HIV-1 infected monozygotic twins: a tale of two outcomes
1 Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas, Health Science Center at Houston, School of Public Health, Brownsville Regional Campus, Brownsville, TX, USA
2 Laboratory of Molecular Retrovirology, Clinical Services Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, MD, USA
3 Clinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
4 Eunice Kennedy Shriver, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA
5 Collaborative Clinical Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
6 CIBIO, Centro de Investigação em Biodiversidade e Recursos Genéticos, Universidade do Porto, Campus Agrário de Vairão, Vairão, Portugal
7 Department of Biochemistry, Genetics and Immunology, University of Vigo, Vigo, Spain
8 Department of Biology, Brigham Young University, Provo, UT, USA
BMC Evolutionary Biology 2011, 11:62 doi:10.1186/1471-2148-11-62Published: 8 March 2011
Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. However, viruses, bacteria and phages provide opportunities to study evolution in both natural and experimental contexts, due to their accelerated rates of evolution and short generation times. Here we investigate HIV-1 evolution by using a natural model represented by monozygotic twins infected synchronically at birth with an HIV-1 population from a shared blood transfusion source. We explore the evolutionary processes and population dynamics that shape viral diversity of HIV in these monozygotic twins.
Despite the identical host genetic backdrop of monozygotic twins and the identical source and timing of the HIV-1 inoculation, the resulting HIV populations differed in genetic diversity, growth rate, recombination rate, and selection pressure between the two infected twins.
Our study shows that the outcome of evolution is strikingly different between these two "replicates" of viral evolution. Given the identical starting points at infection, our results support the impact of random epigenetic selection in early infection dynamics. Our data also emphasize the need for a better understanding of the impact of host-virus interactions in viral evolution.