RNA viruses have an error prone RNA dependent RNA polymerase, large population sizes, and rapid turnover, leading to the hypothesis that RNA viruses evolve over the course of an individual infection under the selective pressure of host immune responses.While this has been observed for chronic infections, to what extent is this observed for viruses that cause acute (shorter than two weeks) infections? How does it vary depending on the nature of host immune pressure? Working with John DeVincenzo and colleagues at the University of Tennessee Center for Health Sciences and at the Broad Institute, we use respiratory syncytial virus infections as a model and deep sequencing of longitudinal samples from an immunocompromised infant, healthy adults, and infants with their first infections to address these and related questions.
