In the past two decades there have been substantial advances in understanding the anti-cancer mechanisms of oncolytic viruses (OVs). OVs can mediate their effects directly, by preferentially infecting and killing tumour cells. Additionally, OVs can indirectly generate anti-tumour immune responses. These differing mechanisms have led to a paradoxical divergence in strategies employed to further increase the potency of oncolytic virotherapies. On one hand, the tumour neovasculature is seen as a vital lifeline to the survival of the tumour, leading some to use OVs to target the tumour vasculature in hopes to starve cancers. Therapeutics causing vascular collapse can potentiate tumour hypoxia, nutrient restriction and pro-inflammatory cytokine release, which has shown promise in oncological studies. On the other hand, the same vasculature plays an important role for the dissemination of OVs, trafficking of effector cells and other therapeutics, which has prompted researchers to find ways of normalizing the vasculature to enhance infiltration of leukocytes and delivery of therapeutic agents. This article describes the recent developments of therapies aimed to shut down versus normalize tumour vasculature in order to inform researchers striving to optimize OV-based therapies.

在过去的二十年里，在理解溶瘤病毒 (OVs) 的抗癌机制方面取得了重大进展。OVs 可以通过优先感染和杀死肿瘤细胞来直接介导它们的作用。此外，OVs 可以间接产生抗肿瘤免疫反应。这些不同的机制导致了用于进一步提高溶瘤病毒疗法效力的策略的矛盾分歧。一方面，肿瘤新血管系统被视为肿瘤存活的重要生命线，导致一些人使用 OV 靶向肿瘤血管系统，以期让癌症挨饿。导致血管塌陷的治疗剂可以加强肿瘤缺氧、营养限制和促炎细胞因子的释放，这在肿瘤学研究中显示出前景。另一方面，相同的脉管系统在 OV 的传播、效应细胞的运输和其他治疗方面发挥着重要作用，这促使研究人员寻找使脉管系统正常化的方法，以增强白细胞的浸润和治疗剂的递送。本文描述了旨在关闭与正常化肿瘤血管系统的疗法的最新进展，以便为努力优化基于 OV 的疗法的研究人员提供信息。