近日，加拿大多伦多大学教授Karen L. Maxwell及其研究团队揭示了前噬菌体阻断细胞表面受体以保护其病毒后代。该研究于2025年7月16日发表于国际一流学术期刊《自然》杂志上。

据悉，在微生物群落中，病毒主题竞争宿主细胞，并进化出多种机制来抑制竞争对手。一种策略是重复感染排斥，即已建立的病毒感染可以防止同一细胞的继发性感染。这一现象已被证明在真核病毒的传播中起着重要作用。

在这里，研究团队确定了细菌病毒（噬菌体）中的重复感染排斥蛋白发挥类似的作用，促进病毒在细菌群落中的传播。该课题组描述了一种能调控常见噬菌体——IV型菌毛动态的噬菌体蛋白Zip。这种被称为Zip的蛋白质并没有废除它们的活性，而是对其进行微调，在不消耗健康成本的情况下提供强大的噬菌体防御。值得注意的是，Zip还可以防止新释放的噬菌体后代的内化和破坏，课题组将这种现象称为抗克罗诺斯效应，这是希腊神话中吞噬其后代的神。Zip活性促进细菌溶原群落中游离噬菌体的积累，从而增强病毒的传播。

研究团队进一步证明了抗克罗诺斯效应在不同的噬菌体编码的重复感染排斥系统中是保守的。他们的研究结果确定了保护噬菌体后代的重复感染排斥系统的机制基础，并为细菌和真核系统之间的病毒防御机制的保护提供了见解。

附：英文原文

Title: Prophages block cell surface receptors to preserve their viral progeny

Author: Taylor, Vronique L., Patel, Pramalkumar H., Shah, Megha, Yusuf, Ahmed, Burk, Cayla M., Sztanko, Kristina M., Gitai, Zemer, Davidson, Alan R., Koch, Matthias D., Maxwell, Karen L.

Issue&Volume: 2025-07-16

Abstract: In microbial communities, viruses compete for host cells and have evolved diverse mechanisms to inhibit competitors. One strategy is superinfection exclusion, whereby an established viral infection prevents a secondary infection of the same cell1. This phenomenon has been shown to have an important role in the spread of eukaryotic viruses. Here we determine that superinfection exclusion proteins in bacterial viruses (bacteriophages, hereafter phages) perform a similar role, promoting viral spread through the bacterial community. We characterize a phage protein that alters the dynamics of a common phage receptor, the type IV pilus. This protein, known as Zip, does not abrogate pilus activity, but fine-tunes it, providing a strong phage defence without a fitness cost. Notably, Zip also prevents internalization and destruction of newly released phage progeny, a phenomenon that we call the anti-Kronos effect after the Greek god who consumed his offspring. Zip activity promotes the accumulation of free phages in bacterial lysogen communities, thereby enhancing viral spread. We further demonstrate that the anti-Kronos effect is conserved across diverse prophage-encoded superinfection exclusion systems. Our results identify the mechanistic basis of a superinfection exclusion system that safeguards phage progeny and provide insights into the conservation of viral defence mechanisms among bacterial and eukaryotic systems.

DOI: 10.1038/s41586-025-09260-z

Source: https://www.nature.com/articles/s41586-025-09260-z