cell activation but strong for antigen-suppressing reactions. We also discuss alternative models of cross-immunity and possible extensions of the model.

中文翻译：

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由病原体感染引发的自身免疫性疾病：数学模型。

人类中许多无法治愈的疾病与自身免疫有关，最初是由病毒感染引起的。据推测，该病毒的抗原表位与宿主机体的抗原相似，因此可以逃避免疫监视。病毒感染会激活免疫系统，从而导致病毒清除。感染后，增强的免疫系统可能开始攻击宿主的细胞，组织和器官。在这项研究中，我们开发了一个简单的数学模型，其中我们确定了触发自身免疫反应所需的条件。该模型考虑了T辅助（Th）细胞，病毒，自身抗原和记忆T细胞的动力学。病毒感染导致病毒丰度随时间增加，这被Th细胞数量增加所抑制。为了将病毒从体内清除，即使体内不存在病毒，Th细胞的水平也必须保持在一定的阈值以上，以防止病毒复制。这种作用是通过在暂时性病毒感染过程中产生的记忆T细胞来实现的。因此，我们研究了病毒感染后增强免疫应答所需的条件，并得出结论：对于阴性选择和T细胞活化，交叉免疫必须弱，而对于抗原抑制反应则必须强。我们还将讨论交叉免疫的替代模型以及该模型的可能扩展。我们研究了病毒感染后增强免疫应答所需的条件，并得出结论：对于阴性选择和T细胞活化，交叉免疫必须弱，而对于抗原抑制反应则必须强。我们还将讨论交叉免疫的替代模型以及该模型的可能扩展。我们研究了病毒感染后增强免疫应答所需的条件，并得出结论：对于阴性选择和T细胞活化，交叉免疫必须弱，而对于抗原抑制反应则必须强。我们还将讨论交叉免疫的替代模型以及该模型的可能扩展。