The spread of viruses among cells, organs, and hosts is often mediated by structures that carry multiple viral genome copies, such as polyploid virions, virion aggregates, occlusion bodies, virus-containing lipid vesicles, and virological synapses. These structures increase the multiplicity of infection, defined as the number of viral genomes that initiate infection. High multiplicities of infection may promote the emergence of social-like virus–virus interactions, such as cooperation to evade immunity and/or antiviral treatments and division of labor, but also of noncooperative interactions such as negative dominance and interference. Collective infectious units may be exploited for retarding drug-resistance evolution, for producing attenuated viruses, or for codelivering different genetic variants of a virus to target cells/hosts.
Collective Infectious Units in Viruses. Trends Microbiol. 02 March 2017 doi: 10.1016/j.tim.2017.02.003
Increasing evidence indicates that viruses do not simply propagate as independent virions among cells, organs, and hosts. Instead, viral spread is often mediated by structures that simultaneously transport groups of viral genomes, such as polyploid virions, aggregates of virions, virion-containing proteinaceous structures, secreted lipid vesicles, and virus-induced cell-cell contacts. These structures increase the multiplicity of infection, independently of viral population density and transmission bottlenecks. Collective infectious units may contribute to the maintenance of viral genetic diversity, and could have implications for the evolution of social-like virus-virus interactions. These may include various forms of cooperation such as immunity evasion, genetic complementation, division of labor, and relaxation of fitness trade-offs, but also noncooperative interactions such as negative dominance and interference, potentially leading to conflict.