Abstract
BackgroundReplicate 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.ResultsDespite 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.ConclusionsOur 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.
Highlights
Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science
We used monozygotic twins infected at birth from the same blood transfusion contaminated with Human Immunodeficiency Virus 1 (HIV-1) to study the association of population genetic and phylogenetic diversity with disease progression and clinical outcomes
We documented that these twins had very different clinical outcomes with twin A being relatively healthy compared to twin B. Associated with this slower disease progression in twin A, we found phylogenetic differences, higher growth rates, and higher genetic diversity in the HIV population and higher recombination rates in rt
Summary
Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. 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. RNA viruses serve as exciting models for testing this theory because of their potential for rapid evolution. A striking feature of the Human Immunodeficiency Virus 1 (HIV-1) is the rapid population dynamics resulting in a high degree of genetic diversity within and between infected individuals [5,6]. The virus can capitalize on this genetic diversity to evade a host immune response [7,8]. Viral evolution can be strongly shaped through antiviral pressure applied by the host’s immune system [11,12]
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