Who to piggyback?

A new study suggests that, rather than "Killing-the-Winner", phages instead "Piggyback-the-Winner"

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Phages (viruses that infect bacteria) come in two flavours: lytic and lysogenic. Lytic phages lyse their hosts to release progeny, whereas lysogenic phages replicate by integrating into their host's genome. Based on these lifestyles, lysogeny has been postulated to promote viral survival when hosts are less abundant, whereas lytic phages have been proposed to follow a "Kill-the-Winner" model in which increased host abundance enables increased viral replication.

However, a recent study in Nature challenges these notions by showing that the relative abundance of virus-like particles (VLP) declines as host density increases; and that the the abundance of hallmark genes encoded by lysogenic viruses increases as microbial abundance increases. Collectively, these data suggest that, as host abundance increases, there is a lytic to lysogenic switch in phage lifestyle, supporting a "more microbes, fewer viruses" model that the authors termed "Piggyback-the-Winner". Notably, this holds true in multiple habitats, including in coral reefs, in the deep ocean, in polar lakes, in rivers, lakes and soils, and in animal-associated environments.

Given the importance of lytic/lysogenic switches in regulating the role of phages in multiple ecosystems, it'll be interesting to see how this study changes our understanding of how these viruses mediate important ecological and biogeochemical processes.

Claudio Nunes-Alves

Senior Editor, Nature Microbiology

I'm a senior editor at Nature Microbiology, interested in all things bacteria, virus, archaea, fungi and parasites (but I mostly handled articles focusing on bacterial physiology, evolution, parasites and archaea). Before joining Nature, I studied biochemistry at the University of Porto, Portugal, as an undergrad; and was a grad student and post-doc in the labs of Margarida Correia-Neves (ICVS, Braga, Portugal), Sam Behar (Brigham and Women's Hospital and Harvard Medical School, Boston, MA, and then at UMass Medical School, Worcester, MA) and Christophe Benoist (at Harvard Medical School, Boston, MA), where I studied multiple aspects of immunity to tuberculosis.