In contrast to the classical notion that virions function as independent infectious units, recent work has shown that viruses are often transmitted as more complex structures, such as aggregates of virions or lipid vesicles harboring multiple infectious particles ("collective infectious units"). These recent discoveries lay the groundwork for the evolution of social interactions, a previously unappreciated facet of viruses. This project has investigated how collective infectious units drive virus-virus interactions. To do so, we have used the conceptual framework provided by the theory of social evolution, which had previously been validated in different types or organisms, but not in viruses. Our model systems have included enteroviruses, vesicular stomatitis viruses, baculoviruses and bacteriophages. Experimental work with these viruses has been complemented by simulations and modeling. We have shown that collective spread can provide viruses with an immediate fitness benefit that is most relevant during the early stages of infection. These benefits stem from faster production of viral progeny, which can help viruses stay ahead of innate immune responses. However, in the long term, collective spread may favor the emergence of defective viruses that function as social cheaters and have a negative impact on viral fitness. The emergence of cheaters depends on a number of factors, such as the genetic composition of collective infectious units, the spatial structure of the population, and the frequency with which collective infectious units are formed. The results of this project have been published in 16 original research articles and eight reviews, opinion articles or book chapters. The results have also been presented in multiple invited talks and congresses, as well as in journals, blogs and interviews aimed at the general public.
