Viral biogeography revealed by signatures in Sulfolobus islandicus genomes
Article first published online: 30 OCT 2008
© 2008 The Authors. Journal compilation © 2008 Society for Applied Microbiology and Blackwell Publishing Ltd
Volume 11, Issue 2, pages 457–466, February 2009
How to Cite
Held, N. L. and Whitaker, R. J. (2009), Viral biogeography revealed by signatures in Sulfolobus islandicus genomes. Environmental Microbiology, 11: 457–466. doi: 10.1111/j.1462-2920.2008.01784.x
- Issue published online: 18 JAN 2009
- Article first published online: 30 OCT 2008
- Received 26 June, 2008; accepted 24 August, 2008.
Viruses are a driving force of microbial evolution. Despite their importance, the evolutionary dynamics that shape diversity in viral populations are not well understood. One of the primary factors that define viral population structure is coevolution with microbial hosts. Experimental models predict that the trajectory of coevolution will be determined by the relative migration rates of viruses and their hosts; however, there are no natural microbial systems in which both have been examined. The biogeographic distribution of viruses that infect Sulfolobus islandicus is investigated using genome comparisons among four newly identified, integrated, Sulfolobus spindle-shaped viruses and previously sequenced viral strains. Core gene sequences show a biogeographic distribution where viral genomes are specifically associated with each local population. In addition, signatures of host–virus interactions recorded in the sequence-specific CRISPR (clustered regularly interspaced short palindromic repeats) system show that hosts have interacted with viral communities that are more closely related to local viral strains than to foreign ones. Together, both proviral and CRISPR sequences show a clear biogeographic structure for Sulfolobus viral populations. Our findings demonstrate that virus–microbe coevolution must be examined in a spatially explicit framework. The combination of host and virus biogeography suggests a model for viral diversification driven by host immunity and local adaptation.