The genomes of penaeid shrimps and other crustaceans harbor endogenous nimaviruses, relatives of the devastating pathogen white spot syndrome virus (WSSV). Endogenous nimaviruses do not seem to cause disease in shrimp, and their gene sequences are so divergent that they do not cause false positives in PCR or antigen tests targeting WSSV. The discovery of endogenous nimaviruses proved extremely useful to investigate the evolution of WSSV, as it was previously thought to be an "orphan" virus whose relatives were not discovered at all. However, the reason why they are present remained unknown.
Genomic analyses revealed that endogenous nimaviruses insert exclusively into specific nucleotide motifs occurring in repetitive sequences, especially microsatellites. Penaeid endogenous nimaviruses target (TAACC/GGTTA)n repeats, which typically occur in the telomeres of arthropod chromosomes but are also dispersed throughout the chromosomes in penaeid shrimps. Motif-specific integration is enabled most likely by virus-encoded DNA recombination enzymes, the integrases. These observations suggest that endogenous nimaviruses are genomic parasites colonizing "niches" defined by repetitive sequences in the shrimp genome. Repeat-specific integration, which targets redundant parts of the host genome, can be seen as an adaptive tactic to minimize the possibility of destroying host genes, which could be lethal.
Endogenous nimaviruses challenge our conventional understanding of what viruses are and how they behave. With the discovery of diverse, benign relatives of WSSV, it appears that viruses may have the potential to coexist with, rather than harm, the host. The next challenge will be to uncover the mechanisms and evolutionary drivers that lead some viruses to become lethal pathogens, while others evolve into genomic “free-loaders”.