Alzheimer’s disease (AD) is a multifactorial disease triggered by environmental factors in combination with genetic predisposition. Infectious agents, in particular herpes simplex virus type 1 (HSV-1), are gradually being recognised as important factors affecting the development of AD. However, the mechanism linking HSV-1 and AD remains unknown. Of note, HSV-1 manipulates the activity of cofilin-1 to ensure their efficient infection in neuron cells. Cofilin-1, the main regulator of actin cytoskeleton reorganization, is implicating for the plastic of dendritic spines and axon regeneration of neuronal cells. Moreover, dysfunction of cofilin-1 is observed in most AD patients, as well as in mice with AD and ageing. Further, inhibition of cofilin-1 activity ameliorates the host cognitive impairment in an animal model of AD. Together, dysregulation of cofilin-1 led by HSV-1 infection is a potential link between HSV-1 and AD. Herein, we critically summarize the role of cofilin-1-mediated actin dynamics in both HSV-1 infection and AD, respectively. We also propose several hypotheses regarding the connecting roles of cofilin-1 dysregulation in HSV-1 infection and AD. Our review provides a foundation for future studies targeting individuals carrying HSV-1 in combination with cofilin-1 to promote a more individualised approach for treatment and prevention of AD.

阿尔茨海默氏病（AD）是由环境因素与遗传易感性结合触发的多因素疾病。感染因子，特别是1型单纯疱疹病毒（HSV-1），逐渐被认为是影响AD发生的重要因素。但是，连接HSV-1和AD的机制仍然未知。值得注意的是，HSV-1操纵cofilin-1的活性以确保它们在神经元细胞中的有效感染。Cofilin-1是肌动蛋白细胞骨架重组的主要调节剂，与树突棘的可塑性和神经元细胞的轴突再生有关。而且，在大多数AD患者以及患有AD和衰老的小鼠中观察到cofilin-1功能障碍。此外，抑制cofilin-1活性可改善AD动物模型中的宿主认知障碍。一起，HSV-1感染导致的cofilin-1失调是HSV-1与AD之间的潜在联系。在这里，我们批判性地总结了cofilin-1介导的肌动蛋白动力学分别在HSV-1感染和AD中的作用。我们还提出了关于cofilin-1失调在HSV-1感染和AD中的联系作用的几种假设。我们的综述为今后针对携带HSV-1和cofilin-1的个体开展研究提供了基础，以促进更具个性化的治疗和预防AD的方法。