Abstract
Despite their simplicity, viruses exhibit certain types of social interactions. Situations in which a given virus achieves higher fitness in combination with other members of the viral population have been described at the level of transmission, replication, suppression of host immune responses, and host killing, enabling the evolution of viral cooperation. Although cellular coinfection with multiple viral particles is the typical playground for these interactions, cooperation between viruses infecting different cells is also established through cellular and viral-encoded communication systems. In general, the stability of cooperation is compromised by cheater genotypes, as best exemplified by defective interfering particles. As predicted by social evolution theory, cheater invasion can be avoided when cooperators interact preferentially with other cooperators, a situation that is promoted in spatially structured populations. Processes such as transmission bottlenecks, organ compartmentalization, localized spread of infection foci, superinfection exclusion, and even discrete intracellular replication centers promote multilevel spatial structuring in viruses.
Highlights
WHY SOCIAL VIRUSES?Consider a single cell coinfected by N identical viral particles, versus N cells infected by one viral particle each
High multiplicity of infection (MOI) regimes favor the emergence of defective interfering particles (DIPs), which function as molecular parasites of the normal virus (2, 3)
A general principle derived from social evolution theory is that, for cooperative traits to be maintained in populations, cooperators should preferentially interact with other cooperators
Summary
Consider a single cell coinfected by N identical viral particles, versus N cells infected by one viral particle each. The benefits provided to others come at the cost of reducing the fitness of the cooperator (altruism), as has been suggested for certain viral proteins involved in immunity evasion (6–8). This direct fitness cost needs to be compensated for selection to favor altruism. For cooperative interactions such as altruism to be evolutionarily stable, these have to be nonrandom, meaning that they should preferentially involve cooperators and thereby exclude cheaters Applying these principles to viruses should help us understand, predict, and even manipulate processes such as immune evasion, virulence, lysis regulation, and the emergence of defective viruses, among others. Genetically related members of the viral population, excluding cheaters and making cooperation evolutionarily sustainable
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