自然杀伤（NK）细胞是先天性淋巴细胞，参与免疫应答，抵抗病毒感染和肿瘤。为了对抗它们，病毒和肿瘤采取策略来逃避NK细胞介导的免疫监视。在本综述中，我们探讨了病毒采取的免疫逃避策略，重点关注人类巨细胞病毒（HCMV）和严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的例子。我们将选择的病毒逃避机制分为三类进行分类研究：（1）为抑制性受体NKG2A提供配体，（2）下调激活性受体NKG2D的配体，（3）诱导免疫抑制细胞因子转化生长因子（TGF）-β。对于每一类机制，我们比较了病毒和肿瘤的免疫逃避，回顾了在癌症治疗中克服逃避的潜在机会。我们认为，对病毒和NK细胞之间的宿主-病原体相互作用进行深入研究，不仅可以加深我们对病毒免疫逃避的理解，还可以揭示NK细胞如何应对这种逃避尝试的方式。因此，由于病毒和肿瘤的免疫逃避之间的相似之处，我们提议从抗病毒NK细胞反应中获得的见解可能为设计未来的肿瘤免疫治疗提供有价值的经验。该文章受版权保护，保留所有权利。该文章受版权保护，保留所有权利。

Natural killer (NK) cells are innate lymphocytes that participate in immune responses against virus-infected cells and tumors. As a countermeasure, viruses and tumors employ strategies to evade from NK cell-mediated immunosurveillance. In this review, we examine immune evasion strategies employed by viruses, focusing on examples from human cytomegalovirus (HCMV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We explore selected viral evasion mechanisms categorized into three classes: (1) providing ligands for the inhibitory receptor NKG2A, (2) down-regulating ligands for the activating receptor NKG2D, and (3) inducing the immunosuppressive cytokine transforming growth factor (TGF)-β. For each class, we draw parallels between immune evasion by viruses and tumors, reviewing potential opportunities for overcoming evasion in cancer therapy. We suggest that in-depth investigations of host-pathogen interactions between viruses and NK cells will not only deepen our understanding of viral immune evasion but also shed light on how NK cells counter such evasion attempts. Thus, due to the parallels of immune evasion by viruses and tumors, we propose that insights gained from anti-viral NK cell responses may serve as valuable lessons that can be leveraged for designing future cancer immunotherapies. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.