UCLA

In viral infections and cancer tumours, negative health outcomes often correlate with increasing genetic diversity. Possible evolutionary processes for such relationships include mutant lineages escaping host control or diversity, per se, creating too many immune system targets. Another possibility is social heterosis where mutations and replicative errors create clonal lineages varying in intrinsic capability for successful dispersal; improved environmental buffering; resource extraction or effective defence against immune systems. Rather than these capabilities existing in one genome, social heterosis proposes complementary synergies occur across lineages in close proximity. Diverse groups overcome host defences as interacting 'social genomes' with group genetic tool kits exceeding limited individual plasticity. To assess the possibility of social heterosis in viral infections and cancer progression, we conducted extensive literature searches for examples consistent with general and specific predictions from the social heterosis hypothesis. Numerous studies found supportive patterns in cancers across multiple tissues and in several families of RNA viruses. In viruses, social heterosis mechanisms probably result from long coevolutionary histories of competition between pathogen and host. Conversely, in cancers, social heterosis is a by-product of recent mutations. Investigating how social genomes arise and function in viral quasi-species swarms and cancer tumours may lead to new therapeutic approaches.