Multicomponent viral systems face specific challenges when enduring population bottlenecks. These systems can lose coding information due to the lack of co-encapsidation of all the genetic information, at least in a proportion of the capsids in a population. Moreover, bottlenecks can also impact one of the main potential advantages of multicomponent systems: the regulation of gene expression through changes in gene copy frequencies at the population level. How these systems cope with population bottlenecks is far from being clear. Here, two non-exclusive scenarios are described. In the first scenario, population bottlenecks during host infection allow for the isolation of within-host populations with different gene frequencies, leaving the door opened for the selection of populations with adaptive gene frequencies. The second scenario postulates that viruses could influence bottleneck size, at least at certain steps of their life cycle, to limit random changes in gene frequencies. Examples of viral mechanism impacting bottleneck size at cell infection are available and, intriguingly, they can lead to either increases or reductions in bottleneck size. This situation opens the way for putative trade-offs on both gene frequencies and bottleneck sizes that could differ among multicomponent systems.